Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production.
Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production.
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DOI：
10.1172/jci16521
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发表时间：
2003-01
期刊：
影响因子：
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通讯作者：
Michael W. Rajala;S. Obici;P. Scherer;L. Rossetti
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文献类型：
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作者：
Michael W. Rajala;S. Obici;P. Scherer;L. Rossetti
据推测，脂肪源性激素β-淀粉样蛋白将肥胖与胰岛素抵抗和糖尿病联系起来。在这里，输注的抗胰岛素或抵抗素样分子-β（β-Mbeta）迅速诱导严重的肝脏，但不是外周胰岛素抵抗。在存在生理性高胰岛素血症的情况下，输注纯化的重组葡萄糖酸，使循环葡萄糖酸水平增加约2倍至15倍，抑制葡萄糖代谢，使得需要较低的葡萄糖输注速率以将血浆葡萄糖浓度维持在基础水平。葡萄糖生成速率的显著增加完全解释了β-葡萄糖醛酸和β-葡萄糖醛酸对体内胰岛素作用的影响。这些结果支持了一个新的脂肪和肠道来源的循环蛋白家族调节肝脏胰岛素作用的观点。
The adipose-derived hormone resistin is postulated to link obesity to insulin resistance and diabetes. Here, the infusion of either resistin or the resistin-like molecule-beta (RELMbeta) rapidly induced severe hepatic but not peripheral insulin resistance. In the presence of physiologic hyperinsulinemia, the infusion of purified recombinant resistin, increasing circulating resistin levels by approximately twofold to 15-fold, inhibited glucose metabolism such that lower rates of glucose infusion were required to maintain the plasma glucose concentration at basal levels. The effects of resistin and RELMbeta on in vivo insulin action were completely accounted for by a marked increase in the rate of glucose production. These results support the notion that a novel family of fat- and gut-derived circulating proteins modulates hepatic insulin action.