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Impaired adaptation of energy intake induces severe obesity in aged mice on a high‐fat diet

机译:能量摄入适应性受损会导致高脂饮食的老年小鼠严重肥胖

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摘要

High‐fat diet (HFD) feeding induces inflammation in various tissues, including the nodose ganglion and hypothalamus, resulting in obesity and metabolic disorders. In this study, we investigated the effect of short‐term HFD on aged and young mice. Aged mice easily gained weight during short‐term HFD feeding, and required many days to adapt their energy intake. One‐day HFD in aged mice induced inflammation in the distal colon, but not in the nodose ganglion or hypothalamus. The anorexic effect of glucagon‐like peptide‐1 (GLP‐1) was attenuated in aged mice. Intraperitoneal administration of GLP‐1 did not induce expression of genes that regulate feeding in the hypothalamus of aged mice. mRNA expression of the gene encoding the GLP‐1 receptor (Glp1r) in the nodose ganglion was significantly lower in aged mice than in young mice. Our findings suggest that adaptation of energy intake regulation was attenuated in aged mice, causing them to become obese in response to short‐term HFD feeding.
机译:高脂饮食(HFD)会引起各种组织(包括结节神经节和下丘脑)发炎,从而导致肥胖和代谢异常。在这项研究中,我们调查了短期HFD对老年和年轻小鼠的影响。老年小鼠在短期HFD喂养期间很容易体重增加,并且需要很多天才能适应其能量摄入。衰老小鼠的一日HFD诱导远端结肠发炎,但未在结节神经节或下丘脑中引起炎症。胰高血糖素样肽-1(GLP-1)的厌食作用在衰老小鼠中减弱。腹膜内给予GLP-1不会诱导调节老年小鼠下丘脑进食的基因的表达。结节神经节中编码GLP-1受体(Glp1r)的基因的mRNA表达明显低于年轻小鼠。我们的研究结果表明,衰老小鼠的能量摄入调节适应性减弱,导致它们因短期HFD喂养而变得肥胖。

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