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Updated: Jun 4, 2025

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
A famsin-glucagon axis mediates glucose homeostasis
Aijun Long1, Yazhuo Wang2, Yihua Guo3
1State Key Laboratory of Membrane Biology, MOE Key Laboratory of Bioinformatics, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, China; Metabolic Syndrome Research Center, Department of Geriatrics, The Second Xiangya Hospital of Central South University, Changsha, China.
Abstract:
Glucagon is essential for glucose homeostasis, and its dysregulation is associated with diabetes. Despite extensive research, the mechanisms governing glucagon secretion remain incompletely understood. Here, we unveil that famsin, a gut-secreted hormone, promotes glucagon release and modulates glucose homeostasis. Mechanistically, famsin binds to its receptor OLFR796 in mice (OR10P1 in humans), initiating calcium release in the endoplasmic reticulum of islet α cells. This process triggers glucagon secretion, consequently promoting hepatic glucose production through glucagon signaling. Furthermore, deficiency of famsin signaling reduces hepatic glucose production and lowers blood glucose levels, underscoring the significance of the famsin-glucagon axis in glucose homeostasis. Therefore, our findings establish famsin as a crucial regulator of glucagon secretion and provide valuable insights into the intricate gut-islet-liver interorgan crosstalk that maintains glucose homeostasis.
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