脂肪生成
自噬
脂肪组织
脂肪细胞
串扰
胰岛素抵抗
生物
细胞生物学
白色脂肪组织
内分泌学
胰岛素
生物化学
细胞凋亡
光学
物理
作者
Farman Ali Khan,Haroon Khan,Ajmal Khan,Masao Yamasaki,Naima Moustaid‐Moussa,Ahmed Al‐Harrasi,Shaikh Mizanoor Rahman
标识
DOI:10.1016/j.biopha.2022.113715
摘要
White adipose tissue expands rapidly due to increased adipocyte number (hyperplasia) and size (hypertrophy), which results in obesity. Adipogenesis is a process of the formation of mature adipocytes from precursor cells. Additionally, obesity-related metabolic complications, such as fatty liver and insulin resistance, are linked to adipogenesis. On the contrary, autophagy is a catabolic process; essential to maintain cellular homeostasis via the degradation or recycling of unnecessary or damaged components. Importantly, autophagy dictates obesity and adipogenesis. Hence, a clear understanding of how autophagy regulates adipogenesis is crucial for drug development and the prevention and treatment of obesity and its associated disorders, such as type 2 diabetes, cardiovascular disease, and cancer. In this review, we highlighted recent findings regarding the crosstalk between adipogenesis and autophagy, as well as the molecules involved. Furthermore, the review discussed how bioactive compounds regulate adipogenesis by manipulating autophagy and underlying molecular mechanisms. Based on in vitro and animal studies, we summarized the effects of bioactive compounds on adipogenesis and autophagy. Hence, human studies are necessary to validate the effectiveness and optimal dosage of these bioactive compounds.
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