DGAT1 Reduces Palmitic Acid-induced Insulin Resistance Without Rescuing ER Stress In C2C12 Cells | 14831
Journal of Obesity & Weight Loss Therapy
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Pathological elevation of plasma free fatty acids (FFAs) induces insulin resistance (IR). Previous work demonstrates that palmitic
acid (PA) affects ectopic lipid distribution, which is associated with endoplasmic reticulum (ER) stress and IR, is rescued by
oleic acid (OA). The exact mechanisms how different saturation FFAs regulate insulin signaling are poorly understood, especially
in skeletal muscle where most of the blood glucose is consumed. We investigated the potential role of PA and OA in the lipid
metabolism and insulin signal in C2C12 cells (mouse myoblast cell line). We found that diacylglycerol (DAG) was accumulated
significantly in PA treatment with a time- and dose-dependent manner, suggesting that triacylglycerol (TAG) synthesis was
blocked in the step of DAG to TAG. Overexpression of DAG acyltransferase 1 (DGAT1) efficiently converted DAG to TAG
but overexpression of DGAT2 had almost no effect. In addition, PA-reduced phosphorylation of AKT was rescued by DGAT1
overexpression without affecting splicing of XBP-1 and phosphorylation of PERK. The data indicate that PA incorporation into
non-toxic TAG was stopped at toxic DAG and DGAT1 could reduce PA-induced IR without rescuing PA-induced ER stress.
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