Low Muscle Insulin Sensitivity in Poorly Controlled T2D is Associated with Incomplete Skeletal Muscle Fatty Acid

The mechanisms responsible for progressively worsening glycemic control are poorly understood. In a study by Gavin TP, et al. it was observed that “lower skeletal muscle mitochondrial respiratory capacity is associated with low insulin sensitivity and the development of T2D.” The insulin sensitivity in skeletal muscle was investigated, and the difference between well (WCD) and poorly (PCD) controlled T2D was determined. They also determined if the “skeletal muscle insulin sensitivity was different between well (WCD) and poorly (PCD) controlled T2D, and if the difference was associated with differences due to mitochondrial respiratory function.” It was determined that both insulin sensitivity (SI) and acute response to glucose (AIRg) were lower in PCD as compared to WCD. The study concluded that the “current results suggest that greater skeletal muscle incomplete FAO [fatty acid oxidation] in poorly controlled T2D is due to elevated β oxidation and is associated with worsening muscle insulin sensitivity.”

Gavin TP, Ernst JM, Kwak H-B, Caudill SE, Reed MA, Garner RT, Nie Y, Weiss JA, Pories WJ, Dar M, Lin C-T, Hubal MJ, Neufer PD, Kuang S, Dohm GL. High incomplete skeletal
muscle fatty acid oxidation explains low muscle insulin sensitivity in poorly controlled T2D. J Clinical Endocrinology & Metabolism. 2017 15 November.

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