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首页> 外文期刊>Molecular Nutrition and Food Research >Vinegar as a functional ingredient to improve postprandial glycemic control-human intervention findings and molecular mechanisms
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Vinegar as a functional ingredient to improve postprandial glycemic control-human intervention findings and molecular mechanisms

机译:醋作为改善餐后血糖控制的功能成分-人为干预发现和分子机制

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摘要

Type 2 diabetes prevalence worldwide is increasing and the burden is particularly high in Asian countries. Identification of functional food ingredients to curb the rise of diabetes among various Asian population groups is warranted. Vinegar is widely consumed throughout Asia, where the principle bioactive component is acetic acid. This review has collated data from human intervention trials to show that vinegar consumption seems more effective in modulating glycemic control in normal glucose-tolerant individuals than in either type 2 diabetics or in those with impaired glucose tolerance. The molecular mechanisms by which vinegar can improve glycemic control have been presented using human, animal and cell culture data. These mechanisms include (i) activation of the free fatty acid receptor 2 (FFAR2) receptors localized in the enteroendocrine L-cells of the intestinal lumen, leading to increased glucagon like peptide 1 (GLP-1) secretion, (ii) increased 5' adenosine monophosphate-activated protein kinase (AMPK) activation, leading to increased fatty acid oxidation and decreased hepatic gluconeogenesis, (iii) lowering of free fatty acid in circulation, potentially leading to improved insulin sensitivity, (iv) increased blood flow to the peripheral tissues and (v) increased satiety, leading to lower food intake. The review also discusses why these mechanisms appear more effective in nondiabetics than in diabetics.
机译:世界范围内2型糖尿病的患病率正在增加,在亚洲国家,负担尤其重。必须确定功能性食品成分,以遏制各种亚洲人群中糖尿病的发作。醋在整个亚洲被广泛消费,那里的主要生物活性成分是乙酸。这篇综述收集了来自人类干预试验的数据,结果表明,与2型糖尿病患者或糖耐量受损的患者相比,食用醋对调节葡萄糖耐量正常的人的血糖控制似乎更为有效。使用人,动物和细胞培养数据已经提出了醋可以改善血糖控制的分子机制。这些机制包括(i)激活位于肠腔内肠内分泌L细胞中的游离脂肪酸受体2(FFAR2)受体,导致胰高血糖素样肽1(GLP-1)分泌增加,(ii)5'增加腺苷单磷酸激活的蛋白激酶(AMPK)激活,导致脂肪酸氧化增加和肝糖异生减少,(iii)循环中游离脂肪酸的降低,可能导致胰岛素敏感性提高,(iv)流向周围组织的血流增加(v)饱腹感增加,导致食物摄入减少。这篇综述还讨论了为什么这些机制在非糖尿病患者中比在糖尿病患者中更有效。

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