Over the last few decades, obesity and associated diseases such as type 2 diabetes (T2D) have developed to reach an endemic scale. However, the mechanisms linking obesity and T2D are still poorly understood. Recent studies suggest that fat accumulation in skeletal muscle might be an early event leading to T2D.
In healthy people, dietary fat accumulates in adipose tissue. This tissue is devoted to store fat after a meal and release it to fuel energy needs (for example during fasting and exercise). On the other hand, skeletal muscle is specialized to burn fat. A number of recent studies indicate that obese and diabetic subjects accumulate fat within lipid droplets in skeletal muscle, which may contribute to the pathogenesis of type 2 diabetes (T2D).
A key feature of T2D is the development of a systemic insulin resistance, i.e. a failure of insulin to adequately reduce blood sugar levels in response to a meal and promote glucose uptake in skeletal muscle. In a review from the journal Hormone Molecular Biology and Clinical Investigation, researchers have demonstrated that disrupted lipid droplet dynamics can give rise to toxic lipids that block the action of insulin in skeletal muscle.
Their review aims to discuss recent literature linking muscle fat storage and insulin resistance and to highlight potential therapeutic strategies to prevent lipotoxicity and T2D.
Understanding the dynamic of lipid droplet in skeletal muscle may help unravel novel targets to prevent lipotoxicity and metabolic diseases.
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