Hepatic glucagon action: beyond glucose mobilization

胰高血糖素 葡萄糖稳态 胰高血糖素受体 内分泌学 肠促胰岛素 内科学 脂肪性肝炎 分解代谢 胰岛素 激素 平衡 碳水化合物代谢 生物 脂肪肝 化学 医学 新陈代谢 糖尿病 胰岛素抵抗 2型糖尿病 疾病
作者
Sarina Kajani,Rhianna C. Laker,Ekaterina L. Ratkova,Sarah Will,Christopher J. Rhodes
出处
期刊:Physiological Reviews [American Physiological Society]
卷期号:104 (3): 1021-1060 被引量:3
标识
DOI:10.1152/physrev.00028.2023
摘要

Glucagon’s ability to promote hepatic glucose production has been known for over a century, with initial observations touting this hormone as a diabetogenic agent. However, glucagon receptor agonism [when balanced with an incretin, including glucagon-like peptide 1 (GLP-1) to dampen glucose excursions] is now being developed as a promising therapeutic target in the treatment of metabolic diseases, like metabolic dysfunction-associated steatotic disease/metabolic dysfunction-associated steatohepatitis (MASLD/MASH), and may also have benefit for obesity and chronic kidney disease. Conventionally regarded as the opposing tag-team partner of the anabolic mediator insulin, glucagon is gradually emerging as more than just a “catabolic hormone.” Glucagon action on glucose homeostasis within the liver has been well characterized. However, growing evidence, in part thanks to new and sensitive “omics” technologies, has implicated glucagon as more than just a “glucose liberator.” Elucidation of glucagon’s capacity to increase fatty acid oxidation while attenuating endogenous lipid synthesis speaks to the dichotomous nature of the hormone. Furthermore, glucagon action is not limited to just glucose homeostasis and lipid metabolism, as traditionally reported. Glucagon plays key regulatory roles in hepatic amino acid and ketone body metabolism, as well as mitochondrial turnover and function, indicating broader glucagon signaling consequences for metabolic homeostasis mediated by the liver. Here we examine the broadening role of glucagon signaling within the hepatocyte and question the current dogma, to appreciate glucagon as more than just that “catabolic hormone.”
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