Increased VLDL-TG fatty acid storage in skeletal muscle in men with type 2 diabeteS

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Abstract

Context: Lipoprotein lipase (LPL) activity is considered the rate-limiting step of very-low-densitylipoprotein triglycerides (VLDL-TG) tissue storage, and has been suggested to relate to the development of obesity as well as insulin resistance and type 2 diabetes. Objective: The objective of the study was to assess the relationship between the quantitative storage of VLDL-TG fatty acids and LPL activity and other storage factors in muscle and adipose tissue. In addition, we examine whether such relations were influenced by type 2 diabetes. Design: We recruited 23 men (12 with type 2 diabetes, 11 nondiabetic) matched for age and body mass index. Postabsorptive VLDL-TG muscle and subcutaneous adipose tissue (abdominal and leg) quantitative storage was measured using tissue biopsies in combination with a primed-constant infusion of ex vivo triolein labeled [1-14C]VLDL-TG and a bolus infusion of ex vivo triolein labeled [9,10-3H]VLDL-TG. Biopsies were analyzed for LPL activity and cellular storage factors. Results: VLDL-TG storage rate was significantly greater in men with type 2 diabetes compared with nondiabetic men in muscle tissue (P = 0.02). We found no significant relationship between VLDL-TG storage rate and LPL activity or other storage factors in muscle or adipose tissue. However, LPL activity correlated with fractional VLDL-TG storage in abdominal fat (P = 0.04). Conclusions: Men with type 2 diabetes have increased VLDL-TG storage in muscle tissue, potentially contributing to increased intramyocellular triglyceride and ectopic lipid deposition.Neithermuscle nor adipose tissue storage rates were related to LPL activity. This argues against LPL as a rate-limiting step in the postabsorptive quantitative storage of VLDL-TG.

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APA

Andersen, I. R., Søndergaard, E., Sørensen, L. P., Nellemann, B., Gormsen, L. C., Jensen, M. D., & Nielsen, S. (2017). Increased VLDL-TG fatty acid storage in skeletal muscle in men with type 2 diabeteS. Journal of Clinical Endocrinology and Metabolism, 102(3), 831–839. https://doi.org/10.1210/jc.2016-2979

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