血浆非酯化脂肪酸(NEFA)在2型糖尿病:病理生理学的证据

Kailash Chandra, V. Jain, S. Jain
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引用次数: 1

摘要

2型糖尿病(T2DM)是一种以血糖水平升高以及脂质和蛋白质代谢受损为特征的代谢功能障碍[1,2]。脂肪酸的动员在胰岛素抵抗中增强,这是由于激素抑制脂肪分解的失败,进一步增加了血浆NEFA水平的增加。这反过来又会导致炎症和进一步的胰岛素抵抗。胰岛素抵抗与胰岛β细胞功能障碍互补导致高血糖。胰岛素抵抗可能在T2DM发病前数年未被发现。胰岛素抑制脂肪组织中储存脂肪的脂解和肝脏中的糖异生。它还增加了最佳细胞功能、修复和生长所需蛋白质的合成,并刺激GLUT-4蛋白的易位,导致葡萄糖转运到肌肉细胞[4]。胰岛素抵抗是一种代谢功能障碍,通常由炎症增加介导。
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Plasma Non-Esterified Fatty Acids (NEFA) in Type 2 Diabetes Mellitus: Evidence on Pathophysiology
Type 2 diabetes mellitus (T2DM) is a metabolic dysfunction characterized by elevated levels of blood glucose as well as impaired lipid and protein metabolism [1,2]. The mobilization of fatty acids is augmented in insulin resistance due to the failure of lipolysis inhibition by the hormone that further augments the increase in plasma NEFA levels. This in turn, results in inflammation as well as further insulin resistance [3]. The complementation of insulin resistance with dysfunction of pancreatic islet β-cells leads to hyperglycemia. Insulin resistance may persist unnoticed for several years prior to onset of T2DM. Insulin inhibits lipolysis of stored fat in adipose tissue and gluconeogenesis in liver. It also increases the synthesis of proteins needed for the optimal cellular function, repair, growth, and stimulates the translocation of the GLUT-4 protein leading to increased transport of glucose into the muscle cells [4]. Insulin resistance is a metabolic dysfunction that is often mediated by increased inflammation.
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