Paracrine signaling in islet function and survival.


Journal

Journal of molecular medicine (Berlin, Germany)
ISSN: 1432-1440
Titre abrégé: J Mol Med (Berl)
Pays: Germany
ID NLM: 9504370

Informations de publication

Date de publication:
04 2020
Historique:
received: 20 08 2019
accepted: 11 02 2020
revised: 05 02 2020
pubmed: 19 2 2020
medline: 16 6 2021
entrez: 19 2 2020
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 32067063
doi: 10.1007/s00109-020-01887-x
pii: 10.1007/s00109-020-01887-x
pmc: PMC7899133
mid: NIHMS1571236
doi:

Substances chimiques

Ghrelin 0
Insulin 0
Somatostatin 51110-01-1
Pancreatic Polypeptide 59763-91-6
Glycogen 9005-79-2
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

451-467

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK114356
Pays : United States

Commentaires et corrections

Type : ErratumIn

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Auteurs

Sean M Hartig (SM)

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, 77030, USA.
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, 77030, USA.

Aaron R Cox (AR)

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, TX, 77030, USA. racox@bcm.edu.

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