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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Lifelong caloric restriction reprograms hepatic fat metabolism in mice
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Lifelong caloric restriction reprograms hepatic fat metabolism in mice

机译：终身热量限制可重编程小鼠肝脂肪代谢

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摘要

Calorie lowering slows the aging process and extends life span in diverse species by so far unknown mechanisms. The inverse linear relationship between calorie intake and life span suggests that regulators of energy metabolism are of importance in aging. The present study shows that lifelong caloric restriction in mice induces a metabolic adaptation with reduced lipogenesis and enhanced lipolysis and ketogenesis. This process, that is, the reprogramming of hepatic fat metabolism, is associated with a marked rise of fibroblastic growth factor 21 as a putative starvation master regulator. Due to the life span-extending properties of fibroblastic growth factor 21, the rise in fibroblastic growth factor 21 might contribute to the markedly better health status found in mice upon lifelong caloric restriction feeding. In addition, adropin, known as a peptide that controls lipid homeostasis, is significantly upregulated, underlining the diminution of lipogenesis that was further substantiated by decreased expression of liver-X-receptor α and its target genes sterol regulatory element-binding protein-1c, fatty acid synthase, and member 1 of human transporter subfamily ABCA upon lifelong caloric restriction feeding.
机译：热量降低降低了迄今为止未知的机制，延缓了衰老过程并延长了各种物种的寿命。卡路里摄入量与寿命之间的反线性关系表明，能量代谢的调节剂在衰老中很重要。本研究表明，小鼠终生的热量限制会诱导脂肪代谢减少，脂解和生酮作用增强的代谢适应。该过程，即肝脂肪代谢的重新编程，与作为假定的饥饿主调节剂的成纤维细胞生长因子21的显着升高有关。由于成纤维细胞生长因子21的寿命延长特性，成纤维细胞生长因子21的增加可能有助于终生限制热量摄食小鼠体内的健康状况。此外，称为控制脂质体内稳态的肽的adropin被显着上调，突显出脂肪生成的减少，这一点进一步被肝脏X受体α及其靶基因固醇调节元件结合蛋白1c的表达降低所证实，脂肪酸合成酶，以及终身热量限制摄食的人转运蛋白亚家族ABCA的成员1。

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