Insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift

dc.contributor.authorNolan, Christopher
dc.contributor.authorPrentki, Marc
dc.date.accessioned2020-01-02T22:55:26Z
dc.date.issued2019
dc.date.updated2019-08-04T08:22:51Z
dc.description.abstractWhile few dispute the existence of the metabolic syndrome as a clustering of factors indicative of poor metabolic health, its utility above that of its individual components in the clinical care of individual patients is questioned. This is likely a consequence of the failure of clinicians and scientists to agree on a unifying mechanism to explain the metabolic syndrome. Insulin resistance has most commonly been proposed for this role and is generally considered to be a root causative factor for not only metabolic syndrome but also for its associated conditions of non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), obesity-related type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). An alternative view, for which evidence is mounting, is that hyper-responsiveness of islet β-cells to a hostile environment, such as westernised lifestyle, is primary and that the resulting hyperinsulinaemia drives the other components of the metabolic syndrome. Importantly, within this new conceptual framework, insulin resistance, while always a biomarker and state of poor metabolic health, is not considered to be harmful, but a protective adaptive response of critical tissues including the myocardium against insulin-induced metabolic stress. This major shift in how metabolic syndrome can be considered puts insulin hypersecretion into position as the unifying mechanism. If shown to be correct, this new conceptual framework has major implications for the future prevention and management of the metabolic syndrome, including its associated conditions of NAFLD, PCOS, obesity-related T2D and ASCVD.en_AU
dc.description.sponsorshipThis work was supported in part by grants from the Canadian Institutes of Health Research (M.P.) and the National Health and Medical Research Council [project grant 1128442 (C.J.N.)].en_AU
dc.format.mimetypeapplication/pdfen_AU
dc.identifier.issn1479-1641en_AU
dc.identifier.urihttp://hdl.handle.net/1885/196471
dc.language.isoen_AUen_AU
dc.provenancehttp://sherpa.ac.uk/romeo/issn/1479-1641/..."Author's post-print on author's personal website, departmental website, institutional website, institutional repository or other repositories, including PubMed Central" from SHERPA/RoMEO site (as at 17/01/2020).
dc.publisherSAGE Publicationsen_AU
dc.relationhttp://purl.org/au-research/grants/nhmrc/1128442en_AU
dc.rights© The Author(s) 2019en_AU
dc.sourceDiabetes and Vascular Disease Researchen_AU
dc.titleInsulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shiften_AU
dc.typeJournal articleen_AU
dcterms.accessRightsOpen Access
local.bibliographicCitation.issue2en_AU
local.bibliographicCitation.lastpage127en_AU
local.bibliographicCitation.startpage118en_AU
local.contributor.affiliationNolan, Christopher, College of Health and Medicine, ANUen_AU
local.contributor.affiliationPrentki, Marc, University of Montrealen_AU
local.contributor.authoremailrepository.admin@anu.edu.auen_AU
local.contributor.authoruidNolan, Christopher, u1820721en_AU
local.description.notesImported from ARIESen_AU
local.identifier.absfor110306 - Endocrinologyen_AU
local.identifier.absfor110201 - Cardiology (incl. Cardiovascular Diseases)en_AU
local.identifier.absseo920103 - Cardiovascular System and Diseasesen_AU
local.identifier.absseo920104 - Diabetesen_AU
local.identifier.ariespublicationu5786633xPUB768en_AU
local.identifier.citationvolume16en_AU
local.identifier.doi10.1177/1479164119827611en_AU
local.identifier.scopusID2-s2.0-85061820096
local.identifier.uidSubmittedByu5786633en_AU
local.publisher.urlhttps://uk.sagepub.com/en-gb/eur/homeen_AU
local.type.statusAccepted Versionen_AU

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