Chapter

The Islets of Langerhans

Volume 654 of the series Advances in Experimental Medicine and Biology pp 421-445

Date:

Molecular Pathways Underlying the Pathogenesis of Pancreatic α-Cell Dysfunction

  • Dan KawamoriAffiliated withDepartment of Cellular and Molecular Physiology, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School
  • , Hannah J. WeltersAffiliated withDepartment of Cellular and Molecular Physiology, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School
  • , Rohit N. KulkarniAffiliated withDepartment of Cellular and Molecular Physiology, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School Email author 

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Abstract

Glucagon plays a critical role in glucose homeostasis by counteracting insulin action, especially during hypoglycemia. Glucagon secretion from pancreatic α-cells is regulated by various mechanisms including glycemia, neural input, and secretion from neighboring β-cells. However, glucagon secretion is dysregulated in diabetic states, causing exacerbation of glycemic disorders. Recently, new therapeutic approaches targeting excess glucagon secretion are being explored for use in diabetes treatment. Therefore, understanding the molecular mechanism of how glucagon secretion is regulated is critical for treating the α-cell dysfunction observed in diabetes.

Keywords

Diabetes Hypoglycemia Pancreatic islets α-cells Glucagon Secretion Insulin GABA Zinc Somatostatin GLP-1 Counter regulation Neurotransmitters and nervous systems Development Hypertrophy