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Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production

Pancreatic islet β-cells exhibit tremendous plasticity for secretory adaptations that coordinate insulin production and release with nutritional demands. This essential feature of the β-cell can allow for compensatory changes that increase secretory output to overcome insulin resistance early in Typ...

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Autores principales: Rohli, Kristen E., Boyer, Cierra K., Blom, Sandra E., Stephens, Samuel B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8869698/
https://www.ncbi.nlm.nih.gov/pubmed/35204835
http://dx.doi.org/10.3390/biom12020335
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author Rohli, Kristen E.
Boyer, Cierra K.
Blom, Sandra E.
Stephens, Samuel B.
author_facet Rohli, Kristen E.
Boyer, Cierra K.
Blom, Sandra E.
Stephens, Samuel B.
author_sort Rohli, Kristen E.
collection PubMed
description Pancreatic islet β-cells exhibit tremendous plasticity for secretory adaptations that coordinate insulin production and release with nutritional demands. This essential feature of the β-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 β-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 β-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 β-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 β-cell function during the pathogenesis of T2D.
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spelling pubmed-88696982022-02-25 Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production Rohli, Kristen E. Boyer, Cierra K. Blom, Sandra E. Stephens, Samuel B. Biomolecules Review Pancreatic islet β-cells exhibit tremendous plasticity for secretory adaptations that coordinate insulin production and release with nutritional demands. This essential feature of the β-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 β-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 β-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 β-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 β-cell function during the pathogenesis of T2D. MDPI 2022-02-20 /pmc/articles/PMC8869698/ /pubmed/35204835 http://dx.doi.org/10.3390/biom12020335 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Rohli, Kristen E.
Boyer, Cierra K.
Blom, Sandra E.
Stephens, Samuel B.
Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title_full Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title_fullStr Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title_full_unstemmed Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title_short Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production
title_sort nutrient regulation of pancreatic islet β-cell secretory capacity and insulin production
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8869698/
https://www.ncbi.nlm.nih.gov/pubmed/35204835
http://dx.doi.org/10.3390/biom12020335
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