脂肪组织
内分泌学
内科学
能量稳态
吻素
葡萄糖稳态
脂肪因子
脂联素
生物
平衡
瘦素
下丘脑
医学
胰岛素抵抗
胰岛素
肥胖
作者
Chunyu Liang,Xuehan Li,Ge Song,Søren Fisker Schmidt,Lingyu Sun,Jianhao Chen,Xinliang Pan,Haotian Zhao,Yi Yan
标识
DOI:10.1096/fj.202302598rr
摘要
Abstract Kisspeptin signaling regulates energy homeostasis. Adiposity is the principal source and receiver of peripheral Kisspeptin, and adipose Kiss1 metastasis suppressor (Kiss1) gene expression is stimulated by exercise. However, whether the adipose Kiss1 gene regulates energy homeostasis and plays a role in adaptive alterations during prolonged exercise remains unknown. Here, we investigated the role of Kiss1 role in mice and adipose tissues and the adaptive changes it induces after exercise, using adipose‐specific Kiss1 knockout (Kiss1 adipoq−/− ) and adeno‐associated virus‐induced adipose tissue Kiss1‐overexpressing (Kiss1 adipoq over ) mice. We found that adipose‐derived kisspeptin signal regulates lipid and glucose homeostasis to maintain systemic energy homeostasis, but in a sex‐dependent manner, with more pronounced metabolic changes in female mice. Kiss1 regulated adaptive alterations of genes and proteins in tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OxPhos) pathways in female gWAT following prolonged aerobic exercise. We could further show that adipose Kiss1 deficiency leads to reduced peroxisome proliferator‐activated receptor gamma co‐activator 1 alpha (PGC‐1α) protein content of soleus muscle and maximum oxygen uptake (VO 2 max) of female mice after prolonged exercise. Therefore, adipose Kisspeptin may be a novel adipokine that increases organ sensitivity to glucose, lipids, and oxygen following exercise.
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