Adropin and insulin resistance: Integration of endocrine, circadian, and stress signals regulating glucose metabolism.
Adropin and insulin resistance: Integration of endocrine, circadian, and stress signals regulating glucose metabolism.
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DOI：
10.1002/oby.23249
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发表时间：
2021-11
期刊：
影响因子：
--
通讯作者：
Havel PJ
中科院分区：
文献类型：
--
作者：
Butler AA;Havel PJ
Dysregulation of hepatic glucose production (HGP) and glucose disposal leads to type 2 diabetes (T2D). Hyperglycemia results from declining ability of insulin to reduce HGP and increase glucose disposal, and inadequate ß-cell compensation for insulin resistance. Hyperglucagonemia resulting from reduced suppression of glucagon secretion by insulin contributes to hyperglycemia by stimulating HGP. These actions of pancreatic hormones are normally complemented by peptides secreted by cells distributed throughout the body. This regulatory network has provided new therapeutics for obesity and T2D (e.g., GLP-1). Other peptide hormones being actively investigated show promise in preclinical studies. Recent experiments using mice and nonhuman primates indicate the small-secreted peptide hormone adropin regulates glucose metabolism. We discuss recent expression profiling data indicating hepatic adropin expression increases with oxidative stress and declines with fasting or in the presence of hepatic insulin resistance, and how adropin interacts with the pancreatic hormones, insulin, and glucagon to modulate glycemic control.
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11.4
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Thapa D;Stoner MW;Zhang M;Xie B;Manning JR;Guimaraes D;Shiva S;Jurczak MJ;Scott I
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