\\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!
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"1891",leadTitle:null,fullTitle:"Management of Technological Innovation in Developing and Developed Countries",title:"Management of Technological Innovation in Developing and Developed Countries",subtitle:null,reviewType:"peer-reviewed",abstract:"It is widely accepted that technology is one of the forces driving economic growth. 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Staphylococcus spp. and Streptococcus spp. that are Gram positive cocci are the main pathogens in several infections. Virulence factors such as usual and unusual surface proteins encoded by resistance genes are the main causes of pathogenesis. Multidrug-resistant pathogens that are the main causes of morbidity and mortality worldwide have the ability to synthesize a number of destructive enzymes encoded by resistance genes such as ?-lactamases. Resistant pathogens such as methicillin-resistant Staphylococcus aureus (MRSA), Streptococcus pneumoniae, Group A, and Group B Streptococcus have emerged throughout the world. To eliminate these resistant pathogens that cause untreatable, acute, and chronic infections, different new antimicrobials must be developed and used. The goal of this book is to provide the latest information about the above topics.",isbn:"978-1-78984-473-3",printIsbn:"978-1-78984-472-6",pdfIsbn:"978-1-78985-941-6",doi:"10.5772/intechopen.77863",price:119,priceEur:129,priceUsd:155,slug:"staphylococcus-and-streptococcus",numberOfPages:120,isOpenForSubmission:!1,hash:"b9ddbf132ac8ea9d2a7613836e5a27ca",bookSignature:"Sahra Kırmusaoğlu",publishedDate:"March 11th 2020",coverURL:"https://cdn.intechopen.com/books/images_new/8032.jpg",keywords:null,numberOfDownloads:2489,numberOfWosCitations:0,numberOfCrossrefCitations:1,numberOfDimensionsCitations:1,numberOfTotalCitations:2,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 24th 2018",dateEndSecondStepPublish:"January 29th 2019",dateEndThirdStepPublish:"March 30th 2019",dateEndFourthStepPublish:"June 18th 2019",dateEndFifthStepPublish:"August 17th 2019",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:"Edited by",kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"179460",title:"Dr.",name:"Sahra",middleName:null,surname:"Kırmusaoğlu",slug:"sahra-kirmusaoglu",fullName:"Sahra Kırmusaoğlu",profilePictureURL:"https://mts.intechopen.com/storage/users/179460/images/system/179460.jpeg",biography:"Dr. Kırmusaoğlu, PhD, is an assistant professor of Microbiology\nat the Department of Molecular Biology and Genetics, T.C. Haliç\nUniversity. She specialized in Microbiology at Abant Izzet Baysal\nUniversity (Biology Department), Turkey. Her previous experience\nincludes laboratory manager at microbiology laboratories in several\nresearch and private hospitals. Throughout her career, she collaborated\nwith academicians/researchers from Abant Izzate Baysal University (AIBU), Middle East Technical University (METU), and Istanbul\nUniversity Cerrahpaşa Faculty of Medicine, and has participated in various research projects.\nDr. Kırmusaoğlu’s research interests include medical microbiology, pathogenic bacteria, bacterial biofilms, antibiofilm and antibacterial activity, bacterial drug resistance, pathogen–host interactions, pathogenesis, molecular microbiology, and microbiota. She has published several international research articles, books, book chapters, and congress proceedings.\nShe is also the editor of Disinfection, Bacterial Pathogenesis and Antibacterial Control,\nand Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods\npublished by IntechOpen. In addition to these, she wrote the book Genel Biyoloji Laboratuvar\nKılavuzu (General Biology Laboratory Manual) published by Hipokrat Publisher.\nShe has contributed to a chapter translation of the book Sherris Medical Microbiology\nby Ryan et al. as one of the translation authors of Sherris Tıbbi Mikrobiyoloji, which is a\nTurkish translated book edited by Prof. Dr. Dürdal Us and Prof. Dr. Ahmet Başustaoğlu.",institutionString:"Haliç University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"6",totalChapterViews:"0",totalEditedBooks:"5",institution:{name:"Haliç University",institutionURL:null,country:{name:"Turkey"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"409",title:"Bacteriology",slug:"biochemistry-genetics-and-molecular-biology-microbiology-bacteriology"}],chapters:[{id:"70748",title:"Introductory Chapter: An Overview of the Genus Staphylococcus and Streptococcus",slug:"introductory-chapter-an-overview-of-the-genus-em-staphylococcus-em-and-em-streptococcus-em-",totalDownloads:273,totalCrossrefCites:0,authors:[{id:"179460",title:"Dr.",name:"Sahra",surname:"Kırmusaoğlu",slug:"sahra-kirmusaoglu",fullName:"Sahra Kırmusaoğlu"}]},{id:"66603",title:"Virulence Factors of Streptococcus mutans Related to Dental Caries",slug:"virulence-factors-of-em-streptococcus-mutans-em-related-to-dental-caries",totalDownloads:384,totalCrossrefCites:0,authors:[{id:"282054",title:"Ph.D.",name:"María Alejandra",surname:"Bojanich",slug:"maria-alejandra-bojanich",fullName:"María Alejandra Bojanich"},{id:"292367",title:"Mr.",name:"Mariano Daniel",surname:"Orlietti",slug:"mariano-daniel-orlietti",fullName:"Mariano Daniel Orlietti"}]},{id:"68220",title:"Toward Better Understanding on How Group A Streptococcus Manipulates Human Fibrinolytic System",slug:"toward-better-understanding-on-how-group-a-em-streptococcus-em-manipulates-human-fibrinolytic-system",totalDownloads:240,totalCrossrefCites:0,authors:[{id:"290636",title:"Dr.",name:"Ruby",surname:"Law",slug:"ruby-law",fullName:"Ruby Law"},{id:"300264",title:"Dr.",name:"Adam J.",surname:"Quek",slug:"adam-j.-quek",fullName:"Adam J. 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From chapter submission and review, to approval and revision, copy-editing 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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Among severalfactors thathave been postulated to contribute to DM epidemic, environmentalfactors have drawn particular attention because of the rapidity of the increase in type 2 or the so called ‘maturity on- set’ diabetes mellitus. Nobuko Seike, Mitsuhiko Noda and Takashi Kadowaki [2] evaluated the association between alcohol consumption and the risk of type 2 DM,it was pointed out that type 2 diabetes mellitus is closely related to life style factors including diet, physical activities, alcohol and smoking as well as obesity and a family history of diabetes. According to the researchers, in Japan the prevalence of diabetes mellitus both for men over age 50 and women over 60 well exceeds 10% and most have type 2 DM which is associated with excessive energy intake, lack of physical exercise and obesity. In addition, Mayes and Botham[3]revealed that obesity – particularly, abdominal obesity(a diet related disorder) is a risk factor for increased mortality, hypertension, type 2 DM, hyperlipidaemia and various endocrine dysfunctions.
On the other hand,type 1 DM, or ’Juvenile DM’ or ‘insulin-dependent’ diabetes is less common than type 2. Only 10% of all diabetics have type 1.
Type 1 diabetes occurs when the pancreas produces no insulin at all. It tends to emerge in childhood or early adulthood (before the age of 40) and must be regulated by regularly injecting insulin. Although the exact cause of type 1 diabetes is currently unknown, it is widely believed that majority of type 1 diabetes is of the immune-mediated nature, where beta cell loss is a T-cell mediatedautoimmune attack [4].
With type 1 diabetes, the immune system attacks cells in the pancreas. This destroys or damages them enough to stop the production of insulin. A number of experts attribute this occurrence to a viral infection.
Genetics are also thought to play a part in the cause of type 1 diabetes; it has often been seen to run in families.
People who have a close relative (parent or sibling) with type 1 diabetes have a 6% chance of developing type 1 diabetes too.
In some instances, type 1 diabetes can be caused by a condition of the pancreas known as ‘chronic pancreatitis’. Chronis pancreatitis causes an inflammation of the pancreas and can cause serious damage to the cells that produce insulin [5].
It is a well known fact that DM being a metabolic, endocrine disorder is directly connected to carbohydrate, lipid and protein metabolism. As a result, nutrition therapy forms an integral part of diabetes management and diabetes self - management education. It is also well established that diabetes is caused by either a lack of Insulin secretion or by insulin resistance. The resultant disease or metabolic disturbance leads to hyperglycaemia and dyslipidemia in the short term, as well as long term complications such as retinopathy, neuropathy and nephropathy. Besides, persons with diabetes are 2 to 4 times more likely to develop coronary artery disease or to suffer a stroke. Findings from the diabetic control and complication trials (DCCT) and the United Kingdom prospective Diabetes study(UKPDS) clearly indicate that the maintenance of near normal blood glucose level dramatically reduces the chronic complications associated with this disorder. In addition, reducing elevated blood lipids levels has been shown to lower the incidence of acute coronary events in other at-risk populations. Research have shown that before the advent of insulin therapy in the early 20th century, medical nutrition therapy (MNT) was the only form of therapy for DM[6].
However, there are many misconceptions concerning nutrition and diabetes [7]. Moreso, most diabeticsare confused with conflicting nutrition advice and opinions. And itis commonly believed that diabetes cannot be completely cured, but it may bemore easily regulated and controlled with the right diet. With strict adherenceto nutritionist’s advice, diabetic patientsmay be able to significantly improve their quality of life. There islittledataon the role nutrition played in diabetes managementin ourenvironment, hence,the need fora reviewlike this.
A number of nutritional factors have been found to influence the development of type 1 diabetes or type 1-related autoimmunity. One study has found, for example, that eating vegetables daily during pregnancy reduced the risk of a child\'s developing type 1-associated autoimmunity [8]. Another found that higher iron intake (via infant formula or supplements) in the first four months of life was associated with a higher risk of developing type 1 diabetes[9]. However, other studies have not found associations between diet and type 1 diabetes development. For example, Virtanen et al.[10] found only a weak protective effect of a few foods eaten during pregnancy and the development of type 1 related autoimmunity in the offspring (those foods were butter, low-fat margarine, berries, and coffee; most foods showed no association).
Norris et al.[11] found that dietary intake of omega-3 fatty acids, found in fish, flax seeds, walnuts, soy, canola, and greens, is protective against the development of type 1 diabetes-related autoantibodies in children at genetic risk of type 1 diabetes. Omega-3s can reduce inflammation, and the lack of omega-3s in Western diets may predispose people to inflammation. Yet the same authors later found that omega-3 levels were not associated with later development of type 1 in these children [12]. So, it is possible that omega-3s may be protective against type 1 autoantibody development, but be less significant later in the disease process.
An earlier study of the same children found that the mother\'s dietary intake of omega-3 fatty acids during pregnancy did not affect the risk of autoimmunity in children [13]. Cod liver oil, however, taken during pregnancy, has been associated with a reduced risk of type 1 diabetes in offspring. Both omega-3 fatty acids and vitamin D are present in this oil, and either or both may play a role [14].
Virtanen et al.[15] found that the fatty acids associated with milk and ruminant meat fat consumption were associated with an increased risk of type 1 related autoimmunity. Linoleic acid, however, was associated with lower levels of autoimmunity, in children genetically at risk of type 1 diabetes.
A group of people with metabolic syndrome (a group of conditions common in people with type 1 or 2 diabetes) were given omega-3 fatty acid supplements or a placebo for six months. Those taking the supplements were found to have lower markers of autoimmunity and inflammation, as well as more weight loss, compared to people who did not take the supplements [16].
Adequate intake of omega-3s during pregnancy may also decrease the risk of obesity in the offspring. Higher levels of omega-6 fatty acids in relation to omega-3s in umbilical cord blood has been associated with higher obesity in children at age 3 [17].
The presence of environmental contaminants in food may also play a role in the effects of nutritional factors. Some contaminants may interfere with the beneficial effects of foods. For example, in a study linking insulin resistance to persistent organic pollutants, the researchers concluded that beneficial aspects of omega-3 fatty acids in salmon oil could not counteract the harmful effects caused by the persistent organic pollutants in that oil [18].
Fish is one source of omega-3 fatty acids, but according to an editorial in the American Journal of Clinical Nutrition (AJCN), it may be better to rely on plant-based sources instead [19]. Studies on fish consumption and type 2 diabetes are inconsistent: some show that higher dietary intake of omega 3s decreases the risk of type 2, some show no connection, and some even show that higher fish consumption increases the risk of type 2 diabetes [20,21]. It may be that the chemicals in fish can explain these inconsistencies. A study shows that plant-based omega 3s have different effects than marine-based omega 3s in relation to type 2 diabetes [22], it was opined that this may be possibly due to the contaminants present in fish.
A high fat diet, especially one high in saturated fats, has been linked to type 2 diabetes and insulin resistance. It appears that saturated fatty acids (but not unsaturated fats) activate immune cells, which produce an inflammatory protein, which in turn then makes cells more insulin resistant [23].Mothers who consumed higher levels of trans fats had an increased risk of excess body fat, and so did their breastfed infants [24].
Can the effects of a high fat diet be passed down to subsequent generations? In animal studies, a high-fat diet that causes obesity in mothers can affect the metabolism and weight of her offspring. But what about a high fat diet in fathers? In one study, the female offspring of heavier father rats (fed a high-fat diet) had defects in their insulin and glucose levels, like their fathers. Unlike their fathers, they were not heavier than the controls [25]. Other researchers fed mice a high fat diet with fat composition similar to a standard Western diet, and then bred them and fed them the same diet for multiple generations. Over four generations, the offspring became gradually heavier, and developed higher insulin levels, despite not eating more calories. The diet was associated with changes in gene expression [26].
The glycemic index(GI) is a measurement of how high a certain food raises blood glucose levels after it is eaten. Foods that have a high glycemic index will cause blood glucose to rise more, triggering insulin production (in people who still produce insulin), then leading to falling blood glucose levels. One prospective study has found that a higher glycemic index diet leads to a faster progression to type 1 diabetes. The group of people on this diet, however, did not have higher levels of autoantibodies, showing that the diet may affect disease progression but not disease initiation. The mechanisms involved may include oxidative stress, caused by high blood glucose levels after meals, or perhaps insulin resistance. Whatever the mechanism, a high glycemic index diet may place additional stress on beta cells that are already under an autoimmune attack [27].
Evidence favouring the active reduction of blood lipids continues to accumulate and several major diabetes associations now recommendthat diabetic patients should reduce fat intake and increase carbohydrate intake to approximately 50% of total calories[1]. High fibre foods has been advocated [28]. It was highlightedthat, although before detailed advice can be given, comparative data on the physiological effects of carbohydrate foods maybe required.
The consumption of sugar-sweetened beverages has been associated with type 2 diabetes, obesity, and metabolic syndrome. A meta-analysis of a 11 prospective studies (of over 300,000 people) found that those who consumed 1-2 sweetened beverages per day had a 26% greater risk of developing type 2 diabetes than those who consumed fewer than one serving per month. The risk was 20% higher for developing metabolic syndrome. Sugar-sweetened beverages include soft drinks, fruit drinks, iced tea, and energy/vitamin water drinks [29].
High-fructose corn syrup is another sweetener linked to obesity. Rats given access to high-fructose corn syrup gained more weight than those given access to sucrose, despite eating the same number of calories [30].
A few studies have found that higher zinc levels in drinking water may be protective against type 1 diabetes. For example, Zhao et al. [31], found that higher levels of zinc and magnesium were associated with lower rates of type 1 diabetes in southwest England. In Norway, a study found that higher zinc levels in water was associated with a lower risk of type 1 diabetes, but the association was not statistically significant [32]. In Finland, a study found that low zinc levels in drinking water was associated with a higher incidence of type 1 diabetes [33].
Nicotinamide, is a component of vitamin B3 that has been shown to protect against diabetes in animals, and prevent beta cell damage [34]. Even better, one study found that it prevented the development of type 1 diabetes in children with type 1-associated autoantibodies [35].
On the basis of these and other studies, a large, double-blind, placebo-controlled trial was conducted in Europe, the U.S. and Canada, called the European Nicotinamide Diabetes Intervention Trial (ENDIT). This trial gave nicotinamide to first degree relatives of people with type 1 diabetes who already had developed type 1-associated autoantibodies. Unfortunately, it found no difference in the development of diabetes between the two groups during the 5 year follow-up period. The study gave high doses of the vitamin, up to 3 g/day (30-50 times higher than the RDA) [34].
Another double-blind, placebo controlled study in Sweden gave high doses of anti-oxidants (including nicotinamide, vitamin C, vitamin E, Beta-carotene, and selenium) to people after they were already diagnosed with type 1 diabetes and also found that they had no effect in protecting the beta cells against the damage of free radicals [36]. There is no evidence linking the anti-oxidants alpha- or beta-carotene levels and the development of type 1 related autoimmunity in another study as well [37].
Uusitalo et al. [38] also found that if pregnant women took anti-oxidants and trace minerals (including retinol, beta-carotene, vitamin C, vitamin E, selenium, zinc, or manganese) during pregnancy, there was no effect on the risk of the child\'s developing type 1-related autoimmunity.
Czernichow et al.[39] found that anti-oxidant supplements were not protective against metabolic syndrome, a group of conditions common in people with type 1 or 2 diabetes. Yet they also found that the people who had the highest levels of some anti-oxidants (beta-carotene, vitamin C, and vitamin E) in the beginning of the study, presumably due to a diet rich in plant foods, did have a lower risk of developing metabolic syndrome.
While these studies did not find promising results concerning anti-oxidant supplements, they also did not find that these supplements did any harm.
Free radicals may play a role in the inflammatory process that destroys the beta cells in type 1 diabetes [36]. Therefore, anti-oxidants have been thought to protect the body from oxidative stress due to the production of free radicals. But, there is some animal evidence that anti-oxidant supplements may also increase insulin resistance, showing that the relationship may not be so simple. When the researchers gave certain mice an anti-oxidant, they were more likely to become insulin resistant [40]. Perhaps this finding could help explain why anti-oxidant supplements have not been found to be protective against type 1 diabetes.
Advanced Glycation End products (AGEs)are found in heat processed foods and have been linked to type 1 and type 2 diabetes in animal studies. They appear to predispose people to oxidative stress and inflammation, and may affect the fetus if the mother consumes them during pregnancy. A study has found that the level of AGEs that a mother eats are correlated with insulin levels in the baby. It found that if mothers have high AGE levels, and infant food is high in AGEs, it may raise the risk of diabetes in the offspring [41].
Researchers fed mother rats a diet that was deficient in protein, and found higher rates of diabetes in the offspring. They also found that one of the offspring\'s genes was "silenced"-- a gene associated with type 2 diabetes development. Nutrition, then, may have effects on gene expression that are linked to type 2 diabetes development [42].
In contemporary time, Medical NutritionTherapy (MNT) is used to describedietary prescriptions [43].
MNT for diabetesaim to achieve the following objectives:
Achieve and maintain near normal blood glucose goals
Achieve and/ or maintain optimal blood lipid levels
Achieve and/ or maintain normal blood pressure
Prevent, delay or treat nutrition related complications
Provide adequate kcalories for achievement of reasonable body weight
Provide optimal nutrition for maximizing health and for growth, development, pregnancy, and lactation
Body of knowledge shows that, with respect to carbohydrates, the key emphasis of MNTfor diabetes mellitus is on the total amount of carbohydrate in terms of energy intake [44].As far as the type of carbohydrates to be ingested is concerned, the guidelines for MNT in DM clearly stress the value of selecting vegetables, fruits and grains, so that the starches consumed will include adequate amounts of both fibre and micronutrients[43].
Research findings shows specific interests in the role that dietary fiber may play in the nutritional management of DM. Benefit of fiber were found with regard to glycaemic control, HDL and LDL cholesterol and triacylglycerols [45]. However, a 3- month study by Jenkins et al.[46] did not find a metabolic advantage of high fiber over low fiber cereals. Also, a study carried out by Erasmus et al. [47],showed that treatment with guar gum does not lower the postprandial glucose level in both non- diabetic and diabetic Nigerian subjects.
The American Diabetes Association [7] gave the following guidelines:
Which can achieve much if the following dietary principles are observed ;
Integrate and syncronise with the time of action of insulin treatment – patient on insulin therapy should eatat consistent time simultaneously with the time of action of insulin preparation used. This will help to minimize the peak of blood glucose as well as incidence of hypoglycaemia.
Reduce saturated fat because diabetics are prone to having coronary heart disease and dietary restriction may reduce the risk.
Keep salt intake low: salt intake must be reduced by diabetics because it has high risk of developing hypertension. However, intake of essential nutrients should be adequateamong growing patients.
Exercise: For planned exercise, reduction in insulin dosage may be the preferred choice to prevent hypoglycemia. Additional carbohydrate may be needed for unplanned exercise. Moderate-intensity exercise increases glucose uptake by 2–3 mg kg−1 min−1 above usual requirements. Thus, a 70-kg person would need 8.4–12.6 g (10–15) carbohydrate per hour of moderate physical activity. More carbohydrate would be needed for intense activity.
Metabolic profile: Improved glycaemic control with insulin therapy is often associated with increased body weight. Because of the potential for weight gain to adversely affect glycaemia, lipids, blood pressure, and general health, prevention of weight gain is desirable.
A change in dietary regimen has a greater potential to improve type 2 diabetes, therefore, the following guidelines will serve a useful purpose.
Because many persons with type 2 diabetes are overweight and insulin resistant, medical nutrition therapy should emphasize lifestyle changes that result in reduced energy intake and increased energy expenditure through physical activity. Therefore, reducing body weight by eating few calories and taking regular exercise. Also, increased physical activity can lead to improved glycaemia, decreasing insulin resistance, and reduced cardiovascular risk factors.
Reduce saturated fat and maintaining a reduced plasma low density lipoprotein cholesterol levels.
Eating low glycaemic index foods such as soya beans, apple, grapefruits, peas(groundnuts), increase intake of vegetables, fruits, legumes and whole grain cereal that may mostly have low glycaemic indices.
Keep salt intake low
Fried food is not good for diabetes patients. Wheat bread, lean meat, game meat (bush meat), green, leafy vegetables, garden egg, all these should be encouraged for DMpatients.
Physical activity: Increased physical activity can lead to improved glycaemia, decreased insulin resistance, and reduced cardiovascular risk factors.
From the review by Kayode et al.[1], epidemiological studies (48) have reported that as nations become more affluent, the nature of the people’s carbohydrate consumption changes such that the ratio of complex (starches) to simple carbohydrates decreases. It has been suggested that this change in dietary pattern is responsible for the occurrence of various diseases, such as atherosclerosis, diabetes and hyperlipidaemia. One proposed physiological basis underlying such suggestions is a traditionally held tenet that simple carbohydrates are more readily available for immediate absorption by the gut than are more complex carbohydrates and that they therefore produce a greater and faster rise in postprandial plasma glucose and insulin responses than do the supposedly more gradually digested and absorbed complex carbohydrate. Consequently, diets restricted in simple carbohydrates have been recommended in disease states in which control of plasma glucose and/or insulin is felt to be important. However, there is dearth of sufficient laboratory data to substantiate the role nutrition plays in the management of diabetes mellitus.
To be able to effectively manage diabetes with the aid of dietary control, patient’s education, understanding, and participationis vital since the complications of diabetes are far less common and less severe in people who have well- managed blood glucose levels. Also, there is reductionin expenses incurred due tothis metabolic disorderwhich research shows was a major drain on health and productivity – related resources of government and otheremployers of labour.
Given the associated higher risks of cardiovascular disease, lifestyle modifications(whichincludes smoking habits, sedentary life, lack of regular exercise etc,) are strongly recommended. Besides, regularexercise, coupled with bloodpressure, cholesterol levels,body weight, HbA1C measurementsis advocated among peoplewith diabetes.
Omega-3 fatty acids may be protective against type 1 diabetes, but more studies would be necessary to confirm this finding. Eating high glycemic-index foods may accelerate the progression of type 1 diabetes, but this association should also be confirmed. Taking anti-oxidant supplements does not appear to reduce the risk of type 1 diabetes, but it is possible that a diet high in anti-oxidants may still be protective.
More research is highly imperative on the epidemiological and laboratory aspects of the role of nutrition in the management of diabetes mellitus.
Our sincere appreciation goes to Professors S.A Shoyinka and J.I Anetor, for their invaluable contributions.
Oxidoreductases, which includes oxidase, oxygenase, peroxidase, dehydrogenase, and others, are enzymes that catalyze redox reaction in living organisms and in the laboratory [1]. Interestingly, oxidoreductases catalyze reaction involving oxygen insertion, hydride transfer, proton extraction, and other essential steps. The substrate that is oxidized is considered as hydrogen or electron donor, whereas the substrate that is reduced during reaction as hydrogen/electrons acceptor. Most commonly, oxidoreductase enzymes use NAD, FAD, or NADP as a cofactor [2]. Organisms use this group of enzymes for synthesis of biomolecules, degradation and removal of molecules, metabolism of exogenous molecules like drugs, and so on [3, 4, 5]. Their biochemical property such as efficiency, specificity, good biodegradability, and being studied well make it fit well for industrial purposes. As a result, oxidoreductases are being utilized in nutrition, food processing, medicine, and other chemical synthesis. In the near future, oxidoreductase may be utilized as the best biocatalyst in pharmaceutical, food processing, and other industries [6, 7].
Enzymes like oxidoreductase play great and significant function in the field of disease diagnosis, prognosis, and treatment [8]. By analyzing the activities of enzymes and changes of certain substances in the body fluids, a number of disease conditions can be diagnosed [9, 10]. The determination of the activity of the oxidoreductases is helpful in understanding the metabolic activity of different organs [8, 11]. For example, the activity of oxidoreductase enzymes in Krebs cycle is significantly increased during skin infection [12].
There are different disease conditions resulting from deficiency (quantitative and qualitative) and excess of oxidoreductase, which may contribute to the metabolic abnormalities and decreased normal performance of life [13, 14]. For example, relative decreases in the activities of NADH dehydrogenase and ubiquinol-cytochrome c oxidoreductase are highly associated with the developments of peripheral arterial disease. Another best example is mutation of p450 oxidoreductase (POR) gene, which leads to insufficiency of P450 enzymes characterized by defective steroidogenesis. Similarly, deficiency of mitochondrial acetaldehyde dehydrogenase disturbs normal metabolism of alcohol and leads to accumulation of acetaldehyde [8, 15, 16]. These conditions in turn affect the normal development and reproduction.
Oxidoreductases are a family of enzymes that catalyze redox reactions. Oxidoreductases catalyze the transfer of electrons from oxidant to reductant [4]. Generally, oxidoreductases catalyze reactions which are similar to A– + B → A + B– where A is the oxidant and B is the reductant [17]. Oxidoreductases can be oxidases where a molecular oxygen acts as an acceptor of hydrogen or electrons and dehydrogenases which are enzymes that oxidize a substrate by transferring hydrogen to an acceptor that is either NAD+/NADP+ or a flavin enzyme. Other classes are oxidoreductases enzymes, peroxidases which are localized in peroxisomes and catalyze the reduction of hydrogen peroxide. Hydroxylases are involved in the addition of hydroxyl groups to their substrates, and oxygenases are key in the incorporation of oxygen from molecular oxygen into organic substrates. And reductase enzymes are involved in the catalysis of reduction reaction [2, 3, 18]. In general, oxidoreductase enzymes play an important role in both aerobic and anaerobic metabolism. They are involved in glycolysis, TCA cycle, oxidative phosphorylation, fatty acid, and amino acid metabolism [5, 19, 20].
In glycolysis, the enzyme glyceraldehydes-3-phosphate dehydrogenase catalyzes the reduction of NAD + to NADH. In order to maintain the redox state of the cell, this NADH must be re-oxidized to NAD+, which occurs in the oxidative phosphorylation pathway [21].
A high number of NADH molecules are produced in the TCA cycle. The product of glycolysis, pyruvate, enters the TCA cycle in the form of acetyl-CoA. Except leucine and lysine, all twenty of the amino acids can be degraded to TCA cycle intermediates. And most of the fatty acids are oxidized into acetyl coA through beta oxidation that enter TCA cycle [19, 22].
The precursor for the TCA cycle comes from lipids and carbohydrates, both of which produce the molecule acetyl-CoA. This acetyl-CoA enters the eight-step sequence of reactions that comprise the Krebs cycle, all of which occur inside mitochondria of eukaryotic cells. TCA or Krebs cycle produces NADH and FADH, and the reactions are catalyzed by classes of oxidoreductase enzymes [23].
Living cells use electron transport chain to transfer electrons stepwise from substrates (NADH & FADH2) to a molecular oxygen. The proton gradient which is generated through electron transport chain runs downhill to drive the synthesis of ATP. Electron transport chain and oxidative phosphorylation take place in the matrix of mitochondria, and there are oxidoreductase enzymes impregnated in the inner mitochondrial membrane, which catalyze these reactions and are engaged in energy production. NADH:quinone oxidoreductase, also called NADH dehydrogenase (complex I), is responsible for the transfer of electrons from NADH to quinones, coupled with proton translocation across the membrane. Succinate:quinone oxidoreductase, or succinate dehydrogenase (complex II), is an enzyme of the Krebs cycle, which oxidizes succinate and reduces quinones, in the absence of proton translocation. Quilon:cytochrome c oxidoreductase (complex III), which transfers electrons from quinols to cytochrome c and cytochrome c:oxygen oxidoreductase, an aa3-type enzyme (complex IV), which receives these electrons and transfers it to oxygen are both oxidoreductase enzymes involved in electron transport chain and oxidative phosphorylation [19, 24, 25] (Figure 1).
Oxidoreductase enzymes involved in electron transport chain and oxidative phosphorylation [18].
Liver is the principal organ for drug metabolism. The body uses different strategies to metabolize drugs like oxidation, reduction, hydrolysis, hydration, conjugation, condensation, or isomerization. The main goal of drug metabolism is to make the drug more hydrophilic and excrete easily. Enzymes involved in drug metabolism are found in many tissues and organs but are more concentrated in the liver. Rates of drug metabolism may vary among individuals. Some individuals metabolize a drug so rapidly; in others, metabolism may be so slow and have different effects. Genetic factors, coexisting disorders (particularly chronic liver disorders and advanced heart failure), and drug interactions are responsible factors for variation of rate of drug metabolism among individuals [26].
Generally, drug metabolism can be in three phases. In phase I drug metabolism, oxidoreductase enzymes such as cytochrome P450 oxidases add polar or reactive groups into drugs (xenobiotics). In phase I reaction, drugs are introduced into new or modified functional group through oxidation, reduction, and hydrolysis. In Phase II reactions, modified compounds are in conjugation with an endogenous substance, e.g., glucuronic acid, sulfate, and glycine. Phase II reactions are synthetic, and compounds become more polar and thus, more readily excreted by the kidneys (in urine) and the liver (in bile) than those formed in nonsynthetic reactions. At the end, in phase III reaction, the conjugated drugs (xenobiotics) may be further processed, before being recognized by efflux transporters and pumped out of cells. The metabolism of drug often converts hydrophobic compounds into hydrophilic products that are more readily excreted [27].
In normal cases, human body wants to remove or detoxify any compounds that cannot be metabolized otherwise utilized to serve the needs of the body. This removal process is carried out mainly by the liver. The liver has classes of oxidoreductase enzymes that are extremely effective at detoxification and removal of drugs from the body [5, 18].
Oxidation and metabolism of a high number of drugs and endogenous molecules are catalyzed by a class of oxidoreductase enzymes called cytochrome P450 monooxygenases. Even though they are distributed throughout the body, cytochrome P450 enzymes are primarily concentrated in liver cells. The CYP2D6 isozymes play a great role in metabolizing certain opioids, neuroleptics, antidepressants, and cardiac medications. Currently it is going to be understood that difference in the genes for CYP450 enzymes play to inter-individual differences in the serum concentrations of drug metabolites, resulting in interpatient variability in drug efficacy and safety [28].
Flavin-containing monooxygenases (FMOs) (EC 1.14.13.8) are a family of microsomal NADPH-dependent oxidoreductase, responsible for oxygenation of nucleophilic nitrogen, sulfur, phosphorus, other drugs, and endogenous molecules. Different variants of mammalian FMOs play a significant role in the oxygenation of nucleophilic xenobiotics. FMO utilizes NADPH as a cofactor and contains one FAD as a prosthetic group. FMOs have a broad substrate specificity and their activity is maximal at or above pH 8.4. FMO is a highly abundant enzyme in the liver endoplasmic reticulum and participates in drug metabolism (activation and detoxification) [29].
Before FMOs bind to a substrate, they activate molecular oxygen. First, flavin adenine dinucleotide (FAD), the prosthetic group of FMO, is reduced by NADPH to form FADH, then oxygen is added into the FAD, and hydro-peroxide FADH-4α-OOH is produced. And then, one oxygen atom is transferred to the substrate [30, 31].
Alcohol dehydrogenase (ADH) and mitochondrial aldehyde dehydrogenase (ALDH) are another family of oxidoreductase responsible for metabolizing ethanol. These enzymes are highly expressed in the liver but at lower levels in many tissues and play a great role in detoxification and easy removal of alcohols. Liver is the main organ for ethanol metabolism. Oxidation of ethanol with these enzymes can become a major energy source especially in the liver, and it can interfere metabolism of other nutrients [32].
The first step in ethanol metabolism is its oxidation to acetaldehyde, and this reaction is catalyzed by enzymes called alcohol dehydrogenases (ADHs). The second reaction in ethanol metabolism is oxidation of acetaldehyde into acetate catalyzed by aldehyde dehydrogenase (ALDH) enzymes. There are different ADH and ALDH enzymes encoded by different genes occurring in several alleles and enzymes that have different alcohol metabolizing capacity; thereby, they influence individuals’ alcoholism risk. These are either through rapid oxidation of ethanol to acetaldehyde where there is more active ADH or slower oxidation of acetaldehyde into acetate where there are less active ALDH enzymes. Excess accumulation of acetaldehyde is toxic, which results in different adverse reactions and produces nausea, skin rash, rapid heartbeat, etc. Most commonly, single-nucleotide polymorphisms (SNPs) are responsible for ADH and ALDH gene variants, and these may occur on both coding and non-coding regions of the gene [33, 34].
Monoamine oxidase is a very important oxidoreductase enzyme mainly responsible for degradation of amine neurotransmitters like norepinephrine, epinephrine, serotonin, and dopamine. Oxidation of different endogenous and exogenous biogenic amines may produce other active or inactive metabolites. Monoamine oxidase (MAO) is found in two isozyme forms: monoamine oxidase A (MAO-A) preferentially deaminates serotonin, norepinephrine, epinephrine, and dietary vasopressors such as tyramine, and MAO-B preferentially deaminates dopamine and phenethylamine. They are integral flavoproteins components of outer mitochondrial membranes in neurons and glia cell. The two isozymes of MAO differ based on substrate specificity and sensitivity to different inhibitors [35].
Monoamine oxidase enzymes catalyze the primary catabolic pathway for 5-HT oxidative deamination. Serotonin is converted into 5-hydroxy-indoleacetaldehyde, and this product is further oxidized by a NAD-dependent aldehyde dehydrogenase to form 5-hydroxyindoleacetic acid (5-HIAA). Immunohistochemical techniques and in situ hybridization histochemistry techniques are used to study the neuroanatomical localization and biochemical nature of the two forms of MAO [36].
Different antidepressant drugs like phenelzine and tranylcypromine inhibit the activity of monoamine oxidase. These are a result of MAO metabolizes biogenic amines such as 5-HT, DA, and NE. In addition, different dopaminergic neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) are metabolized by MAO [37].
Another essential class of oxidoreductase enzyme is NADPH-cytochrome P450 reductase (CPR). It is a membrane-bound protein localized in the ER membrane. PR involves in the detoxification and activation of a number of xenobiotics. CPR uses FAD and FMN as cofactors, and it transfers the hydride ion of NADPH to FAD, and then FAD transfers electrons to FMN and other oxidases. Finally, it reduces the P450 enzyme heme center to activate molecular oxygen. Thus, electrons transfer from NADPH to the P450 heme center by CPR, which is central for P450-catalyzed metabolism. Flow of electron can be expressed as follows:
Human cytochrome P450 reductase is encoded by the POR gene. It is a 78-kDa multi domain diflavin reductase that binds both FMN and FAD and is attached to the cytoplasmic side of the endoplasmic reticulum via a transmembrane segment at its N-terminus [5, 15, 38].
Several industries such as pharmaceutical, foods, biofuel production, natural gas conversion, and others have used enzyme catalysis at commercial scale [39]. Classes of oxidoreductase enzymes are becoming a target by a number of industries. The family of oxidoreductase like heme-containing peroxidases and peroxygenases, flavin-containing oxidases and dehydrogenases, and different copper-containing oxidoreductases is involved in synthesis and degradation of interested products by the above industries and they are biocatalysts of interest for establishing a bio-based economy. Oxidoreductase enzymes have the highest potential in the production of polymer building blocks, sustainable chemicals, and materials from plant biomass within lignocellulose biorefineries [6, 7, 40].
Enzymes are biological catalysts and have great specificity, efficiency, and selectivity in the reaction they catalyze [39]. Oxidoreductase enzymes have different redox-active centers for doing their functions. These unique features of oxidoreductase enzymes make it valuable targets of pharmaceutical and chemical industries. Advancement in recombinant DNA technology, protein engineering, and bioinformatics is a critical event in the application of enzymes in different industries. A number of dug synthesis processes require the involvement of oxidoreductase enzymes [6].
An oxidoreductase is involved in the synthesis of 3,4-dihydroxylphenyl alanine (DOPA), and 3,4-dihydroxylphenyl alanine is a drug used for treatment of Parkinson’s disease [41]. Similarly, a class of oxidoreductase called monoamine oxidase (MAO) catalyzes enantiomeric desymmetrization of bicyclic proline intermediate, which is an important precursor in the synthesis of boceprevir. Boceprevir is a NS3 protease inhibitor that is used for the treatment of chronic hepatitis C infections. Using MAO in this reaction reduces time and waste product generation and is economically cost-competitive and profitable [42]. Its coenzyme specificity makes oxidoreductase an effective biocatalyst in protein engineering [43]. In vitro different oxidoreductase enzymes are involved in regeneration of coenzymes, pyridine nucleotides, NAD(H) and NADP(H). Alcohol dehydrogenase and format dehydrogenase are frequently used enzymes for recycling of coenzymes, and the intermediate products are useful in the synthesis of pharmaceutical drugs such as mevinic acid [44, 45].
Enzymes are biological catalysts and have a number of applications in agricultural fields. Using enzymes has great efficacy and efficiency over chemical catalysts with respect to their productivity, time, cost, quality, and quantity products. There are different classes of oxidoreductase enzymes nowadays involved in fertilizer production, dairy processing, and other food processing in agricultural sector, and their cost-effectiveness and quality product were confirmed by a number of researches [3].
Manipulation of gene cod for different oxidoreductase in plants can also change the characters of plants in a way that it increases productivity and resists adverse effects of herbicide and environmental changes. For example, modification of DNA for glyphosate oxidoreductase (GOX) enzyme that catalyzes the oxidative cleavage of the C▬N bond on the carboxyl side of glyphosate, resulting in the formation of aminomethylphosphonic acid (AMPA) and glyoxylate thereby augmented expression of GOX plants, results in glyphosate herbicide side effect tolerance [46, 47]. Some families of oxidoreductase like xanthine dehydrogenase in plants are used to metabolize reactive oxygen species associated with plant-pathogen and protect plants from stress-induced oxidative damage. Upregulation of xanthine dehydrogenase expression in plants is helpful to increase productivity [48, 49].
Classes of oxidoreductase are also involved in dairy processing. Glucose oxidase produced by fungal species acts as preservatives in dairy products and other foods. The intermediate and end product of glucose oxidase have antimicrobial effect [50]. Isozyme of xanthine oxidoreductase in bovine milk, which catalyzes reduction of oxygen to generate reactive metabolite is used as an anti-microbial agent in the neonatal gastrointestinal tract [51]. Similarly, peroxidases which are a family of oxidoreductase found in higher plants catalyze the oxidation of many compounds including phenolics, in the presence of hydrogen peroxide responsible in browning or darkening of noodles and pasta and associated with a grain quality defect [52]. Protochlorophyllide oxidoreductase (POR), which exists in two isozymes POR A and POR B, plays a vital role in plant chlorophyll synthesis, and manipulation on these genes can induce plant development [53]. In general, there are a number of oxidoreductase enzymes found in plants, and their normal activity is crucial for qualitative and quantitative productivity of crops, and these were confirmed by a number of active researches. Different interventions are also going on at gene level to control the expression of oxidoreductase enzymes in plant as needed [3].
Oxidoreductase enzymes are involved in a number of valuable biochemical reactions in the living organism, and their qualitative and quantitative normality is essential. For example, one important class of oxidoreductase is xanthine oxidoreductase (XOR) that catalyzes oxidative hydroxylation of hypoxanthine to xanthine then to uric acid and over activity XOR leads to hyperuricemia and concomitant production of reactive oxygen species. In turn, hyperuricemia is confirmed as an independent risk factor for a number of clinical conditions such as gout, cardiovascular disease, hypertension, and others. Different urate-lowering drugs or XOR inhibitors are nowadays implemented to prevent and manage hyperuricemia disorder [9].
Another important class of oxidoreductase enzyme is cytochrome P450 oxidoreductase (POR) that is essential for multiple metabolic processes. Cytochrome P450 enzymes are involved in metabolism of steroid hormones, drugs, and xenobiotics. Nowadays, more than 200 different mutations and polymorphisms in POR gene have been identified and cause a complex set of disorders. Deficiency of cytochrome P450 oxidoreductase affects normal production of hormone; specifically, it affects steroid hormones, which are needed for normal development and reproduction. This is highly linked with the reproductive system, skeletal system, and other functions. Signs and symptoms can be seen from birth to adult age with different severities. Individuals with moderate cytochrome P450 oxidoreductase deficiency may have ambiguous external genitalia and have a high chance of infertility but a normal skeletal structure [5, 16, 18].
Aldehyde dehydrogenase 2 (ALDH2) deficiency known as Asian glow or alcohol flushing syndrome is a common genetic health problem that interferes with alcohol metabolism, and ALDH2 is a classical family of oxidoreductase enzymes. It was confirmed that ALDH2 deficiency results in the accumulation acetaldehyde, which is a toxic metabolite of alcohol metabolism and responsible for a number of health challenges like esophageal, head, and neck cancer. A number of researches conclude that acetaldehyde is a group 1 carcinogenic metabolite [33, 54]. Similarly, monoamine oxidase deficiency, which is a family oxidoreductase enzyme, affects the normal metabolism of serotonin and catecholamines. It is a rare X-linked disorder characterized by mild intellectual disability, and behavioral challenges appear at earlier age. Monoamine oxidase-A deficiency that occurs almost exclusively in males has episodes of skin flushing, excessive sweating, headaches, and diarrhea. Monoamine oxidase-A deficiency can be diagnosed by finding an elevated urinary concentration of the monoamine oxidase-A substrates in combination with reduced amounts of the monoamine oxidase products [36, 55].
Mitochondria generate huge amounts of energy (ATP) to eukaryotic cells through oxidation of fats and sugars; and fatty acid β-oxidation and oxidative phosphorylation are two metabolic pathways that are central to this process. Qualitative and quantitative normality of oxidoreductase enzymes involved in oxidative phosphorylation and fatty acid oxidations are essential to get sufficient energy (ATP) form metabolism. Deficiency of a complex I (NADH-CoQ oxidoreductase) is common, and a well-characterized mitochondrial problem causes reduced ATP production [56]. Complex I (NADH-CoQ oxidoreductase) is responsible for recycling of NADH to NAD+, and in turn, this is essential to sustain Krebs cycle and glycolysis. Mutations in both nuclear and mitochondrial DNA for Complex I gene are responsible for mitochondrial disease. Individuals with mitochondrial diseases suffer from an energy insufficiency characterized by myopathies, neuropathy, delayed development, cardiomyopathy, lactic acidosis, and others. Furthermore, since mitochondria are a hub of metabolism, mitochondrial dysfunctions are highly associated with metabolic diseases like hypertension, obesity, diabetes, neurodegenerative diseases, and even aging. Deficiency of complex I leads to elevation of NADH levels in the mitochondria that inhibit pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. This condition completely inhibits Krebs cycle, and it is measured by CO2 evolution from [14C] labeled precursors. Similarly, complex II (succinate:ubiquinone oxidoreductase) deficiency affects both fatty acid oxidation and electron transport chain, and it induces retinopathies and encephalopathies [57, 58].
Deficiency of the pyruvate dehydrogenase complex (PDHC), another class of oxidoreductase enzymes, causes similar clinical and biochemical alteration in energy production with complex I (NADH-CoQ oxidoreductase) [59]. Both TCA cycle and respiratory chain can be affected by succinate dehydrogenase deficiency. Deficiency of oxidoreductase enzymes involved in Krebs cycle affects all carbohydrate, protein, fat, and nucleic acid metabolism as it is a common pathway for metabolism of the above macromolecules [60].
Oxidoreductase enzymes are also involved in bile acid synthesis. Classes of oxidoreductase enzymes called 3beta-hydroxy-Delta (5)-C (27)-steroid oxidoreductase catalyze an early step of bile acids synthesis from cholesterol and are encoded by HSD3B7 gene on chromosome 16p11.2-12. Mutations of HSD3B7 gene affect bile acids synthesis, cause development of progressive liver disease characterized by cholestatic jaundice, malabsorption of lipids, and lipid-soluble vitamins from the gastrointestinal tract, and finally progress to cirrhosis and liver failure [61].
One important biomolecule that acts as a precursor for other molecules and a component of cell membrane is cholesterol. Mammalian cells can get cholesterol from de novo biosynthesis or uptake of exogenously derived cholesterol associated with plasma low-density lipoprotein (LDL). 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which is a class of oxidoreductase, catalyzes the rate-limiting steps of de novo cholesterol biosynthetic pathway and target for manipulation pharmacologically. Under or over activity of HMG-CoA reductase can disturb cholesterol homeostasis and lead to either hypercholesterolemia or hypocholesterolemia. And disturbed cholesterol level associated with number serious clinical problem like atherosclerosis [62, 63].
The authors declare that they have no competing interests.
Mezgeu Legesse Habte drafted the paper and write the literature review.
Etsegenet Assefa assisted in guidance, critical assessment and peer review of the writing. Both authors have given their final approval of this version to be published. Both authors read and approved the final manuscript.
Availability of data and material: All necessary data and materials related to the article are included in the article.
Funding: This review article is not funded by any person or organization (not funded).
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
\n\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\n\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
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\n\nWork - a Chapter, including Conference Papers, and any and all text, graphics, images and/or other materials forming part of or accompanying the Chapter/Conference Paper.
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\n\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\n\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
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\n\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
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Creative Commons Attribution 3.0 Unported (CC BY 3.0) | \n\t\t\t\n\t\t\t 5 October 2011 (2011-10-05) \n\t\t\t | \n\t\t\tCurrently | \n\t\t
The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
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