Current Insights and New Perspectives on the Roles of Hyperglucagonemia in Non-Insulin–Dependent Type 2 Diabetes
Author:
Publisher
Springer Science and Business Media LLC
Subject
Internal Medicine
Link
http://link.springer.com/content/pdf/10.1007/s11906-013-0383-y.pdf
Reference59 articles.
1. Matthaei S, Stumvoll M, Kellerer M, Haring H-U. Pathophysiology and pharmacological treatment of insulin resistance. Endocr Rev. 2000;21:585–618.
2. Mayo KE, Miller LJ, Bataille D, Dalle S, Goke B, Thorens B, et al. International Union of Pharmacology. XXXV. The glucagon receptor family. [Review] [412 refs]. Pharmacol Rev. 2003;55(1):167–94.
3. •• Cryer PE. Glucagon in the pathogenesis of hypoglycemia and hyperglycemia in diabetes. Endocrinology. 2012;153(3):1039–48. This is a comprehensive review on interactions between pancreatic islet alpha-cell glucagon secretion and islet beta-cell insulin secretion. The author argues that in absolute endogenous insulin deficiency (i.e. in type 1 diabetes and in advanced type 2 diabetes), beta-cell failure results in no decrease in beta-cell insulin secretion, and thus no increase in alpha-cell glucagon secretion during hypoglycemia. However, the author also recognizes the increasing evidence that relative hyperglucagonemia, in the setting of deficient insulin secretion, plays a role in the pathogenesis of hyperglycemia in diabetes.
4. Jiang G, Zhang BB. Glucagon and regulation of glucose metabolism. Am J Physiol Endocrinol Metab. 2003;284(4):E671–8.
5. •• Unger RH, Cherrington AD. Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover. J Clin Invest. 2012;122(1):4–12. The primary author is a well-recognized pioneer who advocated for the potential of targeting glucagon and/or GCGRs in the treatment of type 2 diabetes as early as in the 1970s. This is one of best overview articles summarizing the important role of the hormone glucagon in the pathogenesis of type 1 and type 2 diabetes. The authors provide the strong evidence and arguments for targeting glucagon and GCGRs in diabetes, and conclude that glucagon suppression or inactivation may provide therapeutic advantages over insulin monotherapy.
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