Midgut-Derived Activin Regulates Glucagon-like Action in the Fat Body and Glycemic Control
O’Connor, Michael B.
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CitationSong, Wei, Daojun Cheng, Shangyu Hong, Benoit Sappe, Yanhui Hu, Neil Wei, Changqi Zhu et al. "Midgut-Derived Activin Regulates Glucagon-like Action in the Fat Body and Glycemic Control." Cell Metabolism 25, no. 2 (2017): 386-399. DOI: 10.1016/j.cmet.2017.01.002
AbstractWhile high-caloric diet impairs insulin response to cause hyperglycemia, whether and how counter-regulatory hormones are modulated by high-caloric diet is largely unknown. We find that enhanced response of Drosophila adipokinetic hormone (AKH, the glucagon homolog) in the fat body is essential for hyperglycemia associated with a chronic high-sugar diet. We show that the activin type I receptor Baboon (Babo) autonomously increases AKH signaling without affecting insulin signaling in the fat body via, at least, increase of Akh receptor (AkhR) expression. Further, we demonstrate that Activin-β (Actβ), an activin ligand predominantly produced in the enteroendocrine cells (EEs) of the midgut, is up-regulated by chronic high-sugar diet and signals through Babo to promote AKH action in the fat body, leading to hyperglycemia. Importantly, activin signaling in mouse primary hepatocytes also increases glucagon response and glucagon- induced glucose production, indicating a conserved role for activin in enhancing AKH/glucagon signaling and glycemic control.
Citable link to this pagehttps://nrs.harvard.edu/URN-3:HUL.INSTREPOS:37372619
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