A role for adipose tissue de novo lipogenesis in glucose homeostasis during catch-up growth: a Randle cycle favoring fat storage.
A role for adipose tissue de novo lipogenesis in glucose homeostasis during catch-up growth: a Randle cycle favoring fat storage.
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追赶性生长期间脂肪组织从头脂肪生成在葡萄糖稳态中的作用：有利于脂肪储存的兰德尔循环。
作者：
Marcelino H;Veyrat-Durebex C;Summermatter S;Sarafian D;Miles-Chan J;Arsenijevic D;Zani F;Montani JP;Seydoux J;Solinas G;Rohner-Jeanrenaud F;Dulloo AG
追赶生长是2型糖尿病的一个危险因素，其特点是高胰岛素血症和加速体脂恢复。使用一个显示追赶脂肪的半停滞再喂养的大鼠模型，我们以前报道过，在低脂饮食的再喂养过程中，葡萄糖耐量正常，但骨骼肌中胰岛素依赖型葡萄糖的利用减少，脂肪组织中的胰岛素依赖性葡萄糖利用增加，从而伴随着从头开始的成脂能力的增强。在这里，我们报告等卡路里再喂食高脂肪(HF)食物可以钝化体内胰岛素依赖的葡萄糖利用来促进脂肪组织中的新生脂肪生成(DNL)。这些被证明是追赶生长的早期事件，独立于吞噬过度，并先于显性脂肪细胞肥大、脂肪组织炎症或胰岛素信号缺陷的发展。这些结果表明，在追赶生长过程中，增强的DNL作为葡萄糖汇在调节血糖方面发挥了作用，而追赶生长过程中的血糖因暴露于HF饮食而变得迟钝，从而与骨骼肌胰岛素抵抗一起导致糖耐量异常的发展。我们的发现是兰德尔循环假说的扩展，根据该假说，DNL的抑制构成了一种机制，通过该机制，膳食脂质对抗葡萄糖的利用，以甘油三酯的形式储存在脂肪组织中，从而破坏追赶生长过程中的葡萄糖动态平衡。
Catch-up growth, a risk factor for type 2 diabetes, is characterized by hyperinsulinemia and accelerated body fat recovery. Using a rat model of semistarvation-refeeding that exhibits catch-up fat, we previously reported that during refeeding on a low-fat diet, glucose tolerance is normal but insulin-dependent glucose utilization is decreased in skeletal muscle and increased in adipose tissue, where de novo lipogenic capacity is concomitantly enhanced. Here we report that isocaloric refeeding on a high-fat (HF) diet blunts the enhanced in vivo insulin-dependent glucose utilization for de novo lipogenesis (DNL) in adipose tissue. These are shown to be early events of catch-up growth that are independent of hyperphagia and precede the development of overt adipocyte hypertrophy, adipose tissue inflammation, or defective insulin signaling. These results suggest a role for enhanced DNL as a glucose sink in regulating glycemia during catch-up growth, which is blunted by exposure to an HF diet, thereby contributing, together with skeletal muscle insulin resistance, to the development of glucose intolerance. Our findings are presented as an extension of the Randle cycle hypothesis, whereby the suppression of DNL constitutes a mechanism by which dietary lipids antagonize glucose utilization for storage as triglycerides in adipose tissue, thereby impairing glucose homeostasis during catch-up growth.
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影响因子：
7.1
作者：
Aarsland, A;Chinkes, D;Wolfe, RR
通讯作者：
Wolfe, RR
影响因子：
11.1
作者：
Hoffstedt, J.;Forster, D.;Lofgren, P.
通讯作者：
Lofgren, P.
影响因子：
4.9
作者：
Dulloo, A. G.;Jacquet, J.;Montani, J-P
通讯作者：
Montani, J-P
影响因子：
5.8
作者：
Kamel, AF;Norgren, S;Marcus, C
通讯作者：
Marcus, C
影响因子：
6.5
作者：
Letexier, D;Pinteur, C;Beylot, M
通讯作者：
Beylot, M