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Molecular Pathways Underlying the Pathogenesis of Pancreatic α-Cell Dysfunction

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The Islets of Langerhans

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 654))

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.

Dan Kawamori and Hannah J. Welters contributed equally to this work.

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Acknowledgments

We thank Lindsay Huse for excellent assistance with preparation of this chapter. We especially acknowledge the valued and continued support of Cathy and Stan Bernstein for research work in the Kulkarni lab. D.K. is the recipient of a Research Fellowship (Manpei Suzuki Diabetes Foundation, Japan) and a JDRF Postdoctoral Fellowship. H.J.W is the recipient of a fellowship grant from Astra-Zeneca. The authors acknowledge support from the American Diabetes Association Research Grant (R.N.K.) and National Institutes of Health (R.N.K.).

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Kawamori, D., Welters, H.J., Kulkarni, R.N. (2010). Molecular Pathways Underlying the Pathogenesis of Pancreatic α-Cell Dysfunction. In: Islam, M. (eds) The Islets of Langerhans. Advances in Experimental Medicine and Biology, vol 654. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-3271-3_18

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