Regulation of nutrient uptake by AMP-activated protein kinase

Alghamdi, F., Alshuweishi, Y. and Salt, I. P. (2020) Regulation of nutrient uptake by AMP-activated protein kinase. Cellular Signalling, 76, 109807. (doi: 10.1016/j.cellsig.2020.109807) (PMID:33038517)

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Abstract

AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that is a key regulator of energy balance at both the cellular and whole-body level. AMPK acts to stimulate ATP production and reduce ATP consumption when cellular ATP levels fall, thereby normalizing energy balance. Given the central role of AMPK in cellular carbohydrate and lipid metabolism, AMPK activation has been proposed to be a therapeutic target for conditions associated with dysfunctional nutrient metabolism including obesity, type 2 diabetes, hepatic steatosis, cardiovascular diseases and cancer. One way by which increased ATP production can be achieved is by increasing the supply of nutrient substrates. In the 1990s, AMPK activation was demonstrated to stimulate glucose uptake in striated muscle, thereby improving substrate supply for ATP production. Subsequently AMPK activation was postulated to underlie the increase in glucose uptake that occurs during muscle contraction. More recently, however, several lines of evidence have demonstrated that AMPK activation is unlikely to be required for contraction-mediated glucose uptake. Furthermore, despite the importance of AMPK in cellular and whole-body metabolism, far fewer studies have investigated either the role of AMPK in glucose uptake by non-muscle tissues or whether AMPK regulates the uptake of fatty acids. In the present review, we discuss the role of AMPK in nutrient uptake by tissues, focusing on glucose uptake out with muscle and fatty acid uptake.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Alghamdi, Fatmah and Salt, Dr Ian and Alshuweishi, Yazeed Abdullah I
Authors: Alghamdi, F., Alshuweishi, Y., and Salt, I. P.
College/School:College of Medical Veterinary and Life Sciences > School of Cardiovascular & Metabolic Health
College of Medical Veterinary and Life Sciences > School of Molecular Biosciences
Journal Name:Cellular Signalling
Publisher:Elsevier
ISSN:0898-6568
ISSN (Online):1873-3913
Published Online:08 October 2020
Copyright Holders:Copyright © 2020 Elsevier Inc.
First Published:First published in Cellular Signalling 76: 109807
Publisher Policy:Reproduced in accordance with the publisher copyright policy

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
166238Inhibition of vascular Stat Signalling by Amp-Activated Protein Kinase (AMPK).Timothy PalmerBritish Heart Foundation (BHF)PG/12/29276Institute of Cardiovascular & Medical Sciences
169547Inhibition of endothelial mitogen-activated protein kinases by amp-activated protein kinaseIan SaltBritish Heart Foundation (BHF)PG/13/82/30483Institute of Cardiovascular & Medical Sciences
190192The role of AMP-activated protein kinase in adipocyte glucose transport and insulin signallingIan SaltDiabetes UK (DIABETUK)09/0003904Institute of Cardiovascular & Medical Sciences
166848Mechanisms underlying the regulation of endothelial nitric oxide synthesis by glucose and insulin.Ian SaltDiabetes UK (DIABETUK)12/0004489Institute of Cardiovascular & Medical Sciences