The regulatory effects of growth hormone on adipose tissue at physiological and pathological levels and its relationship with obesity
摘要
Growth hormone not only promotes growth and development via inducing insulin-like growth factor-1 produced by the liver but also regulates glucose and lipid metabolism of peripheral organs, including the liver, adipose tissue, and muscle. Particularly, the relationship between growth hormone and adipose tissue has been recognized since the 1950s. More intensive research focusing on it is emerging, fueled by the new conception that adipose tissue is not merely a passive reservoir for fat storage but a highly active organ with endocrine and metabolic capabilities. As for it, earlier findings have illuminated the effects of growth hormone on adipose tissue, including lipolysis and lipogenesis, adipocyte proliferation and differentiation, adipose cytokine secretion, white fat browning, and adipose tissue fibrosis. Subsequently, recent research has uncovered its involvement in promoting adipose tissue aging, regulating the adipose tissue immune microenvironment, and governing adipocyte subgroup composition. More importantly, decreased serum levels of growth hormone detected in patients with obesity are associated with glucose and lipid metabolism dysfunction. Therefore, this review aims to examine the impact of growth hormone on adipose tissue under the physiological context or pathological contexts based on patients and animal models characterized by either excessive or diminished growth hormone action to indicate a complex interplay of mutual regulatory mechanisms between adipose tissue and growth hormone. Subsequently, the alterations of growth hormone levels in obesity and their implications for glucose-lipid metabolism and adipose tissue have also been reviewed. Therefore, the review will offer novel perspectives on the role of growth hormone in the progression of obesity based on the new conception of adipose tissue and its potential use in therapeutic interventions for obesity.