Glucagon blockade restores functional β-cell mass in type 1 diabetic mice and enhances function of human islets

• DOI: 10.1073/pnas.2022142118
• Publication Date: 2021-02-22T21:27:33Z
• Authors: May-Yun Wang; E. Danielle Dean; Ezekiel Quittner-...; Yi Zhu; Kamrul H. Chowdhury; Zhuzhen Zhang; Shangang Zhao; Na Li; Reshing Ye; Young Lee; Yiyi Zhang; Shiuhwei Chen; Xinxin Yu; Derek C. Leonard; Greg Poffenberger; Alison Von Deylen; S. Kay McCorkle; Amnon Schlegel; Kyle W. Sloop; Alexander M. Efanov; Ruth E. Gimeno; Philipp E. Scherer; Alvin C. Powers; Roger H. Unger; William L. Holland
• Keywords: NOD mice

Significance Both type 1 and 2 diabetes are associated with reduced β-cell mass or function, resulting from decreased proliferation increased apoptosis. Understanding the signals governing survival regeneration is critical for developing strategies to maintain healthy populations of these cells in individuals. forms hyperglucagonemia an plasma glucagon:insulin ratio. Glucagon excess contributes metabolic dysregulation diabetic state glucagon receptor antagonism a potential target area treatment prevention diabetes. Our studies presented here suggest that blockade signaling lowers glycemia mouse models while enhancing formation functional production insulin-positive α-cell precursors.