Distribution of losses in an alternator for two different speeds (full excitation field).
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
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From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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The availability of affordable power diodes in the beginning of 1960s paved the way for the widespread use of three-phase claw-pole alternators (or Lundell alternators) for the generation of electric power in motor vehicles. After more than 50 years, this system is still the most economic choice in today’s vehicles due to its low manufacturing cost. However, the efficiency and output power of the Lundell alternators are limited. This is a major drawback for its use in modern vehicles requiring an increase in electrical power. Many alternatives are being considered to replace the Lundell alternator such as the salient pole machines, however they require large investments in manufacturing infrastructure. In this context, this chapter focuses on the improvements of Lundell alternators that could represent the best solutions for the short term. First, we present the conventional automotive generating system, its performance and the limitation of modelling methods. We also discuss various solutions to increase the output power of Lundell alternators without any geometry modification. These include the use of reconfigurable windings and replacement of the diode rectifier by different electronic converters such as a synchronous rectifier or an interleaved PWM rectifier will be considered.
Today, the great majority of electrical generator systems installed on combustion powered vehicles are based on a three-phase wound-field synchronous machine. The conventional automotive generator has a claw pole rotor with a single excitation coil wound axially. It is often named “Lundell” alternator (Fig. 1). The excitation coil is surrounded by two solid iron pole pieces, or claw poles, and is fed via a pair of slip rings and two carbon brushes. The stator is composed of a slotted laminated iron core and a three-phase overlapped winding, wye or delta connected. It is a wave-winding in most cases. Fig. 1 shows a dismantled Lundell alternator (Delcotron 22SI) and its main components. The number of rotor poles for passenger vehicles is generally fixed at 12 poles. The stator has often a single slot per pole and per phase (36 total slots). High power alternators for some applications like buses, trucks or other special vehicles have higher pole numbers (between 14 and 18). Increasing the number of poles reduces the inductance of the stator winding, and as a result, increases the short circuit current. Unfortunately the magnetic losses will also increase due to the higher electrical frequency. So the choice of pole number is actually based on a compromise between the magnetic losses and alternator power requirements. The alternator is coupled to the combustion motor through a belt. In passenger cars the maximum alternator speed (typically 8000 RPM) is about two times more than that of the engine crankshaft (a pulley ratio of 1:2). The Lundell alternator is generally characterized by its form factor (a relatively large diameter compared to its length) which facilitates thermal dissipation.
Dismantled alternator parts: (a) 6 diode full- bridge power rectifier, (b) excitation rectifier, (c) regulator, (d) brush assembly, (e) aluminum rear housing, (f) stator winding, (g) stator laminated core, (h) aluminum front housing, (i) aluminum fan, (j) slip rings, (k) excitation winding, (l) claw-shaped pole pieces.
Fig. 2 shows the simplified schema of a vehicle generation system. Usually six diodes in a full-bridge configuration are used to rectify the output current. The rectifier is divided in two sets of three diodes. The metal casing of the first set is typically pressed into a heat sink (or welded to the heat sink) for better thermal dissipation.
The output power is controlled by regulating the field current. The regulator maintains a constant output voltage on the battery despite the varying alternator speed and variable load conditions. This voltage depends highly on the ambient temperature and the chemical characteristics of the battery and necessitates a temperature compensation by the regulator. The regulator-excitation circuit is often supplied by an additional half- bridge rectifier instead of the battery (Exciter rectifier).
In the alternators with wye connected windings, two or more other auxiliary diodes are connected between the neutral point and the main rectifier output terminals. In this way it is possible to rectify the induced third harmonic voltage and increase the output current at high speeds.
Simplified schema of conventional vehicle generating system with a Lundell alternator.
Performance curves of an alternator are used to show its performance across the whole speed range. Fig. 3 shows the performance curves of a 100A commercial alternator obtained for a battery voltage of 14 V, an ambient temperature of 25 C, and for the maximum excitation current (near 6A).
The output current curve is characterized essentially by three operation points. The first one is the generation starting speed (ΩDG) or 0-Ampere speed at which the alternator reaches its rated voltage without delivering power. The second one is the maximum output current at the highest speed, which corresponds approximately to the DC short-circuit current of the alternator (ISC). Also, a special attention is paid to the output power requirement at engine idle speed (ΩR) at which the alternator must deliver at least the power needed for long-term consumers. No output power is required below the idle speed. Another operating point often mentioned is the speed at rated current (ΩN).
Generally, Lundell alternators are characterized by low efficiency due to important mechanical, copper, and magnetic losses. The efficiency of the alternator varies widely depending on load conditions, alternator speed and alternator size. As shown in Fig. 3, the efficiency is only 53% at idle speed (losses: 675W) and about 42% at 6000 RPM (losses: 2100W). Larger and heavier alternators may be more efficient for the same speed and load conditions, however, this advantage can be compensated by the increase in fuel consumption due to the higher weight (0.1 L/100km fuel consumption for each additional 10 kg for a medium sized vehicle)(Beretta, 2008). Table 1 shows the distribution of losses in an alternator (Beretta, 2008) for two different speeds (full excitation field).
Characteristic of the output maximum current and efficiency as a function of speed for an alternator (Delcotron 22SI type12V-100A) at a battery voltage of 14V, ambient temperature of 25 C and maximum excitation current.
1800 RPM | 6000 RPM | |
Mechanical losses | 2% | 6% |
Excitation losses (rotor) | 7% | 3% |
Magnetic losses (stator) | 21% | 20% |
Copper losses (stator) | 49% | 57% |
power rectifier losses | 21% | 14% |
Distribution of losses in an alternator for two different speeds (full excitation field).
Mechanical losses are generated by brush and bearing friction and losses created by the claw pole rotor and fan (windage losses). The mechanical losses increase considerably at higher speeds (Bosch, 2003). In the current air cooled alternators, one or two fans are used for convection cooling. These fans add to the alternator (aerodynamic) losses and are also responsible for an important part of the alternator audible noise at higher speeds.
As shown in Table 1, the main losses in the alternator are the stator copper losses. Increasing the filling factor will reduce copper losses, however, this is limited by the industrial production constraints (Beretta, 2008).
Other sources of ohmic losses include the losses in the rectifier diodes, regulator losses and and losses occurring due to the contact resistance between the slip rings and brushes.
At nominal excitation current and at lower speeds, the output current is low and the stator is fully saturated due to the weak magnetic reaction. This will result in important magnetic losses in the stator core. Increasing the speed and output current while maintaining the same excitation reduces the flux density in the stator. With this demagnetisation effect the magnetic losses become proportional to speed itself rather than the square of speed (as expected in no-load conditions). Reducing the lamination thickness can lead to a significant reduction of the magnetic losses (0.5 mm or 0.35 mm instead of 1 mm).
Since the claw pole parts are made of solid forged iron, the eddy currents can easily circulate. This will also add to magnetic losses at very low speeds and low loads where the flux density in the air-gap (generated mainly by excitation field) is modulated by the stator slot openings. At higher speeds, the stator magneto-motive force (MMF) produces space harmonic fields in the air-gap which are augmented by the slot openings and again produce claw-pole eddy currents (Boldea, 2006). To reduce magnetic losses in the rotor, it is possible to use a laminated material but the assembly process is more complex (Bretta, 2008).
An efficient cooling method is necessary to limit the temperature in the motor beyond the permissible limits (a junction temperature of 200 C for the diodes and the stator winding).
The thermal dissipation in an alternator is mainly by convection through one or two cooling fans. The small amount of heat generated in the rotor can be dissipated by conduction through alternator bearings.
As an alternative to air cooling, it is possible to cool the alternator more efficiently with a circulation of the engine coolant in the alternator housing. It also reduces the alternator’s noise level by omitting the cooling fan(s).
In order to evaluate the performance of the alternator under variable load conditions, both the machine and rectifier systems shall be modeled with appropriate magnetic and electrical models.
A 3-phase synchronous machine can be modeled by its equivalent circuit as shown in fig. 4. The parameters of the electrical alternator model are derived from the no-load EMF versus rotor field current characteristic EV(jrotor) and the short circuit characteristic ICC(jrotor). The stator cyclic inductance (L(jrotor)) is derived from both tests by applying Eq. 1 where ω is the electrical frequency.
Equivalent circuit model of a 3-phase synchronous machine
A high rotor field current produces magnetic saturation and the stator inductance value decreases. The accuracy of such a model highly depends on the parameters identification or computation method. The armature phase resistance is measured at the rated temperature rise.
It is possible to evaluate analytically the steady state performance of a 3-phase alternator -rectifier system connected to a voltage source (fig. 5) as shown in (Figueroa et al., 2005). This type of modeling uses the electrical equivalent circuit of the machine to directly determine the steady state copper losses, current harmonic contents and DC bus current.
It is faster than a step by step simulation method as employed by simulators for power electronics (PSIM, Saber) and it is well adapted for use within an optimization loop for system evaluation purposes. However, it uses simplifications which compromise the accuracy of the results including rotor saliency, and magnetic losses in the machine.
To evaluate the simulation method, an experimental set-up is used to compare the output performance of the alternator with various rectifier topologies (fig. 6). Torque is measured by a rotating torque sensor and a strain gauge. The alternator is driven by a 5 kW DC motor via a belt and pulley system. A position encoder is also available. The rectifier has been taken out from the machine and the voltage regulator has been removed so that the excitation current could be imposed using an external current source. The same experimental set-up will allow the comparison of various converter topologies and winding configurations for alternators. It has been used for all the experimental work presented in this chapter.
Circuit model of a generation system with a diode rectifier
Test bench, a) converter (b) conventional rectifier, (c) alternator, (d) torque sensor, (e) position sensor, (f) DC motor
Fig. 7 shows the characteristics of the output maximum current and efficiency versus speed provided by the manufacturer along with those obtained by simulation. The simulation slightly overestimates the output current particularly in the central part of the curve. This could be explained by the absence of magnetic losses in the simulation, assumption of a sinusoidal EMF and inaccuracies in parameter identification. Despite these drawbacks, it can be seen that the proposed model is able to provide a current versus speed curve of satisfactory accuracy. In the same figure, it can be seen that the absence of the magnetic and mechanical losses leads to a significant overestimation of the efficiency.
Comparative analysis of simulation and experimental results (from manufacturer) of the alternator output characteristics
The use of a PWM controlled rectifier (fig. 8) instead of a diode rectifier allows for the following main benefits: boosting operation for increasing the output power at low speed and power factor correction in the machine for maximization of output power.
In Lundell alternators, the magnetic circuit is saturated for the rated field current. With a Conventional Diode Rectifier (CDR), the armature reaction always has a demagnetizing effect since the voltage is in phase with the current. In case of controlled rectifiers, the armature reaction can have a magnetizing effect at low speeds depending on the power angle. Therefore, the power increase due to power angle control is less significant than what one could expect when magnetic saturation is increased by the armature reaction. As shown in Fig. 7, the simplified electrical model provides a good current estimation in the case of the diode rectifier while the magnetic saturation of armature field is neglected. This is not the case with a PWM rectifier and the output current is often over estimated by the simulation as shown in fig. 9.
Circuit model of a generation system with a PWM controlled rectifier
The output current obtained by simulation for a diode rectifier and a PWM full-bridge rectifier compared to experimental results
Different magnetic models can be used to compute the parameters of the machine’s equivalent circuit, provided that they take account of magnetic saturation.
A first one is based on a magnetic reluctance network that takes into account the machine geometry and the magnetic material B(H) characteristic (Ostovich et al., 1999). The analytical method based on the reluctance network is fast due to its simplifying assumptions.
A second method is based on 3 Dimensional Finite Element (3D FE) modeling (Küppers & Henneberger, 1997) which is particularly interesting for the analysis and evaluation of saturation and magnetic losses. Finite element methods are the most accurate but are time consuming for a variable speed machine and under variable load conditions.
Fig. 10 shows the results of 3D FE simulation of a claw pole alternator with 36 slots and 12 poles. With the 3D FE modeling, the electrical parameters of the alternator can be directly obtained by applying two methods: a method using the scalar potential and another one using the vector potential (Cros et al., 2008). Fig. 11 shows the output current versus speed characteristics obtained with the electrical parameters of scalar potential and the vector potential models. The right characteristic is between the two curves (Henneron et al., 2004).
The results of 3D FE simulation of a claw pole alternator
Simulated DC current output vs speed characteristics with two 3D FE methods
This section focuses on various possible solutions to increase the output power of Lundell alternators without any geometry modification. This can be achieved by a winding reconfiguration to modify the number of turns per phase. A low number of turns increases power at high speed and a high number of turns improves the idle current. Another way is to rewind the alternator with a lower number of turns and to replace the conventional diode rectifier by an active PWM rectifier. The active rectifier boosts the alternator voltage in order to attain acceptable performances during low speed operation.
The number of turns in the stator winding has a significant effect on the output performances of an alternator connected to a Conventional Diode Rectifier (CDR) and a battery. The output current and the efficiency during high-speed operation can be easily increased by reducing the number of conductors per phase. However, the reduction of the number of turns presents also an unacceptable drawback which is a severe reduction of the output power during idle operation. On the other hand, one should increase the number of turns to improve performance at low speeds.
If the total copper cross section is not modified, the maximum current density is always the same and so the copper losses are not increased. Equation (2) shows the electrical parameters variation of the stator equivalent model (resistance R, cyclical inductance L and no-load flux Φ) according to the number of conductors per slot N when the total copper cross section is kept constant.
Fig. 12 shows a comparison of output characteristics with a number of turns per phase divided by two. The stator winding with the highest number of turns halves the speed of the generation starting point but it produces twice less output current during high-speed operation. One can notice that the winding with twice less turns provides better performance (higher current with lower copper losses) as soon as the speed exceeds 2700 rpm.
Winding reconfiguration is an interesting approach to improve output power, efficiency and satisfy idle current specifications.
One solution is to divide each phase winding in several coil groups and to modify the winding configuration by using several switches. It is then possible to obtain different connections of the coil groups (parallel, series, delta, wye) as a function of the speed. Fig. 13 shows the delta-wye and the series-parallel reconfiguration (Liang et al., 1999).
Influence of winding number of turns on the output performance with a diode rectifier
a) Series- Parallel reconfiguration, b) Wye- Delta winding reconfiguration
One can also use a multi-winding stator with different number of turns to adapt the output characteristics (output current and efficiency) with a single voltage output. In this case, the different windings are connected to different diode rectifiers and must be magnetically decoupled (Cros et al., 2003). In order to compare the relative performance, we consider a given stator with the electrical parameters of a single-winding configuration (L0, R0 and Φ0). Equation (3) shows the new electrical parameters of a m-winding configuration in the same stator.
If we consider m=2, it is possible to optimize the first winding system for the lower speeds and the second one for the higher speeds by choosing the right number of turns in each winding while maintaining the same copper volume per slot. For example, one may use N conductors for the first winding and N/2 conductors for the second one, as shown in fig. 14.
Fig. 15. shows a comparison of output characteristics between a single-winding configuration with N conductors per slot and the double-winding configuration of fig. 14. Note that the double-winding configuration provides higher output current when the speed is greater than 2700 rpm but the current is reduced at low-speed.
Multi- winding alternator with a number of turns equal to N for the first winding and N/2 for the second one.
Performances comparison with a multi-winding stator configuration
To improve the performance over the whole speed range, it is more interesting to use the same number of turns in the two winding systems and make parallel/series reconfigurations at the rectifier outputs as shown in fig. 16. This method is easier to implement than the AC phase winding reconfiguration. It uses only one unidirectional switch and two additional diodes. Fig. 17 shows the performances of a double-winding configuration using the same number of conductors per slot as the original single-winding. A series connection provides the same output current as the original alternator, during low-speed operation when diode voltage drop is neglected. Once the speed exceeds 2700 rpm, a parallel connection is used to obtain higher output current and lower copper losses.
Reconfigurable parallel/series diode rectifiers
Performance of reconfigurable parallel/series diode rectifiers
The winding scheme of a reconfigured alternator compared to the original one (Delcotron 22SI Type 12V-100A) is depicted in Fig. 18. In order to minimize the magnetic coupling, the first 3-phase winding is wound using half stator (18 slots) and the second 3-phase winding using the other half. The new lap windings have the same coil pitch as the original alternator and 12 conductors per slot. The alternator parameters are given in Table 2. The magnetic coupling between the two 3-phase winding systems has been measured for different rotor positions and the maximal measured mutual inductance between them reaches 4% of the measured self-inductance.
Assuming that magnetic coupling is negligible, the electrical parameters of a multiple three phase winding system can be computed from the original alternator parameters (L0, R0, ΦNL0 with N0 conductors per slot). When the same stator is rewound with m three-phase windings and N conductors per slot, the new electrical parameters can be expressed as:
The analysis of these equations and the experimental results (Table 2) confirms that both winding systems are magnetically decoupled.
Original | Rewound | Double-Winding | |
Armature connection | Delta | ||
Pairs of poles | 6 | ||
Stator slots number | 36 | ||
Nominal field current | 6 A | ||
Turns per slot | 11 | 6 | 12 |
Wire cross section | 1.75 mm2 | 3.30 mm2 | 1.65 mm2 |
Resistance at 25°C | 0.1 Ω | 0.035 Ω | 0.07 Ω |
Cyclic Inductance (If = 6A) | 390 µH | 115 µH | 225 µH |
No-load flux (If = 6A) | 28.6 mWb | 15.8 mWb | 16.0 mWb |
Generation-starting speed (If = 6A ) | 910 rpm | 1670 rpm | 1650 rpm |
Output current at 8000rpm (If =6A) | 116 A | 215 A | 218 A |
Efficiency at 8000rpm (If = 6A) | 38 % | 53 % | 53.5 % |
Alternator parameters (Delcotron 22si type 12v-100a)
Winding scheme: (a) original 3-phase Delcotron alternator, (b) double-winding Delcotron alternator
A synchronous rectifier is an interesting alternative to conventional diode rectifiers. The main advantage of such converters is the reduced rectifier losses particularly at higher speeds if MOSFETs with low on-resistance (e.g. 4 mΩ (Beretta, 2008)) are used. Besides, it may be also employed in applications where bidirectional power transfer is required such as stop-start system (Beretta, 2008). In a start-stop system developed by Citroën, the claw-pole machine performs the functions of both starter and alternator. In the starter mode, the phase current and EMF in each phase are synchronised for maximum torque using a position sensor. In the alternator mode, the converter operates as a synchronous rectifier. The voltage drop may be as low as 0.2 V for an output current of 120 A in contrast to 0.8 V to 1.1 V for a diode. The losses can be 60 % lower compared to a diode rectifier (Beretta, 2008). In both modes of operation the switching losses will be much lower than PWM converters due to lower switching frequency. In the alternator mode the switching frequency may be as high as 2800 Hz (at 4000 rpm), however the drain currents are kept close to zero during MOSFET switching (Beretta, 2008).
In order to exploit the alternator at its maximum capabilities, it is interesting to set an optimum power angle as proposed in (Liang et al.,1999) and (Liang et al.,1996). This can be achieved with a PWM full-bridge rectifier (PFBR) as already shown in fig. 8. For each point of operation, the modulation index k and the angle θ between phase voltage and back-EMF are adjusted to maximize the output power with sinusoidal PWM control.
A PFBR is a quite expensive and complex solution; it counts for several active switches and requires rotor position sensing or complex sensorless algorithms (Boldea, 2006). However, like a synchronous rectifier, it offers bidirectional power flow control.
Fig. 19 shows the maximum output current and efficiency obtained by using a sinusoidal PWM and a control technique maximizing output power. It also shows the output current curves obtained with original and rewound alternators connected to a conventional diode rectifier. If compared to the rewound alternator with CDR (RACDR), the PFBR connected to the same alternator increases the output power for speeds below 4000 rpm. (For winding parameters see Table 1). During high speed operation, it is preferable to operate in synchronous rectification mode.
Experimental output current and efficiency vs. speed using a PFBR
The comparison of the output current characteristics with the original alternator shows that the current generated with the PFBR is lower in the range of 1000 to 2000 rpm (Fig. 19). Note that idle power requirement is not satisfied with the PFBR. This is partly due to the magnetic saturation and significant voltage drops across active switches.
If bidirectional power flow is not required, the three single-phase BSBR structure shown in fig. 20 is a simpler solution. It has twice less active switches and all of them are referenced to the ground. Active switches can be reduced to only one using a Boost Switched-Mode Rectifier (BSMR), shown in fig. 21. With this topology, it is not necessary to use a rotor position sensor but the power angle can’t be controlled.
All presented PWM rectifier topologies deliver an output DC current with abrupt current steps and high di/dt’s. These high-amplitude fast-moving current transitions generate RF noise that flows to the battery and then pollutes other loads connected to the battery. Attenuation of these current variations to an acceptable level requires a very large output capacitor. This can lead to considerable efforts to comply with EMC standards (Maxim, 2001). Battery current ripple results in battery heating and a corresponding rise in temperature.
Boost semi-bridge rectifier (BSBR)
Boost switched-mode rectifier (BSMR)
Benefits of interleaved converters on current ripple, components stress and EMI reduction are well known for several different applications (Consoli et al., 2004), (Crebier et al., 2005). The main constraint of interleaved structures is the magnetic coupling between the different windings. Both converters must be connected to different three-phase windings that are not magnetically coupled to avoid a decrease of performances. Fig. 22 shows an example of two interleaved BSMRs with two identical three-phase winding systems having a same back-EMF. Q1 and Q2 are driven by two signals having the same duty-cycle and the same frequency but the phase is shifted by 180 degrees.
Two interleaved BSMRs connected to two identical three-phase windings
Interleaving decreases the current ripple for any value of duty-cycle and it allows for total ripple cancellation when D = 0.5. Equation (5) gives the optimal duty-cycle for a number m of interleaved rectifiers where ki is an integer.
The structure of fig. 23 could be also implemented using the double-winding stator system presented above and two BSMRs operated with fixed optimal duty-cycle (D = 0.5). The rectifier control is thus extremely simple and no position sensing is required. Experimental current waveforms are shown in fig. 23 (left). When comparing the output current ripple with the one obtained with the non-interleaved converter presented in fig. 23 (right), one can appreciate the considerable output current ripple reduction due to interleaving. (from 66A rms to 6.1A rms).
It is also interesting to operate two interleaved BSBRs with a fixed duty-cycle of 0.5 to obtain an ideal ripple cancellation. Hence the simplest control mode consists in driving all the switches of the first converter with the same gate signal and all the switches of the second converter with the same complementary signal. This method doesn’t require additional rotor position sensing. Since the duty cycle is fixed at 0.5, no more control of the power angle is achievable.
The BSBR has a voltage drop per device less than the BSMR. This leads to better performance over the whole speed range
Experimental current waveforms for: left) interleaved BSMRs; right) non-interleaved BSMRs, at 2000rpm with If = 6A. (Vertical scale: 60 A/div, horizontal scale:200 μs/div)
To compare the power improvement provided by the different rectifier topologies, the average power output Pavg. and efficiency avg. are estimated over the same drive cycle (a combination of the two vehicle speed cycles EPA UDDS and EPA US06) using the steady state performance curves with the rated field current. The results are given in Table 2.
Over the same driving cycle, the average power increase with respect to the original alternator ranges from 62% to 67% depending on the topology. The average efficiency has been improved by 10.6 to 11.5 percentage points.
The average output power and the efficiency are very similar for all the structures connected to a rewound machine since all structures regain the conventional diode rectifying mode during high-speed operation. In fact, the controlled rectifier is essentially used at idle speed.
Remarkable differences are although noticeable on the idle mode output power. Note that none of the topologies regains the original idle power. The closest idle power is obtained with the CSPR (-13%). Furthermore, the BSMR and BSBR deliver surprisingly more output power when interleaving is used. This can be partially explained by lower ESR losses in the output capacitor. However, the fact that two different machines are used (single-winding alternator and double-winding alternator) can have an influence too.
The approximate cost estimation for each solution can be derived from the number and ratings of the semiconductors and from the output filter size. It is assumed that the machine cost is not affected by rewinding and the filter size is proportional to the AC ripple component of the output current.
For semiconductors sizing, only rms current ratings are taken in account. In fact, in all topologies, each switch has to withstand the same reverse voltage which corresponds to VOUT (voltage transients neglected). Current ratings are normalized with respect to ISC. Table 3 shows the parts count and their ratings for each topology.
Topology | Pidle | Pavg. | (avg. | ||
Original Alternator | 1059W | 1.0pu | 1454W | 1.0pu | 42.4% |
Rewound alternator with PFBR | 899W | 0.85pu | 2430W | 1.67pu | 53.6% |
Rewound alternator with BSBR | 831W | 0.78pu | 2413W | 1.66pu | 53.9% |
Rewound alternator with BSMR | 779W | 0.74pu | 2350W | 1.62pu | 53.4% |
Double-winding alternator with interleaved BSBR | 869W | 0.82pu | 2419W | 1.66pu | 53.8% |
Double-winding alternator with interleaved BSMR | 799W | 0.75pu | 2353W | 1.62pu | 53.0% |
Double-winding alternator with CSPR | 918W | 0.87pu | 2389W | 1.64pu | 53.5% |
Idle power, average output power and efficiency over the same driving cycle for each topology
In the case of interleaved structures, semiconductor parts are multiplied by two. However, the active silicon area remains the same and distribution of switching power can eventually even be advantageous. Also note that for non-interleaved structures using PWM, the rms value of the ripple component of the output current is about 10 times more significant than with other structures. The resulting filtering requirements for EMC standards compliance can easily lead to bulky and expensive solutions.
Topology | Number of Slow diodes | Slow diode rms current (ISD) | Number of Fast diodes | Fast diode rms current (IFD) | Number of Active switches | Active switch rms current (IQ) | Output current AC ripple (IAC) |
Original Alternator | 6 | 0.52pu | - | - | - | - | 0.04pu |
PFBR | - | - | 6 | 0.52pu | 6 | 0.37pu | 0.48pu |
BSBR | 3 | 0.52pu | 3 | 0.52pu | 3 | 0.37pu | 0.5pu |
BSMR | 6 | 0.52pu | 1 | 1.0pu | 1 | 1.0pu | 0.5pu |
Interleaved BSBR | 6 | 0.26pu | 6 | 0.26pu | 6 | 0.18pu | 0.04*pu |
Interleaved BSMR | 12 | 0.26pu | 2 | 0.5pu | 2 | 0.35pu | 0.04*pu |
CSPR | 12 | 0.26pu | 2 | 0.5pu | 1 | 0.5pu | 0.04pu |
Semiconductor parts count and normalized current ratings for each topology
The low efficiency and the limitation of the output power are major drawbacks of the Lundell alternator. Replacing these alternators with other types of machine is not an economic choice because of their low manufacturing cost. However, improving the performance of existing machines is still the best way for the short term future. This chapter discusses the performance of the conventional automotive alternators and various modeling methods for the simulation of the alternator-rectifiers. Some improvements without geometry modification have been proposed and validated using standard frame of automotive alternator. The results show that the modification of the number of turns and replacing the diode rectifier with other electronic converters could significantly increase the output current and the efficiency. However, there are many other possibilities for enhancing the performance which have not been considered. For example, the transition from 14V to a 42V system, will allow to increase the efficiency of the power electronics rectifier by reducing the conduction losses. The optimization of the claw-pole machine, the use of hybrid structure with permanent magnets, laminations of higher quality, and liquid cooling are alternative methods to enhance the performance.
At present, metformin is the preferred first-line drug used for the treatment of type 2 diabetes mellitus (T2DM) [1, 2, 3, 4]. However, the journey of metformin (1,1-dimethylbiguanide hydrochloride) has not been a simple one. Galega officinalis, also termed as French lilac, Italian fitch, or Spanish sainfoin, the herb metformin derives from, has been known as a traditional medicine since the seventeenth century and was recommended for the treatment of thirst and frequent urination (symptoms of diabetes) by John Hill in 1772. The identification of guanidine and of its related compounds within Galega officinalis, which proved to be able to reduce blood glucose in animals, led to the synthesis of metformin (dimethylbiguanide) in 1922. However, it was only in the 1950s that more information on metformin’s properties was published and when the name of Glucophage, meaning glucose eater, was suggested by Jean Sterne. Metformin was introduced as a treatment for T2DM in 1958 in the UK and in other European countries, whereas in the USA it was approved only in 1994 and started to be used beginning in 1995 [5]. A milestone multicentre trial, the United Kingdom Prospective Diabetes Study (UKPDS) in 1998, showed that the newly T2DM diagnosed patients receiving metformin for more than a decade displayed significant reduction of the cardiovascular events and of diabetes-related death and highlighted that these effects were independent of the glucose-lowering efficacy. Moreover, the potentially beneficial effects of metformin on the macro- and microvasculature have also been revealed [5, 6, 7, 8]. Finally, in a 10-year posttrial analysis, metformin continues to offer cardiovascular benefits [9]. Based on these evidence data, in 2009, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) indicated metformin as the first-line therapy for T2DM [10]. Furthermore, metformin holds a significant role in the delay/prevention of T2DM onset, as shown by the randomised trial conducted in the USA, i.e. the Diabetes Prevention Program (DPP). The study highlighted that metformin reduces the incidence of T2DM by 31% compared to placebo in adults at high risk for T2DM (obese and with impaired glucose tolerance) [11, 12, 13, 14]. Hence, metformin is also recommended as a pharmacologic tool for the prevention of T2DM in subjects with prediabetes, mainly for those with a BMI ≥ 35 kg/m [2], those aged <60 years, and in women with prior gestational diabetes mellitus [15, 16, 17].
Ageing continues to be an intruding topic and an area of great interest, constantly addressed by researchers worldwide. It encompasses a plethora of complex processes that have urged scientists to decipher its underlying mechanisms and to find the possible avenues to postpone its onset and that of its associated diseases [18]. Data from the literature have demonstrated a sustained ageing of the world’s population, estimating a total of around 21.8% of subjects over 60 years old in 2050 and 32.2% in 2100 [19]. Installed as a result of the interaction between genetic, epigenetic, environmental and stochastic factors, ageing involves a progressive decline of the body functions as a consequence of the gradual cellular impairment due to a failure of the repair mechanisms [20, 21, 22, 23]. Age is a major risk factor for the onset of metabolic, cardiovascular, neurodegenerative, immune and malignant diseases [24]. Ageing has been reported to be conditioned by the genetic factor in a proportion of 25–30%, while the remaining 70–75% is ruled by the environmental factor, making it a possible target for therapeutic tools among which metformin has been found [25, 26].
Beyond its blood glucose-lowering effect, metformin has been described as a drug used for preventing or delaying several conditions associated with ageing [27]. As such, metformin has been proven useful in overweight and obesity [28, 29], hypertension [30], atherosclerosis [31], coronary artery disease [32], dementia [33] and cancer [34]. Moreover, in terms of mortality [35], it has been shown that patients with T2DM under metformin monotherapy had a longer survival than the matched, nondiabetic controls. However, the precise beneficial mechanisms by which metformin performs its non-glycaemic work are yet to be analysed. Hence, given the complex mechanisms of action of metformin, there is a growing interest in approaching and studying the potential anti-ageing effect of this drug. With regard to this interest, some large randomised clinical trials have been recently set up in order to evaluate the potential role of metformin in reducing the burden of age-related diseases. The Investigation of Metformin in Pre-Diabetes on Atherosclerotic Cardiovascular outcomes (VA-IMPACT) trial is a placebo-controlled study started in February 2019 and aimed at shedding light on the potential role of metformin in reducing mortality and cardiovascular morbidity in patients with prediabetes and established atherosclerotic cardiovascular disease. More precisely, the primary outcomes include the time to death from any cause, nonfatal myocardial infarction, stroke, hospitalisation for unstable angina, or symptom-driven coronary revascularisation [27]. The other clinical trial, also a placebo-controlled trial, i.e. Targeting Ageing with Metformin (TAME), investigates subjects who have been diagnosed with one single age-associated disease and will provide insight on the ability of metformin to postpone and/or prevent the installation of a second pathology, such as cancer, CVD and dementia [13, 36]. Finally, more information is needed for a better understanding of the mechanistic targets and therapeutic implications of certain drugs (such as metformin) that might delay/alleviate the development of age-related diseases [37].
Herein, we revisit the mechanisms involved in ageing and the mechanistic target of metformin as a potential anti-ageing drug, and we review the available data on the clinical and experimental results showing the ability of metformin to promote healthspan and longevity.
A large body of evidence has demonstrated that metformin could be considered a geroprotective agent in humans [23]. As explained, the protective role of metformin in survival has been largely demonstrated by the UKPDS multicentre trial in terms of cardiac and all-cause mortality, as compared with usual care [8, 9]. However, given its main role, that is to reduce hyperglycaemia, and knowing that a good control of diabetes correlates with an extended lifespan, the question arises whether metformin could be accounted as a tool to prolong longevity in patients that do not display T2DM. In keeping with this question, a recent systematic review by Campbell et al. [23] summarised the studies in which the effects of metformin on all-cause mortality or diseases of ageing have been compared to the nondiabetic or general population or to diabetics controlling the disease through other means. Overall, the meta-analysis revealed that subjects with T2DM under metformin treatment have a lower rate of all-cause mortality and longer survival than people free of T2DM not using metformin and the general population, suggesting that this drug could be an effective instrument to extend the lifespan of those not affected by T2DM [23, 35, 38, 39, 40]. Moreover, the meta-analysis revealed that subjects with T2DM taking metformin had lower rates of all-cause mortality than those following other therapies, such as insulin or sulphonylurea [23]. Given these results, it may be argued that the outcome is attained by the geroprotective role of metformin resulting in delaying or preventing diseases of ageing, such as cancer or cardiovascular disturbances, which are the two most encountered ageing-related diseases [23, 41]. Firstly, in terms of malignancies, Campbell et al. [23] showed that people with T2DM taking metformin had a lower rate of developing any cancer compared with the general population. Moreover, the risk of developing colorectal, breast or lung cancer in individuals with T2DM on metformin treatment, as compared to those using other therapies, was lower. Secondly, subjects with T2DM following metformin therapy displayed a lower rate of any form of cardiovascular disease with respect to those managing their T2DM through any non-metformin therapy. In addition, although the incidence of stroke was also lower with metformin, for myocardial infarction the effect of the drug seems to be non-significant [23].
Finally, apart from the cardiovascular diseases and cancer, there are also other age-related pathologies that could be targeted by metformin, such as cognitive dysfunction. However, the evidence in patients with T2DM is conflicting with some studies showing a protective role of metformin against cognitive decline, whereas others are arguing that metformin treatment could induce neurodegeneration as well as Parkinson’s and Alzheimer’s disease. Nevertheless, the interpretation of the data is difficult given the possible presence of other concomitant conditions that may contribute to this cognitive decline [42].
Ageing is a complex process that occurs at the molecular, cellular, organ and organismal level that everyone faces in time [43]. It involves the loss of the body’s ability to overcome and respond to stress (homeostenosis) by repair and regeneration, thus leading to various disturbances within the human body [24]. Overall, the ageing processes are of a heterogeneous and heterochronic nature. As a heterogeneous process, ageing can evolve at different rates in diverse organisms, while the heterochronic feature implies that cells and tissues within a single organism can age in an asynchronic manner, finally making chronological age different as compared to biological age [24, 43]. Growing body of evidence has shown that ageing involves multiple mechanisms that inter-relate with and modulate each other. In this respect, two elegant reviews have described nine hallmarks of ageing, which have been classified into primary hallmarks (genomic instability, telomere attrition, epigenetic alterations, and loss of proteostasis) as the main culprit of molecular damage, antagonistic hallmarks (deregulated nutrient sensing, mitochondrial dysfunction, and cellular senescence) with beneficial effects when at low levels, by protecting the human organism against damage, but with deleterious effects when at high levels, and finally, the integrative hallmarks (stem cell exhaustion and altered intercellular communication) that arise when the accumulating damage cannot be balanced by homeostatic mechanisms, thus ultimately inducing ageing [22, 36].
Genomic instability has been revealed to be a major stochastic mechanism of ageing [44, 45]. Broadly, deoxyribonucleic acid (DNA) damage can be induced by both exogenous genotoxic factors, such as ionising radiation and ultraviolet irradiation as well as endogenous genotoxic agents, i.e. products of normal metabolism that lead to the formation of reactive oxygen species (ROS) and subsequently to oxidative stress, that may finally result in deleterious effects on the cell. DNA lesions can cause mutations, block transcription and replication but can also trigger DNA damage response (DDR), which implies mechanisms that intervene and arrest cell cycle progression, resulting in the repair of almost all the alterations that occur within the genome. However, when DNA damage is extensive and prevails over repair, DDR effectors trigger cell death (apoptosis) or cell senescence, contributing to ageing and age-related diseases [46, 47]. In fact, in ageing, DNA damage overtakes DNA repair, leading to genomic instability, a fact sustained by studies showing accumulation of DNA alterations in old tissues [48]. On the other hand, genomic instability has been reported to be a driver of accelerated ageing, widely demonstrated by the presence of hypersensitivity to genotoxins and defects in genome maintenance in progeroid syndromes termed as diseases of accelerated ageing. Collectively, DNA damage as a culprit in ageing is highlighted by the accrual of sources of damage, i.e. oxidative stress (the oxidative stress theory of ageing) associated with the mitochondrial theory of ageing, as mitochondria is the primary source of ROS, increased activation of the DDR, mutations and presence of senescent cells along with a decreased capacity for DNA repair [47]. Among these factors oxidative stress is a well-known pathogenic mechanism and seems to be the most important one [49]. The overproduction of ROS along with a reduced antioxidant defence, i.e. oxidative stress, leads to DNA, protein and lipid damage [50, 51]. Also, ROS lead to age-related DNA lesions acting via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) which controls cytokine and chemokine expression and regulates adhesion molecules [45, 52, 53].
Telomeres are chromosomal end structures that play important roles in the protection of DNA from degradation [54]. In each cell division, 20–200 base pairs are lost within the telomeres, and telomerase is in charge of repairing telomeres after cell division. However, when they reach a certain critical length, i.e. shortening or attrition, the cells stop replicating and die [43]. The shortening process, as the telomerase fails to replicate completely the terminal ends of the DNA molecules, has been reported in ageing [55, 56]. Moreover, in humans, damaged telomerase can cause degenerative defects associated with ageing [57, 58].
Epigenetics meaning “above the genes” is termed as the inheritance of changes in gene function with no modifications in the nucleotide sequence of DNA [43, 59]. Epigenetic changes that comprise alterations in DNA itself as DNA methylation and modifications of histones (acetylation and methylation) as well as of other chromatin-associated proteins and chromatin remodelling can also be involved in ageing [22]. Sirtuins, a family of NAD-dependent deacetylases that act on Lys16 of histone H4, are emerging as a link between cellular transformation and lifespan [59]. Of note, epigenetic alterations seem to be reversible, underpinning the anti-ageing interventions [60]. Moreover, Greer et al. [61] showed transgenerational epigenetic inheritance of longevity in Caenorhabditis elegans suggesting that manipulation of specific chromatin modifiers in parents can induce an epigenetic memory of longevity in descendants.
Proteostasis or protein stability is an important feature of the cells and involves a complex network that coordinates protein synthesis with polypeptide folding, conservation of protein conformation and protein degradation [62, 63]. When damaged, as a consequence of various external and endogenous stress factors, it leads to the accumulation of protein aggregates holding proteotoxic effects and becomes a contributor to ageing and to age-related diseases [63, 64, 65]. In fact, it has been demonstrated that with age, proteostasis becomes compromised, leading to proteotoxicity [43, 62, 66]. More precisely, intracellular damaged protein deposition has been described in age-related diseases such as Alzheimer’s and Parkinson’s [62, 63, 67]. Finally, evidence data have revealed a double-sense link between DNA damage and proteostasis, which jointly induce an increased cellular lesion [63].
Deregulated nutrient sensing represents another important hallmark of ageing [22, 68]. Nutrient sensing is mediated by specific molecular pathways, such as insulin and insulin-like growth factor 1 (IGF-1 informs the cells about the presence of glucose and has the same intracellular signalling pathway as insulin), termed as “insulin and/IGF1-signalling” pathway (IIS) as well as the mechanistic target of rapamycin (mTOR) that senses nutrients, whereas AMP-activated protein kinase (AMPK) and sirtuins detect the energy levels [22, 43]. All these systems named as “nutrient sensing” pathways regulate metabolism and influence ageing [43]. More precisely, current data show that anabolic signalling induces accelerated ageing, while decreased nutrient signalling (attained through caloric restriction) promotes a healthy span and extends longevity [69, 70].
The “insulin and/IGF1-signalling” pathway (IIS) operates on the forkhead box proteins or FOXO family of transcription factors and on the mTOR complexes and has been reported to be the most conserved ageing-controlling pathway. Indeed, mutations that reduce the functions of insulin and IGF-1 receptor or downregulate the intracellular effectors, i.e. AKT, mTOR and FOXO, result in increased lifespan [22, 69, 71].
The mTOR kinase is part of two complex proteins and is sensitive to high levels of amino acids controlling a wide range of cellular functions, mostly anabolic metabolism [72]. It is noteworthy that mTOR is a target of rapamycin (an mTOR inhibitor), an antibiotic that exerts anti-proliferative effects by acting through this specific pathway. Several studies have shown that mTOR manipulation by inducing downregulation is involved in extending longevity [22, 43].
Finally, the AMPK pathway and sirtuins that sense changes in energy levels, i.e. low levels of ATP, act in the opposite direction as compared to IIS and mTOR, their activation leading to increased energy production and decreased ATP utilisation [22, 43]. In fact, caloric restriction seems to activate the AMPK pathway [73]. Finally, upregulation of both AMPK and sirtuins favours healthy ageing [74].
Mitochondrial dysfunction is a feature of ageing that refers to reduced respiratory chain efficiency, resulting in electron leak and diminished ATP production [75]. The consequence of mitochondrial dysfunction, installed across ageing, is the formation of ROS, and the theory of free radicals as a mechanism inducing ageing has been widely discussed [76]. However, this theory has been re-analysed and reconsidered as emerging data show that oxidative stress up to a specific threshold has, in fact, a beneficial effect in prolonging lifespan [77, 78]. More specifically, it seems that ROS in a certain amount may play a role as a trigger of compensatory homeostatic reactions as a response to the ongoing and increasing stress factors that come along with ageing, resulting in facing damage and maintaining survival [79]. Still, when over the specific threshold, ROS change their purpose and induce deleterious age-related effects [77, 80, 81].
Apart from the ROS theory, accumulating data have revealed that impaired mitochondrial function may contribute to ageing through other mechanisms, such as the increase of permeability in response to stress that triggers inflammatory reactions, the damaged interface between the outer mitochondrial membrane and the endoplasmic reticulum as well as reduced biogenesis of mitochondria [22]. Furthermore, it seems that both endurance training and alternate-day fasting have the ability to improve healthspan through mitochondrial degeneration avoidance [82, 83].
Finally, the mitochondrial dysfunction seems to be related to the hormesis which is deemed as an adaptive response of the organism to low doses of a toxic agent or physical condition, such as ROS, that induces the ability of the organism to tolerate higher doses of the same toxic agent [63]. Hence, although severe mitochondrial dysfunction is deleterious, mild respiratory damage may increase lifespan, possibly subsequently to a hormetic response [84]. In fact, data from the literature have shown that metformin could be considered a mild mitochondrial “toxic agent” as it induces a low energy state and activates AMPK [85]. In this respect, Anisimov et al. [74] showed that when administrated early in life, metformin treatment increases life span in mice.
Senescence is an age hallmark that stands out as a response triggered by genomic instability and telomere attrition resulting in growth arrest, thus limiting the proliferation of aged and damaged cells [22, 46, 47, 86]. A second important feature of senescent cells is the development of a peculiar secretome, termed as the senescence-associated secretory phenotype (SASP), which encompasses cytokines, chemokines and proteases, resulting in a pro-inflammatory state [87, 88]. Under normal conditions the SASP is involved in the recruitment of macrophages, neutrophils and natural killer (NK) cells, thus holding a beneficial effect in eliminating the senescent cells. However, across the ageing process, the senescence cells accumulate resulting in increased cytokine production and recruitment of more immune cells, which jointly contribute to the onset of the inflammageing state, a true driver of ageing [36, 87]. Moreover, a declined activity of the immune system, termed as immunosenescence, is installed in aged people, thus impairing the clearance of senescent cells and, in turn, increasing even more the chronic inflammation state. Collectively, senescence, inflammageing and immunosenescence promote ageing and operate together, rendering aged people more susceptible to age-related diseases [87, 89]. Finally, interestingly, mitochondrial dysfunction can also trigger cellular senescence, a process termed as “mitochondrial dysfunction-associated senescence” (MiDAS). MiDAS support the existence of a strong inter-relation between cellular senescence and metabolic dysfunction, highlighting that targeting metabolism may be a proper way to extend lifespan in humans [36].
Stem cell exhaustion, i.e. the progressive decline in the regenerative potential of the stem cells needed for tissue repair, is another characteristic of ageing. As explained, ageing is accompanied by immunosenescence, a condition that results from reduced haematopoiesis and that has several deleterious consequences [22].
Finally, apart from cellular damage, ageing also implies altered intercellular communication. Inflammation is an ageing-associated damage in intercellular communication termed as “inflammageing,” as previously described. Inflammageing may result from multiple causes, such as the accumulation of tissue damage, the reduced ability of the immune system to remove pathogens, the increase of senescent cells that produce pro-inflammatory cytokines, immunosenescence that fails to remove the senescent cells, the activation of the NFkB transcription factor, as well as the onset of a dysfunctional autophagic response [22]. Noteworthy, that inflammation is involved in the pathogenesis of obesity and T2DM, diseases that contribute to the onset of ageing [71]. Apart from inflammation, the intercellular communication has been revealed by the bystander effect referring to senescent cells inducing senescence in neighbouring cells via gap-junction-mediated cell–cell cross talk [90].
Given the aforementioned complex hallmarks of ageing, researchers worldwide have searched for proper tools to obtain the delay of ageing and the avoidance of age-related diseases. Here we find metformin, a drug that has been reported to be useful in modulating some of the age-related features. In fact, in cellular and animal models, metformin has been shown to influence and to hold beneficial effects on the following age related hallmarks [91]: (1) genomic instability [92, 93], (2) telomere attrition [94], (3) epigenetic changes [95], (4) proteostasis [96, 97], (5) nutrient-sensing pathways [98, 99], (6) mitochondrial function [100], (7) cellular senescence [101, 102], (8) stem cell function [103], and (9) low-grade inflammation [104].
Evidence-based data have revealed that metformin holds an important role in extending survival and delaying the onset of age-related diseases in nematode Caenorhabditis elegans [105, 106] and mice [107], but not in Drosophila melanogaster [108, 109]. In this respect, metformin supplementation was shown to increase mean lifespan and to prolong the healthspan of nematode Caenorhabditis elegans (an experimental model often used to study ageing and anti-ageing therapies) via AMPK [106]. Moreover, other authors have shown that metformin has the ability to retard ageing in Caenorhabditis elegans by metabolic alteration of its trophic microbial partner, E. coli. In brief, metformin disrupts the bacterial folate cycle, which reduces the levels of methionine in the worm. Finally, this results in postponing ageing by triggering a metabolic dietary restriction phenomenon and AMPK activation [105, 110]. Based on these results, we might argue another important role of metformin, that of modulating human microbiota, i.e. an increased abundance of E. coli, resulting in an increased production of short-chain fatty acids, such as butyrate and propionate, by which metformin might induce significant positive results in T2DM and might interfere with longevity [36, 111, 112].
In a very recent study, Song et al. [113] used the silkworm, a popular experimental model, to investigate the impact of metformin on lifespan and the underlying molecular pathways. They found that metformin prolonged lifespan without reducing body weight, which suggests that it can increase lifespan by remodelling the animal’s energy distribution strategy. Also, metformin increased fasting tolerance and levels of the antioxidant glutathione and activated APMK. Finally, these results suggest that activity in this pathway may contribute to metformin-induced lifespan extension in silkworm by increasing stress resistance and anti-oxidative capacity, while reducing energy output for silk product [113].
Studies on ageing and lifespan have also been performed on mice, highlighting the potential anti-ageing effect of metformin, resulting in an extended lifespan [114, 115, 116]. Anisimov et al. [116] demonstrated that chronic treatment of female mice with metformin significantly increased mean and maximum lifespan, even without cancer prevention in that model. In a further study, the authors showed that in female mice, metformin increased lifespan and postponed tumours when started at young and middle, but not at the old age [74]. Besides the increase of lifespan in mice, Martin-Montalvo et al. [107] pointed out that metformin seems to mimic some of the benefits of calorie restriction and leads to improved glucose-tolerance test, increased insulin sensitivity and reduced low-density lipoprotein and cholesterol levels without a decrease in the caloric intake. With respect to the mechanisms of action, metformin seems to increase the antioxidant activity, resulting in reductions in both oxidative stress and chronic inflammation [107].
Finally, as previously mentioned, not all experimental models confirm the anti-ageing role of metformin. It is the case of Drosophila fruit fly, another animal model where the authors showed that metformin induced a robust activation of AMPK and reduced lipid stores, but did not increase lifespan. Moreover, they found that when administered in high concentrations, metformin is toxic to flies. Finally, it seems that metformin appears to have evolutionarily conserved effects on metabolism but not on fecundity or lifespan [108].
The main universally accepted role of metformin is to alleviate hyperglycaemia. This outcome is obtained through the inhibition of hepatic gluconeogenesis [117, 118]. Metformin holds an insulin-sensitising action and insulin-induced suppression of endogenous glucose production [119]. Although other organs have been discussed as a target for metformin, such as the gut [120], liver remains the main ground of action, as reduced hepatic uptake of metformin prevents the lowering blood glucose effect [91]. There are several mechanisms by which metformin downregulates gluconeogenesis. Firstly, metformin induces alterations in cellular energetics [117], i.e. by decreasing cellular respiration through inhibition of the complex I mitochondrial respiratory chain [121, 122]. The result of this inhibition is the increase of the ADP:ATP and AMP:ATP ratios, which subsequently activate the cellular energy state sensor AMP-activated protein kinase (AMPK) [91, 110, 123], the key player of metformin. Once activated, AMPK leads to an increase in ATP production and a decrease in ATP consumption [42]. Noteworthy, AMPK is one of the molecular pathways that can modify the rate of ageing [43]. The importance of the activation of AMPK in obtaining the reduction in hepatic glucose production was investigated by Hawley et al. [85] who showed that an AMPK mutant does not respond to metformin treatment. On the other hand, Foretz et al. [124] showed that in AMPK knockout mice, the inhibition of gluconeogenesis is still present and associated with a reduction in energy state, but this happens in response to higher concentrations of metformin as compared to standard treatment. With regard to therapeutic concentrations of metformin, it seems that AMPK activation is mandatory for the suppression of gluconeogenesis [117, 125]. Finally, we have to mention that the activation of AMPK via inhibition of the complex I mitochondrial respiratory chain has been recently debated [126] as physiological/low concentration of metformin, which cannot induce AMP/ATP change, can still activate AMPK [125].
Another effect mediated by AMPK activation by metformin refers to the inhibitory phosphorylation of acetyl-CoA carboxylase (ACC), which leads to increased fatty acid uptake and β-oxidation and hence to improved lipid metabolism and subsequently to improved insulin sensitivity [127]. Furthermore, activated AMPK decreases glucagon-stimulated cyclic AMP (cAMP) accumulation, cAMP-dependent protein kinase (PKA) activity and downstream PKA target phosphorylation and increases cyclic nucleotide phosphodiesterase 4B (PDE4B). The authors provided a new mechanism by which AMPK antagonises hepatic glucagon signalling via phosphorylation-induced PDE4B activation [128]. Moreover, the decreased PKA activity promotes glucose consumption and inhibits glucose output [129]. Finally, metformin inhibits hepatic gluconeogenesis through AMPK-dependent regulation of the orphan nuclear receptor small heterodimer partner (SHP) [130].
Secondly, AMPK-independent mechanisms by which metformin inhibits hepatic gluconeogenesis have been reported [117]. In this respect, Miller et al. [131] point towards the ability of the drug to inhibit adenylate cyclase, reduce levels of cAMP and PKA activity, abrogate phosphorylation of critical protein targets of PKA, and block glucagon-dependent glucose output from hepatocytes through accumulation of AMP and related nucleotides independently of AMPK [131]. In addition, metformin inhibits the mitochondrial glycerophosphate dehydrogenase, resulting in an altered hepatocellular redox state, reduced conversion of lactate and glycerol to glucose and hence decreased hepatic gluconeogenesis [132].
Taken together, given the important role of metformin in inhibiting hepatic gluconeogenesis and therefore in reducing hyperglycaemia and subsequently hyperinsulinemia, jointly, important accelerators of ageing, several studies regard metformin as a potential anti-ageing drug [42, 117]. Metformin works through complex mechanisms that have been demonstrated to be similar to those associated with caloric restriction, a well-known model that underpins extended lifespan and healthspan. More precisely, it seems that both metformin and caloric restriction induce the same gene expression profile [107, 117, 133].
Another important target involved in changing the rate of ageing is mTOR [117]. TOR responds to insulin, amino acids and hormones and is involved in controlling a wide range of cellular functions, such as glucose metabolism, lipid and protein synthesis, inflammation and mitochondrial function [72]. Metformin has been demonstrated to downregulate mTOR in both a AMPK-dependent and AMPK-independent manner [98, 134, 135, 136]. Through stimulation of AMPK, metformin induces suppression of ATP consumption by inhibiting energy needing processes, such as protein synthesis via mTOR [42, 137]. In addition, through downregulation of mTOR signalling and of insulin-like growth factor 1 (IGF-1), metformin influences cell growth, proliferation and autophagy [42].
NF-kB pathway is another key mediator of ageing. As previously described, it is activated by genotoxic, oxidative and inflammatory stress and regulates the expression of cytokines, inflammation, growth factors and genes that regulate apoptosis [45]. Metformin has been demonstrated to inhibit NF-kB resulting in suppressing the inflammatory response via AMPK-dependent and independent pathways [138]. Also, metformin seems to hold the ability to reduce the endogenous ROS production [93] by acting at a mitochondrial level through blockage of the reverse electron flow at the respiratory chain complex 1 [139].
Finally, a very recent pathway has been described by Chen et al. [140]. The authors showed through genetic manipulation that metformin extends the Caenorhabditis elegans lifespan and attenuates age-related fitness decline via a mechanism that requires v-ATPase-Ragulator-AXIN/LKB1 of the lysosomal pathway [140].
In toto, the possible molecular mechanisms by which metformin exerts anti-ageing effects are [13, 91]: (1) inhibition of mitochondrial complex 1 in the electron transport chain and decrease of ROS production [139, 141], (2) activation of AMPK [106, 124, 140, 142, 143, 144], (3) inhibition of mTOR [106, 134, 135, 140], (4) NF-ĸB inhibition [101], and (5) reduced IGF-1 signalling [145].
Ageing encompasses a cluster of processes that induce a gradual decline of the human body functions, a condition that everyone faces in time. Also, ageing is a risk factor for a gamut of disturbances such as cancer, T2DM and cardiovascular and neurodegenerative diseases. Therefore, researchers worldwide strive to find the adequate tools in order to delay/avoid the onset of age-related diseases and hence promote healthspan. In keeping with this aim, metformin emerges as a drug that, beyond its main role to reduce hyperglycaemia, has antitumor effects and works as a protector against cardiovascular and neurodegenerative diseases making it a potential anti-ageing medicine. Importantly, metformin seems to possess positive effects even in nondiabetic subjects. However, the exact mechanisms of action and the molecular pathways involved in ageing that are modulated by metformin are not fully explained, and further studies are warranted for a better understanding of the beneficial effects of this drug.
Mr. Manfredi Rizzo serves as Director, Clinical Medical & Regulatory Affairs, Novo Nordisk Europe East and South. The publication was supported by funds from the National Research Development Projects to finance excellence (PFE)-37/2018–2020 granted by the Romanian Ministry of Research and Innovation.
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