Paracrine signaling in islet function and survival

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, ne...

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Bibliographic Details
Published in:Journal of molecular medicine (Berlin, Germany) Germany), 2020-04, Vol.98 (4), p.451-467
Main Authors: Hartig, Sean M., Cox, Aaron R.
Format: Article
Language:English
Subjects:
Beta cells
Biomedical and Life Sciences
Biomedicine
Diabetes
Diabetes mellitus (insulin dependent)
Feeding behavior
Ghrelin
Glucagon
Glucose
Glucose metabolism
Homeostasis
Human Genetics
Insulin
Insulin secretion
Internal Medicine
Molecular Medicine
Pancreas
Paracrine signalling
Review
Somatostatin
Therapeutic applications
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Summary: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.
ISSN:0946-2716
1432-1440
DOI:10.1007/s00109-020-01887-x