Increased intramuscular lipid storage in the insulin-resistant and endurance-trained state

ArticleinPflügers Archiv - European Journal of Physiology 451(5):606-16 · March 2006with54 Reads
DOI: 10.1007/s00424-005-1509-0 · Source: PubMed
Abstract
Numerous studies have reported a strong correlation between intramuscular triacylglycerol (IMTG) content and insulin resistance. However, the proposed relationship between IMTG accumulation and skeletal muscle insulin resistance is not unambiguous, as trained athletes have been shown to be markedly insulin sensitive despite an elevated IMTG storage. Though the latter has often been attributed to differences in muscle fibre type composition and/or structural characteristics of the intramyocellular lipid deposits, recent studies have failed to provide such evidence. The greater insulin sensitivity despite an elevated IMTG deposition in the endurance-trained state has often been described as a metabolic paradox. However, divergent metabolic events are responsible for the greater IMTG content in the endurance-trained versus insulin-resistant states. The greater IMTG storage in the trained athlete represents an adaptive response to endurance training, allowing a greater contribution of the IMTG pool as a substrate source during exercise. In contrast, elevated IMTG stores in the obese and/or type 2 diabetes patient seem to be secondary to a structural imbalance between plasma free fatty acid availability, fatty acid (FA) storage and oxidation. Therefore, the reported correlation between IMTG content and insulin resistance does not represent a functional relationship, as it is strongly influenced by training status and/or habitual physical activity. It can be argued that the ratio between IMTG content and muscle oxidative capacity represents a more accurate marker of insulin resistance. Interventions to augment mitochondrial density and/or function are likely to improve the balance between FA uptake and oxidation and should be applied to prevent and/or treat insulin resistance.
    • "However, chronic activation of AMPK gamma1 in muscle increases glycogen levels [2], gain-of function gamma2 mutation in the heart causes massive glycogen accumulation [27] and AICAR-induced AMPK activation has also been shown to increase muscle glycogen in mice [17]. The role of AMPK in lipid storage IMTG is unclear, but our data should spur future research into AMPK-regulated IMTG turnover, especially since exercise training (i.e., repeated AMPK activation) can lead to elevated IMTG levels [40]. "
    File · Data · Sep 2016 · International Journal of Molecular Sciences
    • "These findings are in line with the so-called " athlete's paradox " . This term was used to describe the intriguing finding that IMCL levels in athletes were as high as those in obese, sedentary subjects or insulin-resistant subjects [114][115][116][117][118][119][120][121]158,176]. However, the capacity to deplete IMCL during exercise was increased in endurance-trained athletes, further corroborating the fact that IMCL can be considered as local fuel stores that are used during physical exercise in proportion to their pre-exercise content [37,45,47,56,59,62,111,135]. "
    [Show abstract] [Hide abstract] ABSTRACT: In addition to the subcutaneous and the visceral fat tissue, lipids can also be stored in non-adipose tissue such as in hepatocytes (intrahepatocellular lipids; IHCL), skeletal (intramyocellular lipids; IMCL) or cardiac muscle cells (intracardiomyocellular lipids; ICCL). Ectopic lipids are flexible fuel stores that can be depleted by physical exercise and repleted by diet. They are related to obesity and insulin resistance. Quantification of IMCL was initially performed invasively, using muscle biopsies with biochemical and/or histological analysis. ¹H-magnetic resonance spectroscopy (¹H-MRS) is now a validated method that allows for not only quantifying IMCL non-invasively and repeatedly, but also assessing IHCL and ICCL. This review summarizes the current available knowledge on the flexibility of ectopic lipids. The available evidence suggests a complex interplay between quantitative and qualitative diet, fat availability (fat mass), insulin action, and physical exercise, all important factors that influence the flexibility of ectopic lipids. Furthermore, the time frame of the intervention on these parameters (short-term vs. long-term) appears to be critical. Consequently, standardization of physical activity and diet are critical when assessing ectopic lipids in predefined clinical situations.
    Full-text · Article · Sep 2016
    • "However, chronic activation of AMPK gamma1 in muscle increases glycogen levels [2], gain-of function gamma2 mutation in the heart causes massive glycogen accumulation [27] and AICAR-induced AMPK activation has also been shown to increase muscle glycogen in mice [17]. The role of AMPK in lipid storage IMTG is unclear, but our data should spur future research into AMPK-regulated IMTG turnover, especially since exercise training (i.e., repeated AMPK activation) can lead to elevated IMTG levels [40]. "
    File · Data · Aug 2016 · International Journal of Molecular Sciences
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