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首页> 外文期刊>EBioMedicine >Adipose tissue lipolysis, plasma fatty acids, and glucose homeostasis in people with obesity: New pieces that help solve the puzzle
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Adipose tissue lipolysis, plasma fatty acids, and glucose homeostasis in people with obesity: New pieces that help solve the puzzle

机译：肥胖的组织脂肪解，血浆脂肪酸和血糖稳态，肥胖的人：帮助解决难题的新件

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Insulin is the key regulator of plasma glucose concentration, because it potently suppresses hepatic glucose production and stimulates tissue glucose uptake. Obesity is often associated with both insulin resistance and hyperinsulinemia. The concurrence of the two is commonly thought to reflect a homeostatic feedback loop in which the insulin resistance-mediated increase in plasma glucose stimulates insulin secretion from b-cells to maintain euglycemia [1]. Continuous overstimulation of b-cells leads to b-cell dysfunction, i.e., an insufficient b-cell response to the rise in glucose, resulting in hyperglycemia despite hyperinsulinemia and ultimately type 2 diabetes (T2D) [1]. However, it has also been proposed that insulin hypersecretion is the initial defect that causes insulin resistance and the vicious cycle that eventually results in T2D [1]. Alternatively, it has been suggested that insulin resistance and insulin hypersecretion occur simultaneously because they have a common cause adipose tissue dysfunction. According to this hypothesis, enlargement of adipocytes leads to a cascade of events that includes impaired adipose tissue perfusion, inflammation, reduced insulin action on triglyceride lipolysis, and increased fatty acid release into the circulation, which in turn causes both insulin resistance in the liver and muscles and increased insulin secretion from b-cells [1 4]. In this issue of EBioMedicine, Fryk and colleagues [5] describe the results from two studies that provide new insights into this complex relationship.
机译：胰岛素是血浆葡萄糖浓度的关键调节剂，因为它效果抑制了肝葡萄糖的产生并刺激组织葡萄糖摄取。肥胖通常与胰岛素抵抗和高胰岛素血症有关。通常认为这两者的同意反映了稳态反馈回路，其中胰岛素抗性介导的血浆葡萄糖的增加刺激来自B细胞的胰岛素分泌，以维持Euglycemia [1]。 B细胞的连续过度刺激导致B细胞功能障碍，即对葡萄糖升高的B细胞应答，尽管高胰岛素血症和最终型糖尿病（T2D）[1]。然而，还提出了胰岛素的高度折叠是导致胰岛素抵抗和最终导致T2D [1]的恶性循环的初始缺陷。或者，已经提出了胰岛素抵抗和胰岛素的过度，同时发生，因为它们具有常见的原因脂肪组织功能障碍。根据这一假设，脂肪细胞的扩大导致包括受损脂肪组织灌注，炎症，对甘油三酯脂解的胰岛素作用的级联的级联事件，并增加脂肪酸释放到循环中，这反过来导致肝脏胰岛素抵抗来自B细胞的肌肉和增加的胰岛素分泌[14]。在这个问题的eBiomedicine，Fryk和同事[5]描述了两项研究的结果，为这种复杂关系提供了新的见解。

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