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Fatty Acids in Veterinary Medicine and Research

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Siobhan Simpson, Alison Mostyn and Catrin S. Rutland

Submitted: January 25th, 2017 Reviewed: March 9th, 2017 Published: June 21st, 2017

DOI: 10.5772/intechopen.68440

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Fatty acid regulation is an essential process for all animals. A number of studies have shown that diet affects the levels/availability of fatty acids in the body but increasingly an evidence shows that disease states can alter the amounts within the body too. Fatty acid levels and availability have been altered by a number of diseases, disorders and reactions including inflammatory responses, heart disease and heart failure and wound repair. They are also essential during the growth and development stages of animals. The amount of research into the consequences of different fatty acid intake and levels in various disease states and during development has increased in both humans and animals. This review presents an overview of the research undertaken to date and highlights the importance, uses and benefits of understanding the roles of fatty acids in both the healthy animals and animals under differing disorders and diseases.


  • heart disease
  • Inflammation
  • development
  • nutrition
  • cancer
  • pregnancy

1. Introduction to fatty acids

Fatty acids consist of a carboxylic acid with a hydrocarbon chain tail, the length of which varies between fatty acids, as does the presence or absence of double bonds between the carbon atoms and their location [1]. Some fatty acids are ingested in the diet whereas others are synthesized into other fatty acids by elongation and desaturation enzymes [24], see Figures 1 and 2. In mammals, fatty acids are obtained from the diet prior to metabolism or incorporation as components of cells [58]. n-6 polyunsaturated fatty acids (PUFAs) and n-3 PUFAs are the two major groups of fatty acids; the first is obtained from fats and oils, and the latter from fish and seafood products [6]. It is essential that the precursors of both n-6 and n-3 PUFAs are extracted by mammals from their diet as they are not able to convert these fatty acids (FAs) between the two major pathways [9].

Figure 1.

Schematic of linoleic and arachidonic acid biosynthetic pathway derived from KEGG pathway maps [2].

Figure 2.

Schematic of palmitic and oleic acid biosynthesis pathway derived from KEGG pathway maps [2].


2. Inflammation, disease and the immune system

Fatty acids are crucial components of the immune system, providing the structural basis of all cell membranes, acting as signaling molecules, and providing a major substrate for energy production [1, 8, 10]. Many diseases involve inflammatory responses either as a reaction to disease or in the initiation of the disease process; although inflammation itself is not always detrimental, for instance, it is an important aspect of wound repair [1114]. Elevated markers of inflammation are frequently detected in heart failure and cancers although this could be due to the response to disease, or the underlying cause of disease [1519].

Fatty acid-derived eicosanoids are important contributors to the inflammatory response [13, 20, 21]. The n-6 PUFA arachidonic acid is a precursor of the most important pro-inflammatory eicosanoids, while the n-3 PUFA derivatives, eicosapentaenoic acid and docosahexaenoic acid metabolites are considered less inflammatory [20]. Arachidonic acid is released from cell membranes by phospholipase A2 enzymes in response to pro-inflammatory stimuli [2225]. Cyclooxygenase, lipoxygenase and cytochrome P450 enzymes then convert free arachidonic acid into eicosanoids [2629]; however, these enzymes are rate limiting as they similarly convert other fatty acids to their metabolites [20]. It has been suggested that if cyclooxygenase, lipoxygenase and cytochrome P450 enzymes are exposed to increased levels of n-3 fatty acids, the result is fewer arachidonic acid-derived eicosanoids [20, 30].

Due to the difference in the inflammatory response between fatty acid metabolites, it is hypothesized that the fatty acid profiles could differ between diseased and healthy individuals. Indeed, fatty acid profiles have been shown to be altered in blood and tissues in individuals with a range of conditions compared to unaffected individuals in both humans and dogs. These conditions include Crohn’s disease, heart disease, skin disease and cancer [3134], and are discussed in greater detail below.

2.1. The role of fatty acids in Crohns’ disease

An interesting inflammatory response disorder is inflammatory bowel disease, including Crohn’s disease. A number of animal studies, including guinea pigs and rats, have shown novel results in the adipocytes, lipid rafts and fatty acid-derived messenger molecules which indicated that aberrant fatty acid composition could play a role in Crohn’s disease [3538]. This research led directly into looking at the role of FAs in human cases of Crohns’ disease, a disorder which is linked to both inflammation and the immune system. Perinodal adipose tissue (PAT) is a specialized adipose tissue depot which surrounds lymph nodes and acts in a paracrine manner—delivering specific FAs and adipokines directly to the node. Research has demonstrated that PAT associated with the lymph node is present in most animals and humans [39]. Crohn’s disease is associated with altered mesenteric PAT FA content, suggesting impaired delivery of FAs to lymphocytes [40]. For many years, patients with Crohn’s disease have been advised to take dietary fish oils that are rich in n-3 PUFAs, but interestingly patients have naturally (prior to taking supplements) presented with higher levels of n-3 PUFAs than observed in controls with concurrent deficiencies in arachidonic acid (20:4n-6) [4143]. More recent evidence suggests that higher levels of n-6 PUFAs, including linoleic acid (18:2n-6) were most effective at relieving inflammatory symptoms [43]. The biosynthetic links between arachidonic acid (20:4n-6) and linoleic acid (18:2n-6) are shown in Figure 1 and help to understand why an increased linoleic acid intake could reverse the decrease in arachidonic acids observed in patients. A number of animal species develop differing forms of inflammatory bowel disease, therefore understanding whether FAs are affected for the differing types of animals and differing breeds could help to indicate differing dietary or treatment requirements.

2.2. The role of fatty acids in cardiovascular function and disease

A number of links have been made between fatty acid levels and heart disease and heart failure. Human patients with significant left ventricular dilation have a larger percentage of oleic acid and a smaller percentage of arachidonic acid in their blood serum compared to patients with moderate left ventricular dilation [33]. It is also important to highlight that none of the patients involved in the study had a confirmed diagnosis, and although valve disease and coronary artery disease were excluded as the underlying cause of left ventricular dilation, infarction was not. Infarction may have skewed the fatty acid results due to the strong inflammatory nature of myocardial infarction [33, 44].

In cats with hypertrophic cardiomyopathy, differing levels of FAs were observed when compared to cats with no hypertrophic symptoms [45]. Hypertrophic cardiomyopathy cats had higher levels of docosahexaenoic acid, palmitic acid and total n-3 PUFAs and lower levels of linoleic acid. Differential levels of docosatetraenoic acid have been observed in canine myocardial tissue in dogs affected by dilated cardiomyopathy [46]. Mobile lipid content within the myocardium was significantly increased in a 24-hour coronary occlusion canine heart, not only throughout the body but also ‘local’ increases were observed around the heart with cardiac levels up to 10 times higher than the rest of the body [4750]. It has been suggested that increased fatty acid levels alongside a decrease in creatine can lead to diastolic dysfunction, as observed in humans with diabetic cardiomyopathy [51, 52]. Despite the observations in dogs and humans, a study in rats showed increased fatty acids and decreased creatine but no associated diastolic dysfunction was observed [53]. With differing observations between species, more research is needed in order to understand the mechanisms and circumstances under which diastolic alteration occurs. Increased levels of palmitoleic acid have been associated with heart failure, higher levels of behenic acid and stearic acid have been associated with lower risk of developing atrial fibrillation, women with higher circulating pentadecanoic acid are less likely to have a myocardial infarction, hypertensive rats have higher circulating eicosedienoic acid and in renal patients higher circulating C20:5n3 is associated with good cardiac functional measures [5460].

Although the fatty acids themselves play a key role in cardiovascular health and disease, other molecules within the fatty acid utilization cascades play important roles too. Heart-type fatty acid-binding protein (H-FABP) is expressed in cardiomyocytes and despite the name, it is also expressed in renal and skeletal muscle cells [61]. Heart-type fatty acid-binding protein (H-FABP) is used as a prognosis tool biomarker in human cardiac disease as it indicates myocardial stretch and injury in chronic heart failure even in children. Higher levels of H-FABP are associated with a poorer long-term outcome in both adults and children [6165]. Although little work has been carried out in other species, this is an area of research which has potential, in addition to investigating whether H-FABP levels are raised prior to infarction and/or heart disease. A rat model has shown that H-FABP is increased following cardiac injury [66]. It also enables detection via a number of differing methods including EIA, ELISA, fully automated latex-agglutination assay and qualitative lateral-flow assay microparticle enhanced immunoassay [61].

External factors such as diet and surgery can play large roles in fatty acid composition and cardiovascular health. A study looking at differing feeding regimes in obese rats in comparison with lean rats showed that n-3 acyl chains, unsaturated and polyunsaturated fatty acids, were all significantly higher in obese rats than in the lean ones [53]. What was also interesting was the fact that mild, short-term diet changes (food intake was restricted by 20% for two weeks) did not alter the cardiac fatty acid profiles. The obese mice also showed symptoms of early stage obese cardiomyopathy; although interestingly the symptoms of this started to improve upon calorie restriction, an important finding as it showed that mild calorie restriction can be of benefit under these circumstances. Fatty acids are not only an important indicator of heart disease in animals, but also important in situations such as surgery. Increased free fatty acid levels also have been noted in response to heart surgery in pigs especially when heparin is co-administered [67]. In the surgery cases, it was found that the young patients were more affected than older patients and the levels were more likely to rise if cyanosis and prolonged ischemia were present.

Although most of the work into cardiovascular health has concentrated on disease and disorders, a number of suggestions for healthy levels have been put forward as ways of preventing disease. There is some evidence that higher levels of circulating arachidic acid are associated with lower risk of atrial fibrillation and diabetes [57, 68]. Another example is docosahexaenoic acid (n-3 PUFA) which has been implicated as having beneficial effects in a wide range of diseases including heart disease and neurological dysfunction [55, 69].

2.3. Fatty acids and skin disease

There are two main ways in which differing fatty acid profiles contribute to skin disease—as part of inflammation and affecting membrane fluidity. These are not mutually exclusive and it is possible that fatty acids are affecting the development of skin disease via both. People with atopic eczema have been shown to have a different fatty acid profile in their skin than people without atopic eczema. In particular, they have shorter fatty acids within their skin than unaffected individuals. This difference is suggested to lead to impaired skin barrier [70]. Atopic eczema is an inflammatory disease and thus processes of inflammation as discussed earlier will be active in the disease process [71]. As with other cases where a difference in fatty acid profiles has been established between individuals with disease and healthy individuals, it is not clear whether the fatty acid change causes the disease or is a response to disease, or possibly both, but it is a potential novel treatment route. Similar to people with atopic eczema, pruritic dogs have been shown to have a different fatty acid profile compared to dogs with healthy skin [72]. More recently, dogs with atopic dermatitis whose diets were supplemented with n-3 PUFA improved significantly more than those given the placebo [73]. As with human skin disease, it is not clear as to how this works, but it is an additional treatment option and area for further research.

2.4. Cancer associations with fatty acids

Cancer is the result of aberrant cellular processes. Many genes and proteins are differentially expressed in tumor tissue compared to nontumor tissue [7477]. Thus, it is intuitive that fatty acid profiles are likely to be altered in tumors compared to nontumor tissue and this has indeed been demonstrated in breast and prostate cancer [78, 79].

There have been studies showing that differential dietary intake of fatty acids can either reduce or increase risk of disease, including cancer. A meta-analysis of studies relating breast cancer risk with n-3 PUFA intake showed that overall increasing n-3 PUFA intake reduced the risk of developing breast cancer [78]. In transgenic mice in which males develop prostate cancer, n-3 PUFA intake from marine sources suppressed tumorigenesis [80]. This is also the case in people where there is reduced risk of developing prostate cancer with increased intake of marine n-3 PUFAs [8183]. Longer chain n-3 PUFAs from non-marine sources, however, are associated with an increased risk of prostate cancer [79, 82, 83].

While ultimately work is required in whole organisms, cell lines are a valuable starting point for research. Of particular note in relation to veterinary medicine and fatty acids are two studies on canine tumor cell lines. The first is that of canine lymphoma cell lines; in this study, stearidonic acid was shown to sensitize cells to anticancer drugs, even when the cells were previously resistant to drugs [84]. The second study utilized fatty acids themselves as antitumor agents. In this study, a specific fatty acid, trans-10, cis-12 conjugated linoleic acid, was shown to inhibit cell growth and induce apoptosis in canine osteosarcoma cell lines and canine lipomas [85, 86].


3. The effects of fatty acids on fertility and during pregnancy and development

Many animal and human studies have established that restriction of a range of nutrients within the maternal diet throughout pregnancy results in offspring that are programmed to be at increased risk of later hypertension and metabolic disease including diabetes and obesity [8790]. This theory has become known as the “developmental origins of health and disease” (DOHaD) hypothesis. Fatty acid intake has been shown to have effects even before pregnancy as severe undernutrition of specific fatty acids has resulted in low reproductive rates in males and females. For example, in male cats, a linoleic deficient diet results in tubular degeneration of the testes and low fertility rates, and in females, the litters were not viable [91, 92].

Other studies have shown birth defects in offspring from females fed on low fatty acid diets but it also showed that arachidonate was a key contributor to viable offspring [93, 94]. In contrast, excess macronutrient intake has been implicated in the incidence of the metabolic syndrome is emerging in a number of rodent [9597] and sheep studies [98]. Studies linking maternal over-nutrition to adverse offspring health in later life are conspicuously lacking, despite a huge effort in understanding the influence of maternal nutrition and its link to obesity. A number of rodent studies have established that a high-fat maternal diet leads to impaired offspring glucose and lipid metabolism [9597, 99], but the influence of increasing other dietary components has not been investigated, perhaps due to the assumption that a high-fat or “junk food” diet is more prevalent in the western world. Rodent studies of increased fat intake during pregnancy are often associated with an overall decrease in food intake which limits their usefulness [97]. The timing of a nutritional insult is also important in determining the outcome for offspring, differential results have been observed in studies investigating early or late gestational nutritional insults in both animal [100, 101] and human studies [102]. As well as a high-fat diet increasing adipocyte and ectopic lipid accumulation, it may also decrease glycogen deposition in skeletal muscle. Increased plasma free fatty acids impair insulin-stimulated glucose disposal, including glycogenesis and glucose uptake—resulting in reduced skeletal muscle glycogen content [103]. Type-2 diabetes in humans is associated with a reduction in glycogen synthase and tissue glycogen [104], it is unknown whether a sub-optimal maternal diet will result in similar changes in offspring. Recent work has demonstrated that there are physiological [105107] and emerging molecular differences between pigs with low, normal or high birth weights [108111]. Extensive physiological examinations of low and high birth weight pigs, at 12 months of age showed that low birth weight pigs had increased fat depth and glucose intolerance and insulin resistance [105]. Also of interest is that, peroxisome proliferator-activated receptor (PPAR)α expression in skeletal muscle is positively correlated to birth weight in these pigs [110]. In younger pigs (7 or 14 days of postnatal age) designated low, normal or high to birth weight, molecular differences have been observed in adipose tissue and skeletal muscle genes known to regulate lipid metabolism including uncoupling proteins (UCPs), PPARα and γ, fatty acid-binding protein (FABP) 3 and 4 and the glucocorticoid receptor (GR) [108, 109, 111].

The role of PPARs is not just restricted to animals subjected to over-nutrition. Studies of maternal low protein diets in rats have demonstrated that post-weaning, offspring had significantly increased hepatic PPARα expression due to decreased methylation as a result of differences in overall dietary fat intake [112]. PPARs are a nuclear hormone receptor family that have attracted much interest due to their involvement in adipogenesis, lipid metabolism, insulin sensitivity, inflammation and blood pressure [113]. PPARγ regulates transcription of genes involved in lipid metabolism by binding to responsive elements in the promoters of respective genes. This transcription regulation stimulates fatty acid storage in adipose tissue by increasing the storage capacity and the quantity of fatty acids that enter adipocytes and also plays a key role in adipocyte differentiation, promoting the formation of mature lipid-laden adipocytes [114]. The activities of PPARγ are regulated by fatty acids (which are thought to be the endogenous ligands) [115]. PPARγ is often referred to as the “genetic sensor” for fat and a number of dietary studies have demonstrated an increase following high-fat feeding [116, 117], which may provide benefits to the animal by protecting against lipotoxic species [117]. PPARα also acts as a ligand-activated transcription factor and is expressed in tissues which have a high rate of fatty acid catabolism such as skeletal muscle and liver. The fibrate group of drugs has long been utilized as a synthetic ligand for PPARα, but endogenous ligands are still under investigation. Long-chain fatty acyl-CoAs and saturated fatty acids however are known to activate PPARα at micromolar ranges [118]. PPARα has a key role in stimulating lipid oxidation pathways to prevent storage of fats as well as increasing insulin sensitivity and glucose tolerance. The expression of PPARs may represent one of the molecular factors driving excess tissue lipid uptake, storage and production in animals that experienced a sub-optimal environment in utero, in particular low birth weight offspring; ectopic lipid storage, especially intramyocellular, is associated with glucose intolerance and type-2 diabetes [104, 119].

The regulation of fatty acids is also an important factor during the lactation period. A number of studies have shown that the relative fatty acid content of milk differs depending on the species. Donkeys have milk more similar to humans than cows, with lower levels of saturated fats and higher essential fatty acids than cows, more akin to humans [120, 121]. Milk, from humans, dog, and guinea pig are mostly comprised from long-chain fatty acids (48–54 acyl carbon atoms), cow, sheep, and goat, have more short-chain acids (28–54 acyl carbon atoms) and horses tended to have medium-chain fatty acids (26–54 carbon atoms range) [122]. Maternal diet can also have an impact on the fatty acid contents of her milk. This has been shown in many species from mice and sheep to humans [123125]; the pregnancy status of the mother also vastly changes milk fatty acid composition [126]. These are important factors when assessing whether the mother is receiving an appropriate diet, assessing whether she is pregnant or not and whether milk replacement formulae contain the appropriate levels of fatty acids.


4. Fatty acid-binding proteins and lipid modulation

Fatty acids are now recognized as crucial components of cellular signaling cascades, in particular, those regulating lipid metabolism, as described above with PPARs. Research into fatty acids as signaling molecules is in its infancy, but it is well known that fatty acids are ligands for transcription factors. Fatty acids are carried through tissue membranes and in the cytosol by chaperones known as fatty acid-binding proteins (FABPs), of which there are a number of tissue-specific isoforms [127]. Knock-out mice not expressing the adipocyte-specific FABP4 exhibited protection from the metabolic effects (e.g. insulin resistance and hypercholesterolaemia) of a high-fat diet, suggesting FABP4 modulates a number of components of the metabolic syndrome [127]. In skeletal muscle, a fat-rich diet increases the expression of the cytosolic and plasma membrane specific FABP [128].

Insulin resistance is characterized by a decrease in the enzymes and proteins involved in lipid oxidation [129]. Lipogenesis and adipogenesis are modulated by the enzymes acetyl-CoA carboxylase 1 and 2 (ACC1 and ACC2, respectively) and AMP-activated protein kinase (AMPK); both enzymes are potential drug targets to treat obesity and the metabolic syndrome and AMPK has been suggested as a target for metformin [130, 131]. Briefly, ACC1 controls fatty acid biosynthesis and ACC2 controls fatty acid oxidation. ACC1 catalyses the conversion of acetyl-COA to malonyl-CoA, therefore modulating the rate limiting step of long-chain fatty acid biosynthesis in adipose tissue. ACC2 is expressed in skeletal muscle, where the product malonyl-CoA inhibits fatty acid oxidation. The AMPKα subunit is activated during periods of metabolic stress (e.g. increased AMP/ATP ratio) by phosphorylation and inhibits the activity of ACC1 and 2, thus promoting fatty acid oxidation, glucose uptake and inhibits lipid synthesis [132] and thereby reducing ectopic lipid storage. An isocaloric high-fat diet has been shown to inhibit AMPK in rats [133]. Despite great potential for modulation by maternal diet, there are few DOHAD studies of ACC and AMPK expression; however, early studies of an obese pregnant ewe model have shown decreased AMPK signaling in fetal offspring muscle [98].


5. Future fatty acid research and medicine

Although artificially induced disease often only replicates a small aspect of disease and does not reflect the typically longer time scales involved in natural disease progression in both humans and animals [134, 135], these studies can be valuable when compared to naturally occurring diseases in order to understand mechanisms and development. All of the ‘natural population’ studies discussed in this chapter may have their own caveats too. Differences in diet, age, sex and even pre-clinical symptoms and diagnosis can all affect the results observed in both disease and fatty acid states. This chapter has concentrated on development, cardiovascular disease, cancer and immunity but differing fatty acids have been implicated or associated with in a number of diseases and disorders ranging from human, rodent and canine epilepsy through to canine ADHD and reproductive ability [92, 136, 137].

Fatty acid profiling has important potential applications as a diagnosis tool across the species, especially in cases where pre-clinical symptoms are difficult to observe. Although it is not always necessarily known if differences in fatty acid profiles are contributing to the initiation of disease or are a response to disease processes, these differences could be drug targets [26, 138140]. In addition, there are genes that contribute to fatty acid profile composition and if a particular part of the pathway is shown to be different in individuals with disease compared to healthy individuals, these could be likely genes for candidate gene studies in the future [141, 142]. The scientific methodologies available for looking at lipid levels have also progressed over the years; just one example is the use of proton magnetic resonance spectroscopy of protons (H-MRS) to assess cardiac lipids in a non-invasive manner [52]. This is a valuable tool for animal health and welfare, and there are additional uses in looking at metabolism and fatty acids. Much of the present work involves looking at genes and lipid levels of animals intended for the meat industry. An example is the evidence that differing polymorphisms in genes can result in differing meat quality traits. This includes fatty acid synthase (FASN) which was found to correlate with meat weight loss during the first salting of dry-cured ham production [143], meat quality including marbling in cattle [144] and playing a role in the mammary gland and milk in goats and cattle [145, 146], in addition to many other roles. Differing H-FABP polymorphisms/expression levels have also been related to growth rate and size of beef cattle and chickens and could therefore provide useful markers for breeding [147, 148].

Research into the links between fatty acids and differing developmental stages and disease states is increasing in both humans and animals and provides the potential for innovative diagnostic and treatments tools.



This work was supported by the Biotechnology and Biological Sciences Research Council [grant number BB/J014508/1], by generous funding to Catrin S. Rutland from the BBSRC University of Nottingham Doctoral Training Programme.


  1. 1. Fahy E, et al. A comprehensive classification system for lipids. Journal of Lipid Research. 2005;46(5):839-862
  2. 2. Kanehisa M, et al. KEGG as a reference resource for gene and protein annotation. Nucleic Acids Research. 2016;44(D1):D457-D462
  3. 3. Vessby B, et al. Indices of fatty acid desaturase activity in healthy human subjects: Effects of different types of dietary fat. British Journal of Nutrition. 2013;110(5):871-879
  4. 4. Wang Y, et al. Tissue-specific, nutritional, and developmental regulation of rat fatty acid elongases. Journal of Lipid Research. 2005:46(4):706-715
  5. 5. Farvid MS, et al. Dietary linoleic acid and risk of coronary heart disease: A systematic review and meta-analysis of prospective cohort studies. Circulation. 2014 Oct 28;130(18):1568-78. doi: 10.1161/CIRCULATIONAHA.114.010236. Epub 2014 Aug 26
  6. 6. Meyer BJ, et al. Dietary intakes and food sources of omega-6 and omega-3 polyunsaturated fatty acids. Lipids. 2003;38(4):391-398.
  7. 7. Burns CP, et al. Effect of modification of plasma membrane fatty acid composition on fluidity and methotrexate transport in L1210 murine leukemia cells. Cancer Research. 1979;39(5):1726-1732
  8. 8. Kröger J, et al. Erythrocyte membrane fatty acid fluidity and risk of type 2 diabetes in the EPIC-Potsdam study. Diabetologia. 2014;58(2):282-289
  9. 9. Kang JX, et al. Transgenic mice: Fat-1 mice convert n-6 to n-3 fatty acids. Nature. 2004;427(6974):504
  10. 10. Wolters M, et al. Reference values of whole-blood fatty acids by age and sex from European children aged 3-8 years. International Journal of Obesity. 2014;38(S2):S86-S98
  11. 11. Danesh J, et al. Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. British Medical Journal. 2000;321(7255):199-204
  12. 12. Gurtner GC, et al. Wound repair and regeneration. Nature. 2008;453(7193):314-321
  13. 13. Harris RE. Cyclooxygenase-2 (cox-2) blockade in the chemoprevention of cancers of the colon, breast, prostate, and lung. Inflammopharmacology. 2009;17(2):55-67
  14. 14. Mohler, ER, et al. Bone formation and inflammation in cardiac valves. Circulation. 2001;103(11):1522-1528
  15. 15. Aukrust P, et al. Elevated circulating levels of C-C chemokines in patients with congestive heart failure. Circulation. 1998;97(12):1136-1143
  16. 16. Il'yasova D, et al. Circulating levels of inflammatory markers and cancer risk in the health aging and body composition cohort. Cancer Epidemiology Biomarkers & Prevention. 2005;14(10):2413-2418
  17. 17. Leyva F, et al. Uric acid in chronic heart failure: A marker of chronic inflammation. European Heart Journal. 1998;19(12):1814-1822
  18. 18. Pankuweit S, et al. The HLA class II allele DQB1 0309 is associated with dilated cardiomyopathy. Gene. 2013;531(2):180-183
  19. 19. Shiels MS, et al. Circulating inflammation markers and prospective risk of lung cancer. Journal of the National Cancer Institute. 2013 Dec 18;105(24):1871-80. doi: 10.1093/jnci/djt309. Epub 2013 Nov 18.
  20. 20. Bagga D, et al. Differential effects of prostaglandin derived from ω-6 and ω-3 polyunsaturated fatty acids on COX-2 expression and IL-6 secretion. Proceedings of the National Academy of Sciences. 2003;100(4):1751-1756
  21. 21. Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature New Biology. 1971;231(25):232-235
  22. 22. Bonventre JV, et al. Reduced fertility and postischaemic brain injury in mice deficient in cytosolic phospholipase A2. Nature. 1997;390(6660):622-625
  23. 23. Burch RM, Luini A, Axelrod J. Phospholipase A2 and phospholipase C are activated by distinct GTP-binding proteins in response to alpha 1-adrenergic stimulation in FRTL5 thyroid cells. Proceedings of the National Academy of Sciences. 1986;83(19):7201-7205
  24. 24. Lee IT, et al. Cooperation of TLR2 with MyD88, PI3K, and Rac1 in lipoteichoic acid–induced cPLA(2)/COX-2–dependent airway inflammatory responses. The American Journal of Pathology. 2010;176(4):1671-1684
  25. 25. Xu J, et al. Prostaglandin E2 production in astrocytes: Regulation by cytokines, extracellular ATP, and oxidative agents. Prostaglandins, Leukotrienes, and Essential Fatty Acids. 2003. 69(6):437-448
  26. 26. McAdam BF, et al. Systemic biosynthesis of prostacyclin by cyclooxygenase (COX)-2: The human pharmacology of a selective inhibitor of COX-2. Proceedings of the National Academy of Sciences. 1999;96(1):272-277
  27. 27. Morrison AR, Pascoe N. Metabolism of arachidonate through NADPH-dependent oxygenase of renal cortex. Proceedings of the National Academy of Sciences. 1981;78(12):7375-7378
  28. 28. Oliw EH, et al. Arachidonic acid metabolism in rabbit renal cortex. Formation of two novel dihydroxyeicosatrienoic acids. Journal of Biological Chemistry. 1981;256(19):9924-9931
  29. 29. Palmer RMJ, et al. Chemokinetic activity of arachidonic acid lipoxygenase products on leuocyctes of different species. Prostaglandins. 1980;20(2):411-418
  30. 30. Todoric J, et al. Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n−3 polyunsaturated fatty acids. Diabetologia. 2006;49(9):2109-2119
  31. 31. Azordegan N, et al. Carcinogenesis alters fatty acid profile in breast tissue. Molecular and Cellular Biochemistry. 2012;374(1):223-232
  32. 32. Baylin A, Campos H. Arachidonic acid in adipose tissue is associated with nonfatal acute myocardial infarction in the central valley of Costa Rica. The Journal of Nutrition. 2004;134(11):3095-3099
  33. 33. Rupp H, et al. Inverse shift in serum polyunsaturated and monounsaturated fatty acids is associated with adverse dilatation of the heart. Heart. 2010;96(8):595-598
  34. 34. Taugbøl O, Baddaky-Taugbøl B, Saarem K. The fatty acid profile of subcutaneous fat and blood plasma in pruritic dogs and dogs without skin problems. Canadian Journal of Veterinary Research. 1998;62(4):275-278
  35. 35. Pond CM, Mattacks CA. The source of fatty acids incorporated into proliferating lymphoid cells in immune-stimulated lymph nodes. British Journal of Nutrition. 2003;89(3):375-382
  36. 36. Mattacks CA, Sadler D, Pond CM. The effects of dietary lipids on dendritic cells in perinodal adipose tissue during chronic mild inflammation. British Journal of Nutrition. 2004;91(6):883-892
  37. 37. Riol-Blanco L, et al. The neuronal protein Kidins220 localizes in a raft compartment at the leading edge of motile immature dendritic cells. European Journal of Immunology. 2004;34(1):108-118
  38. 38. Morelli AE, Thomson AW. Dendritic cells under the spell of prostaglandins. Trends in Immunology. 2003;24(3):108-111
  39. 39. Pond CM. Paracrine interactions of mammalian adipose tissue. Journal of Experimental Zoology. Part A, Comparative Experimental Biology. 2003;295(1):99-110
  40. 40. Westcott E, et al. Fatty acid compositions of lipids in mesenteric adipose tissue and lymphoid cells in patients with and without Crohn's disease and their therapeutic implications. Inflammatory Bowel Diseases. 2005;11(9):820-827
  41. 41. Miura S, et al. Modulation of intestinal immune system by dietary fat intake: Relevance to Crohn's disease. Journal of Gastroenterology and Hepatology. 1998;13(12):1183-1190
  42. 42. Trebble TM, et al. Peripheral blood mononuclear cell fatty acid composition and inflammatory mediator production in adult Crohn's disease. Clinical Nutrition. 2004;23(4):647-655
  43. 43. Gassull MA, et al. Fat composition may be a clue to explain the primary therapeutic effect of enteral nutrition in Crohn's disease: Results of a double blind randomised multicentre European trial. Gut. 2002;51(2):164-168
  44. 44. Frangogiannis NG. The inflammatory response in myocardial injury, repair and remodeling. Nature Reviews Cardiology. 2014;11(5):255-265
  45. 45. Hall DJ, et al. Comparison of serum fatty acid concentrations in cats with hypertrophic cardiomyopathy and healthy controls. Journal of Feline Medicine and Surgery. 2014;16(8):631-636
  46. 46. Smith CE, et al. Myocardial concentrations of fatty acids in dogs with dilated cardiomyopathy. American Journal of Veterinary Research. 2005;66(9):1483-1486
  47. 47. Evanochko WT, et al. Proton NMR spectroscopy in myocardial ischemic insult. Magnetic Resonance in Medicine. 1987;5(1):23-31.
  48. 48. Bouchard A, et al. Visualization of altered myocardial lipids by 1H NMR chemical-shift imaging following ischemic insult. Magnetic Resonance in Medicine. 1991;17(2):379-389
  49. 49. Straeter-Knowlen IM, et al. 1H NMR spectroscopic imaging of myocardial triglycerides in excised dog hearts subjected to 24 hours of coronary occlusion. Circulation. 1996;93(7):1464-1470
  50. 50. Reeves RC, et al. Demonstration of increased myocardial lipid with postischemic dysfunction (myocardial stunning) by proton nuclear magnetic-resonance spectroscopy. Journal of the American College of Cardiology. 1989;13(3):739-744
  51. 51. Diamant M, et al. Diastolic dysfunction is associated with altered myocardial metabolism in asymptomatic normotensive patients with well-controlled type 2 diabetes mellitus. Journal of the American College of Cardiology. 2003;42(2):328-335
  52. 52. Faller KM, et al. (1)H-MR spectroscopy for analysis of cardiac lipid and creatine metabolism. Heart Failure Reviews. 2013;18(5):657-668
  53. 53. Ruiz-Hurtado G, et al. Mild and short-term caloric restriction prevents obesity-induced cardiomyopathy in young Zucker rats without changing in metabolites and fatty acids cardiac profile. Frontiers in Physiology. 2017;8:42
  54. 54. Djoussé L, et al. Plasma phospholipid concentration of cis palmitoleic acid and risk of heart failure. Circulation: Heart Failure. 2012;5(6):703-709
  55. 55. Eide IA, et al. Plasma levels of marine n-3 fatty acids and cardiovascular risk markers in renal transplant recipients. European Journal of Clinical Nutrition. 2016;70(7):824-830
  56. 56. Fosshaug LE, et al. Altered levels of fatty acids and inflammatory and metabolic mediators in epicardial adipose tissue in patients with systolic heart failure. Journal of Cardiac Failure. 2015;21(11):916-923
  57. 57. Fretts AM, et al. Plasma phospholipid saturated fatty acids and incident atrial fibrillation: The cardiovascular health study. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease. 2014;3(3):e000889
  58. 58. Kim OY, et al. Altered heart and kidney phospholipid fatty acid composition are associated with cardiac hypertrophy in hypertensive rats. Clinical Biochemistry. 2013;46(12):1111-1117
  59. 59. Warensjö E, et al. Biomarkers of milk fat and the risk of myocardial infarction in men and women: A prospective, matched case-control study. The American Journal of Clinical Nutrition. 2010. 92(1):194-202
  60. 60. Wu JHY, et al. Fatty acids in the de novo lipogenesis pathway and risk of coronary heart disease: The Cardiovascular Health Study. The American Journal of Clinical Nutrition. 2011;94(2):431-438
  61. 61. Pelsers MMAL, Hermens WT, Glatz JFC. Fatty acid-binding proteins as plasma markers of tissue injury. Clinica Chimica Acta. 2005;352(1-2):15-35
  62. 62. Zoair A, et al. Serum level of heart-type fatty acid binding protein (h-FABP) before and after treatment of congestive heart failure in children. Pediatric Cardiology. 2015;36(8):1722-1727
  63. 63. Niizeki T, et al. Combination of heart-type fatty acid binding protein and brain natriuretic peptide can reliably risk stratify patients hospitalized for chronic heart failure. Circulation Journal. 2005;69(8):922-927
  64. 64. Niizeki T, et al. Persistently increased serum concentration of heart-type fatty acid-binding protein predicts adverse clinical outcomes in patients with chronic heart failure. Circulation Journal. 2008;72(1):109-114
  65. 65. Cabiati M, et al. High peripheral levels of h-FABP are associated with poor prognosis in end-stage heart failure patients with mechanical circulatory support. Biomarkers in Medicine. 2013;7(3):481-492
  66. 66. Ozdemir C, et al. Heart-type fatty acid binding protein and cardiac troponin I may have a diagnostic value in electrocution: A rat model. Journal of Forensic and Legal Medicine. 2016;39:76-79
  67. 67. Wittnich C, Belanger MP. What factors contribute to the elevation of serum free fatty acids (FFA) in newborns in the cardiac surgical setting? Canadian Journal of Physiology and Pharmacology. 2017
  68. 68. Forouhi NG, et al. Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: The EPIC-InterAct case-cohort study. The Lancet, Diabetes & Endocrinology. 2014;2(10):810-818
  69. 69. D'Ascoli TA, et al. Association between serum long-chain omega-3 polyunsaturated fatty acids and cognitive performance in elderly men and women: The Kuopio Ischaemic Heart Disease Risk Factor Study. European Journal of Clinical Nutrition. 2016;70(8):970-975
  70. 70. van Smeden J, et al. The importance of free fatty acid chain length for the skin barrier function in atopic eczema patients. Experimental Dermatology. 2014;23(1):45-52
  71. 71. Ring J, et al. Guidelines for treatment of atopic eczema (atopic dermatitis) Part II. Journal of the European Academy of Dermatology and Venereology. 2012;26(9):1176-1193
  72. 72. Taugbol O, Baddaky-Taugbol B., Saarem K. The fatty acid profile of subcutaneous fat and blood plasma in pruritic dogs and dogs without skin problems. Canadian Journal of Veterinary Research-Revue Canadienne De Recherche Veterinaire. 1998;62(4):275-278
  73. 73. Muller MR, et al. Evaluation of cyclosporine-sparing effects of polyunsaturated fatty acids in the treatment of canine atopic dermatitis. Veterinary Journal. 2016;210:77-81
  74. 74. Calon A, et al. Stromal gene expression defines poor-prognosis subtypes in colorectal cancer. Nature Genetics. 2015;47(4):320-329
  75. 75. Fehrmann RSN, et al. Gene expression analysis identifies global gene dosage sensitivity in cancer. Nature Genetics. 2015;47(2):115-125
  76. 76. Gillet JP, et al. A gene expression signature associated with overall survival in patients with hepatocellular carcinoma suggests a new treatment strategy. Molecular Pharmacology. 2016;89(2):263-272
  77. 77. van't Veer LJ, et al. Gene expression profiling predicts clinical outcome of breast cancer. Nature. 2002;415(6871):530-536
  78. 78. Zheng JS, et al. Intake of fish and marine n-3 polyunsaturated fatty acids and risk of breast cancer: Meta-analysis of data from 21 independent prospective cohort studies. BMJ-British Medical Journal. 2013;346
  79. 79. Gann PH, et al. Prospective study of plasma fatty acids and risk of prostate cancer. Journal of the National Cancer Institute. 1994;86(4):281-286
  80. 80. Akinsete JA, et al. Consumption of high omega-3 fatty acid diet suppressed prostate tumorigenesis in C3(1) Tag mice. Carcinogenesis. 2012;33(1):140-148
  81. 81. Augustsson K, et al. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiology, Biomarkers & Prevention. 2003;12(1):64-67
  82. 82. Leitzmann MF, et al. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. The American Journal of Clinical Nutrition. 2004;80(1):204-216
  83. 83. Pelser C, et al. Dietary fat, fatty acids, and risk of prostate cancer in the NIH-AARP diet and health study. Cancer Epidemiology, Biomarkers & Prevention. 2013;22(4):697-707
  84. 84. Pondugula SR, et al. Stearidonic acid, a plant-based dietary fatty acid, enhances the chemosensitivity of canine lymphoid tumor cells. Biochemical and Biophysical Research Communications. 2015;460(4):1002-1007
  85. 85. Wong J, et al. Isomer specificity of conjugated linoleic acid on suppression of osteosarcomas. Journal of Nature and Science. 2015;1(4):e67
  86. 86. Long E, et al. Fatty acid profile and gene expression in canine lipoma – a promising treatment target? Advances in Animal Biosciences. 2013;P032
  87. 87. Cettour-Rose P, et al. Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat. A link between catch-up growth and later metabolic syndrome. Diabetes. 2005;54:751-756
  88. 88. Barker DJP, et al. Fetal nutrition and cardiovascular disease in adult life. The Lancet. 1993;341:938-941
  89. 89. Phillips DIW, et al. Size at birth and plasma leptin concentrations in adult life. International Journal of Obesity. 1999;23:1-5
  90. 90. Whorwood CB, et al. Maternal undernutrition during early to midgestation programs tissue-specific alterations in the expression of the glucocorticoid receptor, 11beta-hydroxysteroid dehydrogenase isoforms, and type 1 angiotensin II receptor in neonatal sheep. Endocrinology. 2001;142(7):2854-2864
  91. 91. MacDonald ML, et al. Effects of linoleate and arachidonate deficiencies on reproduction and spermatogenesis in the cat. The Journal of Nutrition. 1984;114(4):719-726
  92. 92. Risso A, et al. Effect of long-term fish oil supplementation on semen quality and serum testosterone concentrations in male dogs. International Journal of Fertility & Sterility. 2016;10(2):223-231
  93. 93. Morris JG. Do cats need arachidonic acid in the diet for reproduction? Journal of Animal Physiology and Animal Nutrition. 2004;88(3-4):131-137
  94. 94. Morris JG, Rogers QR, O'Donnell JA. Lysine requirement of kittens given purified diets for maximal growth. Journal of Animal Physiology and Animal Nutrition. 2004;88(3-4):113-116
  95. 95. Siemelink M, et al. Dietary fatty acid composition during pregnancy and lactation in the rat programs growth and glucose metabolism in the offspring. Diabetologia. 2002;45(10):1397-1403
  96. 96. Taylor PD, et al. Impaired glucose homeostasis and mitochondrial abnormalities in offspring of rats fed a fat-rich diet in pregnancy. American Journal of Physiology. 2005;288(1):R134-R139
  97. 97. Armitage JA, Taylor PD, Poston L. Experimental models of developmental programming: Consequences of exposure to an energy rich diet during development. Journal of Physiology. 2005;565(1):3-8
  98. 98. Zhu MJ, et al. AMP-activated protein kinase signalling pathways are down regulated and skeletal muscle development impaired in fetuses of obese, over-nourished sheep. Journal of Physiology. 2008;586(10):2651-2664
  99. 99. Cerfa ME, et al. Hyperglycaemia and reduced glucokinase expression in weanling offspring from dams maintained on a high-fat diet. British Journal of Nutrition. 2006;95:391-396
  100. 100. Symonds ME, et al. Maternal nutrient restriction during placental growth, programming fetal adiposity and juvenile blood pressure control. Archives of Physiology and Biochemistry. 2003;111(1):45-52
  101. 101. Chadio SE, et al. Impact of maternal undernutrition on the hypothalamic-pituitary-adrenal axis responsiveness in sheep at different ages postnatal. Journal of Endocrinology. 2007;192(3):495-503
  102. 102. Roseboom T, de Rooij S, Painter R. The Dutch famine and its long-term consequences for adult health. Early Human Development. 2006;82(8):485-491
  103. 103. Kelley DE, et al. Interaction between glucose and free fatty acid metabolism in human skeletal muscle. Journal of Clinical Investigation. 1993;92(1):91-98
  104. 104. Savage DB, Petersen KF, Shulman GI. Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiological Reviews. 2007;87(2):507-520
  105. 105. Poore KR, Fowden AL. The effect of birth weight on glucose tolerance in pigs at 3 and 12 months of age. Diabetologia. 2002;45:1247-1254
  106. 106. Poore KR, et al. The effects of birth weight in basal cardiovascular function in pigs at 3 months of age. Journal of Physiology. 2002;539:969-978
  107. 107. Poore KR, Fowden AL. Insulin sensitivity in juvenile and adult large white pigs of low and high birthweight. Diabetologia. 2004;47:340-348
  108. 108. Mostyn A, et al. Influence of size at birth on the endocrine profiles and expression of uncoupling proteins in subcutaneous adipose tissue, lung and muscle of neonatal pigs. American Journal of Physiology. 2005;288(6):R1536-R1542
  109. 109. Mostyn A, et al. The influence of size at birth on lipid storage and peroxisome proliferator activated receptor g (PPARg) expression in adipose tissue (AT). Early Human Development. 2006;82:634
  110. 110. Marten N, et al. The influence of piglet birth weight on peroxisome proliferator activated receptor α (PPARα) expression in skeletal muscle. Proceedings of the Neonatal Society. 2006,
  111. 111. Mostyn A, et al. Differences in FABP3 and FABP4 messenger RNA expression in skeletal muscle and subcutaneous adipose tissue between normal birth weight and low and high birth weight porcine offspring at days 7 and 14 of postnatal life. Proceedings of the Nutrition Society. 2007;66:57A
  112. 112. Lillycrop KA, et al. Dietary protein restriction of pregnant rats induces and folic acid supplementation prevents epigenetic modification of hepatic gene expression in the offspring. Journal of Nutrition. 2005;135(6):1382-1386
  113. 113. Evans RM, Barish GD, Wang Y. PPARs and the complex journey to obesity. Nature Medicine. 2004;10(4):1-7
  114. 114. Rosen ED, Spiegelman BM. PPARg: A nuclear regulator of metabolism, differentiation, and cell growth. The Journal of Biological Chemistry. 2001;276(41):37731-37734
  115. 115. Bays H, Mandarino L, DeFronzo RA. Role of the adipocyte, free fatty acids and ectopic fat in the pathogenesis of type 2 diabetes mellitus: Peroxisomeal proliferator-activated receptor agonists provide a rational therapeutic approach. Journal of Clinical Endocrinology and Metabolism. 2004;89(2):463-478
  116. 116. Vidal-Puig A, et al. Regulation of PPAR gamma gene expression by nutrition and obesity in rodents. Journal of Clinical Investigation. 1996;97(11):2553-2561
  117. 117. Medina-Gomez G, et al. PPAR gamma 2 prevents lipotoxicity by controlling adipose tissue expandability and peripheral lipid metabolism. PLoS Genetics. 2007;3(4):e64
  118. 118. Xu HE, et al. Molecular recognition of fatty acids by peroxisome proliferator-activated receptors. Molecular Cell. 1999;3(3):397-403
  119. 119. Unger RH. Weapons of lean body mass destruction: The role of ectopic lipids in the metabolic syndrome. Endocrinology. 2003;144(12):5159-5165
  120. 120. Chilliard Y, et al. Ruminant milk fat plasticity: Nutritional control of saturated, polyunsaturated, trans and conjugated fatty acids. Annales De Zootechnie. 2000;49(3):181-205
  121. 121. Martemucci G, D'Alessandro AG. Fat content, energy value and fatty acid profile of donkey milk during lactation and implications for human nutrition. Lipids in Health and Disease. 2012;11
  122. 122. Breckenr WC, Kuksis A. Molecular weight distributions of milk fat triglycerides from seven species. Journal of Lipid Research. 1967;8(5):473-478
  123. 123. Innis SM. Impact of maternal diet on human milk composition and neurological development of infants. American Journal of Clinical Nutrition. 2014;99(3):734s-741s
  124. 124. Oosting A, et al. Rapid and selective manipulation of milk fatty acid composition in mice through the maternal diet during lactation. Journal of Nutritional Science. 2015;4
  125. 125. Capper JL, et al. Polyunsaturated fatty acid supplementation during pregnancy alters neonatal behavior in sheep. Journal of Nutrition. 2006;136(2):397-403
  126. 126. Barreiro R, et al. Effects of bovine pregnancy on the fatty acid composition of milk: The significance for humans needs. Food Additional & Contaminants. Part A, Chemistry, Analysis, Control, Exposure Risk & Assessment. 2017:1-9
  127. 127. Makowski L, Hotamisligil GS. Fatty acid binding proteins—the evolutionary crossroads if inflammatory and metabolic responses. J Nutr. 2004 Sep;134(9):2464S-2468S
  128. 128. Roepstorff C, et al. Studies of plasma membrane fatty acid-binding protein and other lipid-binding proteins in human skeletal muscle. Proceedings of the Nutrition Society. 2004;63:239-244
  129. 129. Panarotto D, et al. Insulin resistance affects the regulation of lipoprotein lipase in the postprandial period and in an adipose tissue-specific manner. European Journal of Clinical Investigation. 2002;32:84-92
  130. 130. Zhou G, et al. Role of AMP-activated protein kinase in mechanism of metformin action. Journal of Clinical Investigation. 2001;108(8):1167-1174
  131. 131. Tong L. Acetyl-coenzyme A carboxylase: Crucial metabolic enzyme and attractive target for drug discovery. Cellular and Molecular Life Sciences. 2005;62:1784-1803
  132. 132. Hardie DG, Hawley SA. AMP-activated protein kinase: The energy charge hypothesis revisited. BioEssays. 2001;23(12):1112-1119
  133. 133. Liu Y, et al. High-fat diet feeding impairs both the expression and activity of AMPKa in rats' skeletal muscle. Biochemical and Biophysical Research Communications. 2006;339(2):701-707
  134. 134. Denayer T, Stöhr T, Van Roy M. Animal models in translational medicine: Validation and prediction. New Horizons in Translational Medicine. 2014;2(1):5-11
  135. 135. van der Worp HB, et al. Can animal models of disease reliably inform human studies? PLoS Medicine. 2010;7(3):e1000245
  136. 136. DeGiorgio CM, Taha AY. Omega-3 fatty acids (-3 fatty acids) in epilepsy: Animal models and human clinical trials. Expert Review of Neurotherapeutics. 2016;16(10):1141-1145
  137. 137. Puurunen J, et al. A non-targeted metabolite profiling pilot study suggests that tryptophan and lipid metabolisms are linked with ADHD-like behaviours in dogs. Behavioral and Brain Functions. 2016;12:27 doi: 10.1186/s12993-016-0112-1
  138. 138. Buzzai M, et al. The glucose dependence of Akt-transformed cells can be reversed by pharmacologic activation of fatty acid [beta]-oxidation. Oncogene. 2005;24(26):4165-4173
  139. 139. Kantor PF, et al. The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase. Circulation Research. 2000;86(5):580-588
  140. 140. Serisier S, et al. Fenofibrate lowers lipid parameters in obese dogs. The Journal of Nutrition. 2006;136(7):2037S-2040S
  141. 141. Purushotham A, et al. Hepatocyte-specific deletion of SIRT1 alters fatty acid metabolism and results in hepatic steatosis and inflammation. Cell Metabolism. 2009;9(4):327-338
  142. 142. Stavinoha MA, et al. Diurnal variations in the responsiveness of cardiac and skeletal muscle to fatty acids. American Journal of Physiology—Endocrinology and Metabolism. 2004;287(5):E878-E887
  143. 143. Wang DF, et al. Effects of nutritional level of concentrate-based diets on meat quality and expression levels of genes related to meat quality in Hainan black goats. Animal Science Journal. 2015;86(2):166-173
  144. 144. Jurie C, et al. Adipocyte fatty acid-binding protein and mitochondrial enzyme activities in muscles as relevant indicators of marbling in cattle. Journal of Animal Science. 2007;85(10):2660-2669
  145. 145. Zhu, J.J., et al., Inhibition of FASN reduces the synthesis of medium-chain fatty acids in goat mammary gland. Animal, 2014. 8(9):1469-1478
  146. 146. Chamberlain MB, DePeters EJ. Impacts of feeding lipid supplements high in palmitic acid or stearic acid on performance of lactating dairy cows. Journal of Applied Animal Research. 2017;45(1):126-135
  147. 147. Liang W, et al. Investigation of the association of two candidate genes (H-FABP and PSMC1) with growth and carcass traits in Qinchuan beef cattle from China. Genetics and Molecular Research. 2014;13(1):1876-1884
  148. 148. Li DL, et al. Growth, carcase and meat traits and gene expression in chickens divergently selected for intramuscular fat content. British Poultry Science. 2013;54(2):183-189

Written By

Siobhan Simpson, Alison Mostyn and Catrin S. Rutland

Submitted: January 25th, 2017 Reviewed: March 9th, 2017 Published: June 21st, 2017