Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences

Philip Newsholme; Jordan Rowlands; Roselyn Rose'Meyer; Vinicius Cruzat

doi:10.3390/antiox11010108

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Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences

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Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences

Philip Newsholme, Jordan Rowlands, Roselyn Rose'Meyer and Vinicius Cruzat

Antioxidants, Vol.11(1), pp.1-18

04/01/2022

DOI: https://doi.org/10.3390/antiox11010108

PMID: 35052612

Appears in Recent Faculty of Health Publications

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Abstract

Biochemistry & Molecular Biology

Chemistry, Medicinal

Food Science & Technology

Life Sciences & Biomedicine

Pharmacology & Pharmacy

Science & Technology

insulin

metabolic reprogramming

antidiabetic therapeutics

glucose metabolism

lipid metabolism

islet inflammation

Irreversible pancreatic beta-cell damage may be a result of chronic exposure to supraphysiological glucose or lipid concentrations or chronic exposure to therapeutic anti-diabetic drugs. The beta-cells are able to respond to blood glucose in a narrow concentration range and release insulin in response, following activation of metabolic pathways such as glycolysis and the TCA cycle. The beta-cell cannot protect itself from glucose toxicity by blocking glucose uptake, but indeed relies on alternative metabolic protection mechanisms to avoid dysfunction and death. Alteration of normal metabolic pathway function occurs as a counter regulatory response to high nutrient, inflammatory factor, hormone or therapeutic drug concentrations. Metabolic reprogramming is a term widely used to describe a change in regulation of various metabolic enzymes and transporters, usually associated with cell growth and proliferation and may involve reshaping epigenetic responses, in particular the acetylation and methylation of histone proteins and DNA. Other metabolic modifications such as Malonylation, Succinylation, Hydroxybutyrylation, ADP-ribosylation, and Lactylation, may impact regulatory processes, many of which need to be investigated in detail to contribute to current advances in metabolism. By describing multiple mechanisms of metabolic adaption that are available to the beta-cell across its lifespan, we hope to identify sites for metabolic reprogramming mechanisms, most of which are incompletely described or understood. Many of these mechanisms are related to prominent antioxidant responses. Here, we have attempted to describe the key beta-cell metabolic adaptions and changes which are required for survival and function in various physiological, pathological and pharmacological conditions.

Details

Title: Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences
Creators: Philip Newsholme - Curtin Univ, Curtin Med Sch, Perth, WA 6845, Australia
Jordan Rowlands - Curtin University
Roselyn Rose'Meyer - Griffith Univ, Sch Pharm & Med Sci, Gold Coast, Qld 4222, Australia
Vinicius Cruzat - Torrens University Australia
Publication Details: Antioxidants, Vol.11(1), pp.1-18
Publisher: Mdpi
Number of pages: 18
Grant note: Curtin Medical School and The Curtin Health Innovation Research Institute School of Pharmacy and Medical Sciences, Griffith University Torrens University Faculty of Health Sciences
Identifiers: 991013072491102368
Copyright: (c) 2022 by the Authors. 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/).
Academic Unit: Faculty of Health
Language: English
Resource Type: Journal article

Metabolic Adaptions/Reprogramming in Islet Beta-Cells in Response to Physiological Stimulators-What Are the Consequences

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