Journal article
Nutrient Regulation of Pancreatic Islet beta-Cell Secretory Capacity and Insulin Production
Biomolecules (Basel, Switzerland), Vol.12(2), p.335
02/01/2022
DOI: 10.3390/biom12020335
PMCID: PMC8869698
PMID: 35204835
Abstract
Pancreatic islet beta-cells exhibit tremendous plasticity for secretory adaptations that coordinate insulin production and release with nutritional demands. This essential feature of the beta-cell can allow for compensatory changes that increase secretory output to overcome insulin resistance early in Type 2 diabetes (T2D). Nutrient-stimulated increases in proinsulin biosynthesis may initiate this beta-cell adaptive compensation; however, the molecular regulators of secretory expansion that accommodate the increased biosynthetic burden of packaging and producing additional insulin granules, such as enhanced ER and Golgi functions, remain poorly defined. As these adaptive mechanisms fail and T2D progresses, the beta-cell succumbs to metabolic defects resulting in alterations to glucose metabolism and a decline in nutrient-regulated secretory functions, including impaired proinsulin processing and a deficit in mature insulin-containing secretory granules. In this review, we will discuss how the adaptative plasticity of the pancreatic islet beta-cell's secretory program allows insulin production to be carefully matched with nutrient availability and peripheral cues for insulin signaling. Furthermore, we will highlight potential defects in the secretory pathway that limit or delay insulin granule biosynthesis, which may contribute to the decline in beta-cell function during the pathogenesis of T2D.
Details
- Title: Subtitle
- Nutrient Regulation of Pancreatic Islet beta-Cell Secretory Capacity and Insulin Production
- Creators
- Kristen E. Rohli - University of IowaCierra K. Boyer - University of IowaSandra E. Blom - University of IowaSamuel B. Stephens - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Biomolecules (Basel, Switzerland), Vol.12(2), p.335
- DOI
- 10.3390/biom12020335
- PMID
- 35204835
- PMCID
- PMC8869698
- NLM abbreviation
- Biomolecules
- ISSN
- 2218-273X
- eISSN
- 2218-273X
- Publisher
- Mdpi
- Number of pages
- 24
- Grant note
- DOI: 10.13039/100000005, name: United States Department of Defense, award: PR190353; DOI: 10.13039/100000002, name: National Institutes of Health, award: T32GM008629
- Language
- English
- Date published
- 02/01/2022
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984360045102771
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