Intramuscular triacylglycerol and insulin resistance: Guilty as charged or wrongly accused?

In the paper

“This phenomenon, now well known as the “athletes' paradox”, suggested that lipid droplet accumulation per se is not sufficient to disrupt insulin action.”

In the paper

“cross-sectional studies showing that isolated muscle strips, tissue homogenates or cultured myocytes from severely obese and/or diabetic humans exhibit diminished rates of fat oxidation when compared to specimens derived from healthy control subjects [9,41,46,87].”

What the sources say

• Not checked yetcites [9] Blaak, 2004, Basic disturbances in skeletal muscle fatty acid metabolism in obesity and type 2 diabetes mellitus, Proc. Nutr. Soc. source
• Not checked yetcites [41] Hulver, 2003, Skeletal muscle lipid metabolism with obesity, Am. J. Physiol. Endocrinol. Metab. source
• Not checked yetcites [46] Kelley, 1999, Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss, Am. J. Physiol.
• Not checked yetcites [87] Ukropcova, 2005, Dynamic changes in fat oxidation in human primary myocytes mirror metabolic characteristics of the donor, J. Clin. Invest. source

In the paper

“reports showing that lipid droplet accumulation in highly insulin-sensitive endurance athletes is similar to or even greater than that found in patients with type 2 diabetes [27,89,90].”

What the sources say

• Not checked yetcites [27] Goodpaster, 2001, Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes, J. Clin. Endocrinol. Metab. source
• Not checked yetcites [89] van Loon, 2006, Increased intramuscular lipid storage in the insulin-resistant and endurance-trained state, Pflugers Arch. source
• Not checked yetcites [90] van Loon, 2004, Intramyocellular lipid content in type 2 diabetes patients compared with overweight sedentary men and highly trained endurance athletes, Am. J. Physiol. Endocrinol. Metab. source

In the paper

“Conversely, a generalized limitation in oxidative capacity or a specific impingement of β-oxidation necessitates a compensatory increase in glucose uptake and glycolytic ATP production.”

In the paper

“diet-induced and genetic forms of glucose intolerance were associated with high rates of incomplete fat oxidation [49,50]”

What the sources say

• Not checked yetcites [49] Koves, 2005, Peroxisome proliferator-activated receptor-gamma co-activator 1alpha-mediated metabolic remodeling of skeletal myocytes mimics exercise training and reverses lipid-induced mitochondrial inefficiency, J. Biol. Chem. source
• Not checked yetcites [50] Koves, 2008, Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance, Cell Metab. source

In the paper

“the widely accepted chemiosmotic model of respiration [75], which holds that absolute rates of fuel oxidation under aerobic conditions depend ultimately on ATP turnover (i.e., workload).”

What the sources say

• Not checked yetcites [75] Rich, 2008, A perspective on Peter Mitchell and the chemiosmotic theory, J. Bioenerg. Biomembr. source

In the paper

“In the context of exercise, increased lipid delivery and catabolism allows for glucose/glycogen sparing, which then permits prolonged activity at a given submaximal intensity and/or a burst of anaerobic output in the later stages of an event [35].”

What the sources say

• Not checked yetcites [35] Holloszy, 1984, Adaptations of skeletal muscle to endurance exercise and their metabolic consequences, J. Appl. Physiol. source

In the paper

“Thus, a large body of evidence predicts that a deficit in β- oxidation would increase, not decrease, glucose utilization.”

In the paper

“At a constant work rate, provision of fatty acids inhibits glycolytic flux and glucose oxidation because the lipid substrate provides at least some portion of the acetyl-CoA that feeds the TCA cycle.”

In the paper

“Loss of MCD results in partial CPT1 inhibition [50,88].”

What the sources say

• Not checked yetcites [50] Koves, 2008, Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance, Cell Metab. source
• Not checked yetcites [88] Ussher, 2009, Insulin-stimulated cardiac glucose oxidation is increased in high-fat diet-induced obese mice lacking malonyl CoA decarboxylase, Diabetes source

In the paper

“In aggregate, these studies showed that the early stages of obesity and insulin resistance are accompanied by increased rather than reduced β-oxidation.”

In the paper

“exercise training boosted mitochondrial capacity to completely oxidize lipid substrate [49].”

What the sources say

• Not checked yetcites [49] Koves, 2005, Peroxisome proliferator-activated receptor-gamma co-activator 1alpha-mediated metabolic remodeling of skeletal myocytes mimics exercise training and reverses lipid-induced mitochondrial inefficiency, J. Biol. Chem. source

In the paper

“The aforementioned findings suggested that excessive fat supply, absent physical activity, results in a persistent mismatch between β-oxidation and TCA cycle activity.”

In the paper

“Similar observations emerged from other laboratories that likewise reported increased oxidative capacity, β-oxidation enzyme activities and mitochondrial biogenesis in parallel with high fat feeding and the onset of both obesity and insulin resistance in rodents [26,30,51,85,96].”

What the sources say

• Not checked yetcites [26] Garcia-Roves, 2007, Raising plasma fatty acid concentration induces increased biogenesis of mitochondria in skeletal muscle, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [30] Hancock, 2008, High-fat diets cause insulin resistance despite an increase in muscle mitochondria, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [51] Kraegen, 2008, Muscle insulin resistance: a case of fat overconsumption, not mitochondrial dysfunction, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [85] Turner, 2007, Excess lipid availability increases mitochondrial fatty acid oxidative capacity in muscle: evidence against a role for reduced fatty acid oxidation in lipid-induced insulin resistance in rodents, Diabetes source
• Not checked yetcites [96] Yechoor, 2002, Coordinated patterns of gene expression for substrate and energy metabolism in skeletal muscle of diabetic mice, Proc. Natl. Acad. Sci. U.S.A. source

In the paper

“a growing number of studies have reported a negative association between circulating and/or tissue acylcarnitines and glucose tolerance.”

In the paper

“in vitro measurement of [14C]oleate catabolism revealed disproportionally high rates of incomplete relative to complete fat oxidation in isolated muscle mitochondria from obese compared to lean rodents.”

What the sources say

• Not checked yetcites [49] Koves, 2005, Peroxisome proliferator-activated receptor-gamma co-activator 1alpha-mediated metabolic remodeling of skeletal myocytes mimics exercise training and reverses lipid-induced mitochondrial inefficiency, J. Biol. Chem. source

In the paper

“Human studies have also reported increased plasma acylcarnitine levels in association with insulin resistance and diabetes [1,37,52,64].”

What the sources say

• Not checked yetcites [1] Adams, 2009, Plasma acylcarnitine profiles suggest incomplete long-chain fatty acid beta-oxidation and altered tricarboxylic acid cycle activity in type 2 diabetic African-American women, J. Nutr. source
• Not checked yetcites [37] Huffman, 2009, Relationships between circulating metabolic intermediates and insulin action in overweight to obese, inactive men and women, Diabetes Care source
• Not checked yetcites [52] Lien, 2009, The STEDMAN project: biophysical, biochemical and metabolic effects of a behavioral weight loss intervention during weight loss, maintenance, and regain, OMICS source
• Not checked yetcites [64] Newgard, 2009, A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance, Cell Metab. source

In the paper

“In both the AIF and TXNIP knockout mice protection against diet-induced glucose intolerance was associated with heightened insulin-mediated activation of Akt.”

What the sources say

• Not checked yetcites [38] Hui, 2008, Txnip balances metabolic and growth signaling via PTEN disulfide reduction, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [70] Pospisilik, 2007, Targeted deletion of AIF decreases mitochondrial oxidative phosphorylation and protects from obesity and diabetes, Cell source

In the paper

“This definition was satisfied in both the TFAM and MCK-AIF knockout mouse models.”

In the paper

“the AIF null mice had increased activity of 5′ AMP-activated protein kinase, an energy sensing enzyme that stimulates glucose uptake in response to a rise in the cellular AMP/ATP ratio [43].”

What the sources say

• Not checked yetcites [43] Jessen, 2005, Contraction signaling to glucose transport in skeletal muscle, J. Appl. Physiol. source

In the paper

“Thus, MCD inactivation appeared to encourage glucose uptake and utilization through mechanisms independent of the canonical insulin signaling pathway.”

In the paper

“Deficiency of AIF resulted in subtle disruptions in mitochondrial gene expression and oxidative phosphorylation, resembling those reported in humans with type 2 diabetes [68,70].”

What the sources say

• Not checked yetcites [68] Patti, 2003, Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: potential role of PGC1 and NRF1, Proc. Natl. Acad. Sci. U.S. A. source
• Not checked yetcites [70] Pospisilik, 2007, Targeted deletion of AIF decreases mitochondrial oxidative phosphorylation and protects from obesity and diabetes, Cell source

In the paper

“treatment with the CPT1 inhibitor, etomoxir, prevented lipid-induced insulin resistance in rat L6 myotubes [50].”

What the sources say

• Not checked yetcites [50] Koves, 2008, Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance, Cell Metab. source

In the paper

“the antidiabetic phenotype of the mcd−/− mice suggests that increased fat oxidation is compulsory for the development of lipid-induced glucose intolerance.”

In the paper

“Recent progress in ROS biology indicates that these agents are not merely arbitrary toxins but also act as bona fide participants in signal transduction.”

In the paper

“Taken together, these findings imply that mitochondrial dysfunction and insulin resistance have a common connection to redox imbalance.”

In the paper

“inefficient electron transfer through ETS complexes I and III has been shown to increase the half-life of the superoxide anion and thus generation of the cellular H2O2 [7].”

What the sources say

• Not checked yetcites [7] Berthiaume, 2005, Dietary vitamin E decreases doxorubicin-induced oxidative stress without preventing mitochondrial dysfunction, Cardiovasc. Toxicol. source

In the paper

“production of carnitine conjugates helps to avert mitochondrial dysfunction, owing at least in part to regeneration of free CoA [73,97].”

What the sources say

• Not checked yetcites [73] Ramsay, 2004, Carnitine acyltransferases and their influence on CoA pools in health and disease, Mol. Aspects Med. source
• Not checked yetcites [97] Zammit, 2009, Carnitine, mitochondrial function and therapy, Adv. Drug Deliv. Rev. source

In the paper

“experiments in cultured 3T3-L1 adipocytes showed that several distinct genetic and nutritional maneuvers that reduced oxidative stress blocked insulin resistance caused by dexamethasone and TNFα [36].”

What the sources say

• Not checked yetcites [36] Houstis, 2006, Reactive oxygen species have a causal role in multiple forms of insulin resistance, Nature source

In the paper

“these redox circuits intersect and regulate insulin signaling molecules such as PTEN, SHIP2 and PTP1B [14,38,44,45].”

What the sources say

• Not checked yetcites [14] Brandes, 2009, Thiol-based redox switches in eukaryotic proteins, Antioxid. Redox Signal. source
• Not checked yetcites [38] Hui, 2008, Txnip balances metabolic and growth signaling via PTEN disulfide reduction, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [44] Jones, 2006, Disruption of mitochondrial redox circuitry in oxidative stress, Chem. Biol. Interact. source
• Not checked yetcites [45] Jones, 2008, Radical-free biology of oxidative stress, Am. J. Physiol. Cell Physiol. source

In the paper

“Treatment of genetically obese/diabetic rodents with antioxidant nutrients, such as alpha-lipoic acid and N-acetylcysteine, has been shown to improve insulin action and glucose homeostasis [8,31,36].”

What the sources say

• Not checked yetcites [8] Bitar, 2004, Alpha-lipoic acid mitigates insulin resistance in Goto-Kakizaki rats, Horm. Metab. Res. source
• Not checked yetcites [31] Henriksen, 2006, Exercise training and the antioxidant alpha-lipoic acid in the treatment of insulin resistance and type 2 diabetes, Free Radic. Biol. Med. source
• Not checked yetcites [36] Houstis, 2006, Reactive oxygen species have a causal role in multiple forms of insulin resistance, Nature source

In the paper

“genetic or pharmacological manipulations that lowered mitochondrial ROS production preserved insulin action in lipid-treated myotubes [32] and mice fed a high fat diet [4,32].”

What the sources say

• Not checked yetcites [32] Hoehn, 2009, Insulin resistance is a cellular antioxidant defense mechanism, Proc. Natl. Acad. Sci. U.S.A. source
• Not checked yetcites [4] Anderson, 2009, Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans, J. Clin. Invest. source

In the paper

“The observation that tissue acylcarnitines accumulate in several instances of insulin resistance temps speculation that these metabolites might act as “lipotoxic” culprits.”

In the paper

“oxidant stress is known to activate several of the serine kinases and transcription factors that have been linked to impaired insulin signaling, including c-jun amino-terminal kinases (JNKs), IkB kinase catalytic subunit β (IKK-β), NF-kappa B transcription factor (NF-kB) and protein kinase C (PKC; reviewed in [10,17]).”

What the sources say

• Not checked yetcites [10] Bloch-Damti, 2005, Proposed mechanisms for the induction of insulin resistance by oxidative stress, Antioxid. Redox Signal. source
• Not checked yetcites [17] Chakraborti, 1998, Oxidant-mediated activation of mitogen-activated protein kinases and nuclear transcription factors in the cardiovascular system: a brief overview, Cell. Signal. source

In the paper

“the antidiabetic effects of carnitine were associated with a shift in fuel preference toward glucose oxidation”

What the sources say

• Not checked yetcites [65] Noland, 2009, Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control, J. Biol. Chem. source

In the paper

“Routine physical activity also causes a fiber type shift, favoring conversion from white to red myofibers [35].”

What the sources say

• Not checked yetcites [35] Holloszy, 1984, Adaptations of skeletal muscle to endurance exercise and their metabolic consequences, J. Appl. Physiol. source

In the paper

“CrAT is presumed to play a key role in regulating the activities of mitochondrial enzymes that respond to the acetyl-CoA/CoA ratio, such as pyruvate dehydrogenase and α-ketoglutarate dehydrogenase [73].”

What the sources say

• Not checked yetcites [73] Ramsay, 2004, Carnitine acyltransferases and their influence on CoA pools in health and disease, Mol. Aspects Med. source

In the paper

“Whole body carnitine levels were decreased in insulin resistant states such as advanced age, genetic diabetes and diet-induced obesity.”

What the sources say

• Not checked yetcites [65] Noland, 2009, Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control, J. Biol. Chem. source

In the paper

“Results from a limited number of small scale studies suggest that carnitine supplementation might confer insulin sensitizing actions in glucose intolerant or diabetic humans [16,58,72].”

What the sources say

• Not checked yetcites [16] Capaldo, 1991, Carnitine improves peripheral glucose disposal in non-insulin-dependent diabetic patients, Diabetes Res. Clin. Pract. source
• Not checked yetcites [58] Mingrone, 1999, l-Carnitine improves glucose disposal in type 2 diabetic patients, J. Am. Coll. Nutr. source
• Not checked yetcites [72] Rahbar, 2005, Effect of L-carnitine on plasma glycemic and lipidemic profile in patients with type II diabetes mellitus, Eur. J. Clin. Nutr. source

In the paper

“carnitine-supplemented rodents had robust increases in tissue efflux and urinary excretion of acetylcarnitine.”

What the sources say

• Not checked yetcites [65] Noland, 2009, Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control, J. Biol. Chem. source

In the paper

“Cross-sectional studies have found an inverse relationship between the proportion of type I (red) fibers and risk of developing metabolic disease [82].”

What the sources say

• Not checked yetcites [82] Tanner, 2002, Muscle fiber type is associated with obesity and weight loss, Am. J. Physiol. Endocrinol. Metab. source

In the paper

“This was first described in studies showing that treadmill running caused a 2-fold increase in insulin-stimulated glucose uptake when assessed during the post-exercise period using a rat hindlimb perfusion model [76], and then later reproduced in human studies of one-legged exercise [77] and animals models of electrically stimulated muscle contraction [22].”

What the sources say

• Not checked yetcites [76] Richter, 1982, Muscle glucose metabolism following exercise in the rat: increased sensitivity to insulin, J. Clin. Invest source

In the paper

“Muscle contraction is known to stimulate translocation of the Glut4 glucose transporter via an insulin-independent mechanism (reviewed elsewhere [79]), but the insulin sensitizing properties of contractile activity are evident up to 24 h post-exercise, indicating that additional mechanisms come into play [84].”

What the sources say

• Not checked yetcites [84] Turcotte, 2008, Skeletal muscle insulin resistance: roles of fatty acid metabolism and exercise, Phys. Ther. source

In the paper

“This was first described in studies showing that treadmill running caused a 2-fold increase in insulin-stimulated glucose uptake when assessed during the post-exercise period using a rat hindlimb perfusion model [76], and then later reproduced in human studies of one-legged exercise [77] and animals models of electrically stimulated muscle contraction [22].”

What the sources say

• Not checked yetcites [22] Dolan, 1993, Contractile activity restores insulin responsiveness in skeletal muscle of obese Zucker rats, Biochem. J. source

In the paper

“Muscle contraction is known to stimulate translocation of the Glut4 glucose transporter via an insulin-independent mechanism (reviewed elsewhere [79]), but the insulin sensitizing properties of contractile activity are evident up to 24 h post-exercise, indicating that additional mechanisms come into play [84].”

In the paper

“Although current evidence is far from conclusive, at least in some cases exercise-independent increases in mitochondrial mass and fat oxidation failed to enhance glucose tolerance.”

In the paper

“Oakes et al. reported that a single bout of swim exercise reversed diet-induced insulin resistance in rodents in association with reduced intramuscular levels of malonyl-CoA and long chain acyl-CoAs, whereas IMTG were unchanged [66].”

What the sources say

• Not checked yetcites [66] Oakes, 1997, Diet-induced muscle insulin resistance in rats is ameliorated by acute dietary lipid withdrawl or a single bout of exercise, Diabetes source

In the paper

“Oakes et al. reported that a single bout of swim exercise reversed diet-induced insulin resistance in rodents in association with reduced intramuscular levels of malonyl-CoA and long chain acyl-CoAs, whereas IMTG were unchanged [66].”

What the sources say

• Not checked yetcites [66] Oakes, 1997, Diet-induced muscle insulin resistance in rats is ameliorated by acute dietary lipid withdrawl or a single bout of exercise, Diabetes source

In the paper

“These findings suggest that the antidiabetic effects of an active lifestyle might depend more on the bioenergetic expense of physical work than adaptive remodeling of the muscle.”

In the paper

“This was first described in studies showing that treadmill running caused a 2-fold increase in insulin-stimulated glucose uptake when assessed during the post-exercise period using a rat hindlimb perfusion model [76], and then later reproduced in human studies of one-legged exercise [77] and animals models of electrically stimulated muscle contraction [22].”

What the sources say

• Not checked yetcites [77] Richter, 1989, Effect of exercise on insulin action in human skeletal muscle, J. Appl. Physiol. source

In the paper

“Indeed, it is well recognized that even an acute bout of exercise can lead to complete or near-complete reversal of impaired insulin-stimulated glucose uptake into skeletal muscle of obese humans and rodents [84].”

What the sources say

• Not checked yetcites [84] Turcotte, 2008, Skeletal muscle insulin resistance: roles of fatty acid metabolism and exercise, Phys. Ther. source

In the paper

“MCK-PGC1α mice had increased intramuscular levels of TAG, DAG and lysophosphatic acid when fed the fat-enriched diet [19].”

What the sources say

• Not checked yetcites [19] Choi, 2008, Paradoxical effects of increased expression of PGC-1alpha on muscle mitochondrial function and insulin-stimulated muscle glucose metabolism, Proc. Natl. Acad. Sci. U.S.A. source

In the paper

“Muscle contraction is known to stimulate translocation of the Glut4 glucose transporter via an insulin-independent mechanism (reviewed elsewhere [79]), but the insulin sensitizing properties of contractile activity are evident up to 24 h post-exercise, indicating that additional mechanisms come into play [84].”

What the sources say

• Not checked yetcites [79] Rockl, 2008, Signaling mechanisms in skeletal muscle: acute responses and chronic adaptations to exercise, IUBMB Life source

In the paper

“In these mice, increased DGAT activity in muscle resulted in higher IMTG levels, decreased DAG and ceramide levels, and resistance to diet-induced glucose intolerance.”

What the sources say

• Not checked yetcites [54] Liu, 2007, Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistance, J. Clin. Invest source

In the paper

“Notably, one outcome of acute contraction universally observed in these and other studies (cited below) was the lowering of muscle glycogen.”

What the sources say

• Not checked yetcites [20] Christ-Roberts, 2004, Glycogen synthase: key effect of exercise on insulin action, Exerc. Sport Sci. Rev. source

In the paper

“Accordingly, enhancement of insulin action in these models might be more closely connected to glycogen metabolism than lipid flux [20].”

What the sources say

• Not checked yetcites [20] Christ-Roberts, 2004, Glycogen synthase: key effect of exercise on insulin action, Exerc. Sport Sci. Rev. source

In the paper

“In these mice, increased DGAT activity in muscle resulted in higher IMTG levels, decreased DAG and ceramide levels, and resistance to diet-induced glucose intolerance.”

What the sources say

• Not checked yetcites [54] Liu, 2007, Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistance, J. Clin. Invest source

In the paper

“Oakes et al. reported that a single bout of swim exercise reversed diet-induced insulin resistance in rodents in association with reduced intramuscular levels of malonyl-CoA and long chain acyl-CoAs, whereas IMTG were unchanged [66].”

What the sources say

• Not checked yetcites [66] Oakes, 1997, Diet-induced muscle insulin resistance in rats is ameliorated by acute dietary lipid withdrawl or a single bout of exercise, Diabetes source

In the paper

“These observations help to explain the high lipid levels in trained athletes.”

In the paper

“In line with this scenario, contraction caused a robust reduction in IMTG content of the obese muscles; however, diacylglycerol, monoacylglycerol and long chain acyl-CoAs were either unchanged or increased.”

What the sources say

• Not checked yetcites [83] Thyfault, 2007, Contraction of insulin-resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolism, Am. J. Physiol. Cell Physiol. source

In the paper

“Similarly, a more recent study in humans found a strong correlation between lowering of malonyl-CoA and improved insulin sensitivity, both measured 4 h after one-legged exercise [25].”

What the sources say

• Not checked yetcites [25] Frosig, 2009, Reduced malonyl-CoA content in recovery from exercise correlates with improved insulin-stimulated glucose uptake in human skeletal muscle, Am. J. Physiol. Endocrinol. Metab. source

In the paper

“In these mice, increased DGAT activity in muscle resulted in higher IMTG levels, decreased DAG and ceramide levels, and resistance to diet-induced glucose intolerance.”

What the sources say

• Not checked yetcites [54] Liu, 2007, Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistance, J. Clin. Invest source

In the paper

“It is also important to emphasize that new insights pertaining to biological mechanisms of insulin resistance do not necessarily translate into attractive antidiabetic drug targets.”

In the paper

“Mounting evidence argues against the notion that skeletal muscle insulin resistance is caused by inherent or acquired deficiencies in oxidative metabolism.”

In the paper

“Instead, the early stages of lipid overload and glucose intolerance reflect a pronounced shift in substrate selection, in favor of fat oxidation.”

In the paper

“However, recent studies in genetically modified mouse models challenge this idea.”

In the paper

“Taken together with the phenotype of the MCK-DGAT1 mice, these results build on evidence of a fascinating physical and functional dynamic between lipid droplets, mitochondrial biology and insulin action [57].”

What the sources say

• Not checked yetcites [57] Meex, 2009, Modulation of myocellular fat stores: lipid droplet dynamics in health and disease, Am. J. Physiol. Regul. Integr. Comp. Physiol. source