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非酯化脂肪酸代谢与餐后血脂异常

Non-esterified fatty acid metabolism and postprandial lipaemia.

作者信息

Frayn K N

机构信息

Oxford Lipid Metabolism Group, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, UK.

出版信息

Atherosclerosis. 1998 Dec;141 Suppl 1:S41-6. doi: 10.1016/s0021-9150(98)00216-0.

Abstract

Non-esterified fatty acids (NEFA, or free fatty acids) are an important metabolic fuel. Both the concentration of NEFA and their flux through the circulation vary widely from hour to hour, reflecting nutritional state and physical activity. Inappropriately elevated plasma NEFA concentrations may have a number of adverse effects on both carbohydrate and lipid metabolism. These adverse effects are likely to be most marked in the postprandial period, when NEFA release from adipose tissue is usually suppressed. Although the regulation of NEFA release in the postabsorptive state is well understood in molecular terms, the predominant pathway for release of NEFA in the postprandial state is the action of lipoprotein lipase (LPL) in adipose tissue capillaries on chylomicron-triacylglycerol (TG). Fatty acids released by LPL may either be sequestered in the adipocytes by esterification, or released as NEFA into the plasma. The regulation of this branch-point, which may be of crucial significance for postprandial metabolism, is not well understood. Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. There is considerable indirect evidence that impaired regulation of this step occurs in insulin resistance and other conditions collectively recognised by an elevated concentration of apolipoprotein B (hyper-apo B). Inappropriate release of NEFA in the postprandial period is likely both to reduce the sensitivity of glucose metabolism to insulin and to accentuate postprandial lipaemia. Further study of the regulation of this pathway is much needed.

摘要

非酯化脂肪酸(NEFA,即游离脂肪酸)是一种重要的代谢燃料。NEFA的浓度及其在循环中的通量每小时都有很大变化,反映了营养状态和身体活动情况。血浆NEFA浓度异常升高可能会对碳水化合物和脂质代谢产生多种不利影响。这些不利影响在餐后阶段可能最为明显,此时脂肪组织中NEFA的释放通常会受到抑制。尽管在分子层面上对吸收后状态下NEFA释放的调节已得到充分理解,但餐后状态下NEFA释放的主要途径是脂肪组织毛细血管中的脂蛋白脂肪酶(LPL)对乳糜微粒三酰甘油(TG)的作用。LPL释放的脂肪酸可能通过酯化作用被隔离在脂肪细胞中,或者作为NEFA释放到血浆中。对这个分支点的调节尚未得到很好的理解,而这一分支点对餐后代谢可能至关重要。刺激脂肪酸在组织中潴留的因素包括胰岛素和酰化刺激蛋白。有大量间接证据表明,在胰岛素抵抗以及其他以载脂蛋白B浓度升高(高载脂蛋白B)共同识别的情况下,这一步骤的调节受损。餐后阶段NEFA的不适当释放可能既会降低葡萄糖代谢对胰岛素的敏感性,又会加剧餐后血脂异常。因此,迫切需要对该途径的调节进行进一步研究。

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