A role for suppressed thermogenesis favoring catch-up fat in the pathophysiology of catch-up growth
A role for suppressed thermogenesis favoring catch-up fat in the pathophysiology of catch-up growth
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DOI：
10.2337/diabetes.52.5.1090
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发表时间：
2003-05-01
期刊：
影响因子：
7.7
通讯作者：
Dulloo, AG
中科院分区：
文献类型：
--
作者：
Crescenzo, R;Samec, S;Dulloo, AG
追赶性生长是以后肥胖、2型糖尿病和心血管疾病的危险因素。我们在这里表明，在通过半饥饿生长停滞后，大鼠重新喂食与对照组相同量的低脂饮食，显示1）由于产热减少而导致的较低的能量消耗，这有利于加速脂肪沉积或追赶脂肪，2）正常的葡萄糖，耐受性，但在葡萄糖负荷后，当他们的体脂和血浆游离脂肪酸（FFA）没有超过对照组时，血浆胰岛素较高。高脂饮食的等热量再喂养导致更低的能量消耗和产热，增加脂肪沉积，并导致葡萄糖负荷后更高的血浆胰岛素和血浆葡萄糖升高。逐步回归分析显示，葡萄糖负荷后的血浆胰岛素和胰岛素与葡萄糖的比率通过能量使用效率的变化来预测（即，在产热作用中），而不是通过体脂肪或血浆FFA的绝对量。这些研究表明，抑制产热本身可能有一个主要的作用，在追赶型生长过程中的高胰岛素血症和胰岛素抵抗的发展，并强调了抑制产热专门针对追赶脂肪的追赶型生长和慢性代谢疾病之间的联系的作用。
Catch-up growth is a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases. We show here that after growth arrest by semistarvation, rats refed the same amount of a low-fat diet as controls show 1) lower energy expenditure due to diminished thermogenesis that favors accelerated fat deposition or catch-up fat and 2) normal glucose, tolerance but higher plasma insulin after a glucose load at a time point when their body fat and plasma free fatty acids (FFAs) have not exceeded those of controls. Isocaloric refeeding on a high-fat diet resulted in even lower energy expenditure and thermogenesis and increased fat deposition and led to even higher plasma insulin and elevated plasma glucose after a glucose load. Stepwise regression analysis showed that plasma insulin and insulin-to-glucose ratio after the glucose load are predicted by variations in efficiency of energy use (i.e., in thermogenesis) rather than by the absolute amount of body fat or plasma FFAs. These studies suggest that suppression of thermogenesis per se may have a primary role in the development of hyperinsulinemia and insulin resistance during catch-up growth and underscore a role for suppressed thermogenesis directed specifically at catch-up fat in the link between catch-up growth and chronic metabolic diseases.