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美国牛津糖尿病中心的Karpe F等近期发表的“Fatty acids,obesity,and insulin resistance:time for a reevaluation”(Diabetes,2011,60:2441)。根据他们自己的研究和文献对脂肪酸(FA)在肥胖和IR中的关系撰文提出新认识。首先,非酯化脂肪酸(NEFA)的基本功能现在认为NEFA是将储存在脂肪组织的TG转运到其利用处的转运工具,而不只是供肝、心肌等利用。第二,上身和腹部皮下脂肪堆积是NEFA主要来源,不同于普遍认为只有一小部分NEFA来自腹内脂肪组织。第三,空腹血浆NEFA几乎全部来自脂肪细胞内TG水解,但餐后血浆NEFA约40%～50%来自食物脂肪乳糜颗粒中的TG被LPL水解,脂肪利用被胰岛素抑制,在富含碳水化合物餐后NEFA浓度下降。第四,NEFA升高伴急性IR,常见于肥胖,控制不良的糖尿病患者,IR伴异位脂肪——脂肪组织以外的胰岛素效应组织如骨骼肌细胞脂质增加(细胞TG),反映脂肪清除损害甚于摄取。现撷其精要摘译并如以评论,供广大读作者参考。
Karpe F of the Oxford Diabetes Center recently published “Fatty acids, obesity, and insulin resistance: time for a revaluation” (Diabetes, 2011, 60: 2441). Based on their own research and literature, a new understanding of the relationship of fatty acids (FA) in obesity and IR is emerging. First of all, the basic function of non-esterified fatty acids (NEFA) NEFA is now considered to be stored in fatty tissue of the TG transporter to its use of the transporter, not just the liver, myocardium and so on. Second, subcutaneous fat accumulation in the upper body and abdomen is a major source of NEFA, unlike the general belief that only a small fraction of NEFA is from intra-abdominal adipose tissue. Third, almost all of the fasting plasma NEFA comes from TG lipolysis in adipocytes, but about 40% to 50% of postprandial plasma NEFA is hydrolyzed by LPL from fat-based chylomicrons and fat is inhibited by insulin. In carbohydrate-rich meals After NEFA concentration decreased. Fourth, elevated NEFA with acute IR is commonly seen in obese, poorly controlled diabetic patients and increases in lipid (TG) in insulin-responsive tissues such as skeletal muscle cells other than IR with ectopic fat-adipose tissue, reflecting loss of fat clearance More than intake. Now pick the essence of its translation and as comments, for the majority of readers reference.