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Paracrine signaling in islet function and survival

Authors
  • Hartig, Sean M.1, 1
  • Cox, Aaron R.1
  • 1 Baylor College of Medicine, Houston, TX, 77030, USA , Houston (United States)
Type
Published Article
Journal
Journal of Molecular Medicine
Publisher
Springer-Verlag
Publication Date
Feb 17, 2020
Volume
98
Issue
4
Pages
451–467
Identifiers
DOI: 10.1007/s00109-020-01887-x
Source
Springer Nature
Keywords
License
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Abstract

The pancreatic islet is a dense cellular network comprised of several cell types with endocrine function vital in the control of glucose homeostasis, metabolism, and feeding behavior. Within the islet, endocrine hormones also form an intricate paracrine network with supportive cells (endothelial, neuronal, immune) and secondary signaling molecules regulating cellular function and survival. Modulation of these signals has potential consequences for diabetes development, progression, and therapeutic intervention. Beta cell loss, reduced endogenous insulin secretion, and dysregulated glucagon secretion are hallmark features of both type 1 and 2 diabetes that not only impact systemic regulation of glucose, but also contribute to the function and survival of cells within the islet. Advancing research and technology have revealed new islet biology (cellular identity and transcriptomes) and identified previously unrecognized paracrine signals and mechanisms (somatostatin and ghrelin paracrine actions), while shifting prior views of intraislet communication. This review will summarize the paracrine signals regulating islet endocrine function and survival, the disruption and dysfunction that occur in diabetes, and potential therapeutic targets to preserve beta cell mass and function.

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