Long-term caloric restriction is a conventional and reproducible dietary intervention to improve whole body metabolism, suppress age-related pathophysiology, and extend lifespan. The beneficial actions of caloric restriction are widely accepted to be regulated in both growth hormone/insulin-like growth factor 1-dependent and -independent manners. Although growth hormone/insulin-like growth factor 1-dependent regulatory mechanisms are well described, those occurring independent of growth hormone/insulin-like growth factor 1 are poorly understood. In this review, we focus on molecular mechanisms of caloric restriction regulated in a growth hormone/insulin-like growth factor 1-independent manner. Caloric restriction increases mitochondrial quantity and improves mitochondrial quality by activating an axis involving sterol regulatory element binding protein-c/peroxisome proliferator-activated receptor γ coactivator-1α/mitochondrial intermediate peptidase in a growth hormone/insulin-like growth factor 1-independent manner, particularly in white adipose tissue. Fibroblast growth factor 21 is also involved in this axis. Moreover, the axis may be regulated by lower leptin signaling. Thus, caloric restriction appears to induce beneficial actions partially by regulating mitochondrial quantity and quality in white adipose tissue in a growth hormone/insulin-like growth factor 1-independent manner.

中文翻译：

---

白色脂肪组织中线粒体数量和质量控制对健康寿命的影响：GH/IGF-1独立途径在热量限制介导的代谢重塑中的重要作用

长期热量限制是一种传统的、可重复的饮食干预措施，可改善全身代谢、抑制与年龄相关的病理生理学并延长寿命。人们广泛认为热量限制的有益作用是通过生长激素/胰岛素样生长因子1依赖性和非依赖性方式进行调节的。尽管生长激素/胰岛素样生长因子 1 依赖性调节机制已得到很好的描述，但那些独立于生长激素/胰岛素样生长因子 1 发生的调节机制却知之甚少。在这篇综述中，我们重点关注以生长激素/胰岛素样生长因子 1 独立方式调节热量限制的分子机制。热量限制通过以不依赖于生长激素/胰岛素样生长因子1的方式激活涉及甾醇调节元件结合蛋白-c/过氧化物酶体增殖物激活受体γ辅激活剂-1α/线粒体中间肽酶的轴来增加线粒体数量并改善线粒体质量，特别是在白色脂肪组织中。成纤维细胞生长因子 21 也参与该轴。此外，该轴可能受到较低的瘦素信号传导的调节。因此，热量限制似乎部分地通过以不依赖生长激素/胰岛素样生长因子1的方式调节白色脂肪组织中的线粒体数量和质量来诱导有益作用。