Influence of Gender, Obesity, and Muscle Lipase Activity on Intramyocellular Lipids in Sedentary Individuals

Moro, Cédric; Galgani, José E.; Luu, L.; Pasarica, Magdalena; Mairal, Aline; Bajpeyi, Sudip; Schmitz, Gerd; Langin, Dominique; Liebisch, Gerhard; Smith, Steven R.

doi:10.1210/jc.2009-0053

Cited by 132 publications

(132 citation statements)

References 38 publications

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“…Six young healthy subjects, mean age 22.9 ± 0.4 yrs (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) and mean BMI 26.5 ± 0.5 kg/m 2 (20.1-34.7) were recruited in the study. The protocol was approved by the institutional review board of the Pennington Biomedical Research Center, and all volunteers gave written informed consent.…”

Section: Subjectsmentioning

confidence: 99%

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Regulation of skeletal muscle lipolysis and oxidative metabolism by the co-lipase CGI-58

Badin

Loubière

Coonen

et al. 2012

Journal of Lipid Research

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Section: Subjectsmentioning

confidence: 99%

“…Triacylglycerol hydrolase (TAGH) activity was measured on tissue and cell lysates as previously described ( 19 ). Briefl y, tissue and cell lysates were extracted in a lysis buffer containing 0.25 M sucrose, 1 mM EDTA, 1 mM DTT, 20 µg/ml leupeptin, and 2 µg/ml antipain.…”

Section: Lipase Activity Assaysmentioning

confidence: 99%

Regulation of skeletal muscle lipolysis and oxidative metabolism by the co-lipase CGI-58

Badin

Loubière

Coonen

et al. 2012

Journal of Lipid Research

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“…Importantly, the impaired fatty acid oxidation can lead to the accumulation of specific IMCL intermediates, including long-chain fatty acyl-CoA, diacylglycerol and ceramide, as well as IMCL. 24 Recent studies have revealed that the accumulation of IMCL intermediates might impair insulin signaling 25 and the mitochondrial function. 26 Therefore, IMCL might have a major role in the pathogenesis of insulin resistance.…”

Section: Control Metsmentioning

confidence: 99%

Lower aerobic capacity was associated with abnormal intramuscular energetics in patients with metabolic syndrome

et al. 2011

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Lower aerobic capacity is a strong and independent predictor of cardiovascular morbidity and mortality in patients with metabolic syndrome (MetS). However, the mechanisms are not fully elucidated. We tested the hypothesis that skeletal muscle dysfunction could contribute to the lower aerobic capacity in MetS patients. The incremental exercise tests with cycle ergometer were performed in 12 male patients with MetS with no habitual exercise and 11 age-, sex-and activity-matched control subjects to assess the aerobic capacity. We performed 31 phosphorus-magnetic resonance spectroscopy (MRS) to assess the high-energy phosphate metabolism in skeletal muscle during aerobic exercise. Proton-MRS was also performed to measure intramyocellular lipid (IMCL) content. Peak oxygen uptake (peak VO 2 ; 34.1±6.2 vs. 41.4±8.4 ml kg À1 min À1 , Po0.05) and anaerobic threshold (AT; 18.0±2.4 vs. 23.1±3.7 ml kg À1 min À1 , Po0.01) adjusted by lean body mass were lower in MetS patients than control subjects. Phosphocreatine (PCr) loss during exercise was 1.5-fold greater in MetS, suggesting reduced intramuscular oxidative capacity. PCr loss was inversely correlated with peak VO 2 (r¼À0.64) and AT (r¼À0.60), respectively. IMCL content was threefold higher in MetS and was inversely correlated with peak VO 2 (r¼À0.47) and AT (r¼À0.52), respectively. Moreover, there was a positive correlation between IMCL content and PCr loss (r¼0.64). These results suggested that lean-body aerobic capacity in MetS patients was lower compared with activity-matched healthy subjects, which might be due to the reduced intramuscular fatty acid oxidative metabolism.

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“…The general perception has been that insulin resistance can be attributed to the accumulation of diacylglycerol (DAG) in liver and skeletal muscle (3)(4)(5). The mechanism by which DAG is believed to cause insulin resistance is by the activation of protein kinase C (PKC) e and PKC u leading to phosphorylation and inhibition of insulin receptor substrate 1 and the insulin signaling cascade in both liver (6,7) and skeletal muscle (8)(9)(10).…”

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confidence: 99%

Partial Disruption of Lipolysis Increases Postexercise Insulin Sensitivity in Skeletal Muscle Despite Accumulation of DAG

et al. 2016

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Type 2 diabetes and skeletal muscle insulin resistance have been linked to accumulation of the intramyocellular lipid-intermediate diacylglycerol (DAG). However, recent animal and human studies have questioned such an association. Given that DAG appears in different stereoisomers and has different reactivity in vitro, we investigated whether the described function of DAGs as mediators of lipid-induced insulin resistance was dependent on the different DAG isomers. We measured insulin-stimulated glucose uptake in hormone-sensitive lipase (HSL) knockout (KO) mice after treadmill exercise to stimulate the accumulation of DAGs in skeletal muscle. We found that, despite an increased DAG content in muscle after exercise in HSL KO mice, the HSL KO mice showed a higher insulin-stimulated glucose uptake postexercise compared with wild-type mice. Further analysis of the chemical structure and cellular localization of DAG in skeletal muscle revealed that HSL KO mice accumulated sn-1,3 DAG and not sn-1,2 DAG. Accordingly, these results highlight the importance of taking the chemical structure and cellular localization of DAG into account when evaluating the role of DAG in lipid-induced insulin resistance in skeletal muscle and that the accumulation of sn-1,3 DAG originating from lipolysis does not inhibit insulin-stimulated glucose uptake.

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Influence of Gender, Obesity, and Muscle Lipase Activity on Intramyocellular Lipids in Sedentary Individuals

Abstract: These data suggest that intramyocellular DAG is an independent predictor of insulin resistance in humans and that its levels correlate with lipolytic enzymes activity in skeletal muscle but not with markers of adiposity.

Cited by 132 publications

References 38 publications

Regulation of skeletal muscle lipolysis and oxidative metabolism by the co-lipase CGI-58

Regulation of skeletal muscle lipolysis and oxidative metabolism by the co-lipase CGI-58

Lower aerobic capacity was associated with abnormal intramuscular energetics in patients with metabolic syndrome

Partial Disruption of Lipolysis Increases Postexercise Insulin Sensitivity in Skeletal Muscle Despite Accumulation of DAG

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