Influence of fish oil on skeletal muscle mitochondrial energetics and lipid metabolites during high-fat diet

Lanza, Ian R.; Błachnio-Zabielska, Agnieszka; Johnson, Matthew L.; Schimke, Jill M.; Jakaitis, Daniel R.; LeBrasseur, Nathan K.; Jensen, Michael D.; Nair, K. Sreekumaran; Zabielski, Piotr

doi:10.1152/ajpendo.00584.2012

Cited by 125 publications

(181 citation statements)

References 64 publications

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“…Therefore, it is not possible to definitively conclude whether the improvements in glucose homeostasis seen in obese rats supplemented with flaxseed stem from ALA or EPA/DHA or a combination of all three fatty acids. This is pertinent given that Lanza et al (20) recently reported that whole body glucose tolerance was improved in mice fed a high-fat diet supplemented with menhaden oil, thereby demonstrating that EPA and DHA are capable of improving metabolic health independent of ALA. Future studies in which the FADS pathway is inhibited are required to uncouple the interconversion of ALA to EPA/DHA, and better delineate the relationship of specific PUFAs and insulin sensitivity.…”

Section: Discussionmentioning

confidence: 97%

“…Diets supplemented with omega-3 (n-3) polyunsaturated fatty acids (PUFAs) have been shown to improve glucose tolerance (20,24,30,39); however, the majority of these past studies have examined eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3). Very little is known regarding the effects of ␣-linolenic acid (ALA, 18:3n-3); however, we have previously shown that a diet supplemented with flaxseed (i.e., rich in ALA) prevents obesityinduced insulin resistance (24).…”

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confidence: 99%

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LA and ALA prevent glucose intolerance in obese male rats without reducing reactive lipid content, but cause tissue-specific changes in fatty acid composition

Matravadia

Zabielski

Chabowski

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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While the cause of Type 2 diabetes remains poorly defined, the accumulation of reactive lipids within white adipose tissue, skeletal muscle, and liver have been repeatedly implicated as underlying mechanisms. The ability of polyunsaturated fatty acids (PUFAs) to prevent the development of insulin resistance has gained considerable interest in recent years; however, the mechanisms-of-action remain poorly described. Therefore, we determined the efficacy of diets supplemented with either linoleic acid (LA) or α-linolenic acid (ALA) in preventing insulin resistance and reactive lipid accumulation in key metabolic tissues of the obese Zucker rat. Obese Zucker rats displayed impaired glucose homeostasis and reduced n-3 and n-6 PUFA content in the liver and epididymal white adipose tissue (EWAT). After the 12-wk feeding intervention, both LA- and ALA-supplemented diets prevented whole body glucose and insulin intolerance; however, ALA had a more pronounced effect. These changes occurred in association with n-3 and n-6 accumulation in all tissues studied, albeit to different extents (EWAT > liver > muscle). Triacylglycerol (TAG), diacylglycerol (DAG), ceramide, and sphingolipid accumulation were not attenuated in obese animals supplemented with either LA or ALA, suggesting that preservation of glucose homeostasis occurred independent of changes in reactive lipid content. However, PUFA-supplemented diets differentially altered the fatty acid composition of TAGs, DAGs, and PLs in a tissue-specific manner, suggesting essential fatty acid metabolism differs between tissues. Together, our results indicate that remodeling of the fatty acid composition of various lipid fractions may contribute to the improved glucose tolerance observed in obese rats fed PUFA-supplemented diets.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

LA and ALA prevent glucose intolerance in obese male rats without reducing reactive lipid content, but cause tissue-specific changes in fatty acid composition

Matravadia

Zabielski

Chabowski

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Only C18:0-Cer and C18:1-Cer species were elevated whereas C16:0-Cer remained stable. Recent studies link C16:0-Cer with hepatic insulin resistance [49,50] whereas skeletal muscle C18-derived ceramides account for majority of Cer accumulation in HFD animals [51], mice with uncontrolled STZ-diabetes [52] and in obese, diabetic patients [53]. Inhibition of de novo sphingolipid synthesis by myriocin also had greatest impact on C18:0-and C18:1-Cer species and was accompanied by significant improvement in both the whole-body and skeletal muscle insulin sensitivity.…”

Section: Discussionmentioning

confidence: 99%

The Crucial Role of C18-Cer in Fat-Induced Skeletal Muscle Insulin Resistance

Błachnio-Zabielska

Chacińska

Vendelbo

et al. 2016

Cell Physiol Biochem

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Background/Aims: Muscle bioactive lipids accumulation leads to several disorder states. The most common are insulin resistance (IR) and type 2 diabetes. There is an ongoing debate which of the lipid species plays the major role in induction of muscle IR. Our aim was to elucidate the role of particular lipid group in induction of muscle IR. Methods: The analyses were performed on muscle from the following groups of rats: 1. Control, fed standard diet, 2 HFD, fed high fat diet, 3. HFD/Myr, fed HFD and treated with myriocin (Myr), an inhibitor of ceramide de novo synthesis. We utilized [U¹³C] palmitate isotope tracer infusion and mass spectrometry to measure content and synthesis rate of muscle long-chain acyl-CoA (LCACoA), diacylglycerols (DAG) and ceramide (Cer). Results: HFD led to intramuscular accumulation of LCACoA, DAG and Cer and skeletal muscle IR. Myr-treatment caused decrease in Cer (most noticeable for stearoyl-Cer and oleoyl-Cer) and accumulation of DAG, possibly due to re-channeling of excess of intramuscular LCACoA towards DAG synthesis. An improvement in insulin sensitivity at both systemic and muscular level coincided with decrease in ceramide, despite elevated intramuscular DAG. Conclusion: The improved insulin sensitivity was associated with decreased muscle stearoyl- and oleoyl-ceramide content. The results indicate that accumulation of those ceramide species has the greatest impact on skeletal muscle insulin sensitivity in rats.

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“…Mitochondrial CL PUFA content is in turn positively correlated with cytochrome c oxidase activity [77]. In humans, some studies suggest that PUFA-containing diets induce mitochondrial biogenesis [78], while other studies provide evidence that some functions of mitochondrial respiration might be improved [79]. In all cases, the effect of a PUFA-containing diet on mammalian muscle mitochondrial phospholipids appears to be mostly limited to their FA composition and not on the classes of phospholipids.…”

Section: Impact Of Diet On Skeletal Muscle Mitochondrial Phospholipidsmentioning

confidence: 99%

Looking Beyond Structure: Membrane Phospholipids of Skeletal Muscle Mitochondria

Heden

Neufer

Funai

2016

Trends in Endocrinology & Metabolism

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Skeletal muscle mitochondria are highly dynamic and capable of tremendous expansion to meet cellular energetic demands. Such proliferation in mitochondrial mass requires a synchronized supply of enzymes and structural phospholipids. While transcriptional regulation of mitochondrial enzymes has been extensively studied, there is limited information on how mitochondrial membrane lipids are generated in skeletal muscle. Herein we describe how each class of phospholipids that constitute mitochondrial membranes are synthesized and/or imported, and summarize genetic evidence indicating that membrane phospholipid composition represents a significant modulator of skeletal muscle mitochondrial respiratory function. We also discuss how skeletal muscle mitochondrial phospholipids may mediate the effect of diet and exercise on oxidative metabolism.

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Influence of fish oil on skeletal muscle mitochondrial energetics and lipid metabolites during high-fat diet

Abstract: Influence of fish oil on skeletal muscle mitochondrial energetics and lipid metabolites during high-fat diet.

Cited by 125 publications

References 64 publications

LA and ALA prevent glucose intolerance in obese male rats without reducing reactive lipid content, but cause tissue-specific changes in fatty acid composition

LA and ALA prevent glucose intolerance in obese male rats without reducing reactive lipid content, but cause tissue-specific changes in fatty acid composition

The Crucial Role of C18-Cer in Fat-Induced Skeletal Muscle Insulin Resistance

Looking Beyond Structure: Membrane Phospholipids of Skeletal Muscle Mitochondria

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