Type 2 diabetes across generations: from pathophysiology to prevention and management
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Nolan, Christopher; Damm, Peter; Prentki, Marc
Description
Type 2 diabetes is now a pandemic and shows no signs of abatement. In this Seminar we review the pathophysiology of this disorder, with particular attention to epidemiology, genetics, epigenetics, and molecular cell biology. Evidence is emerging that a substantial part of diabetes susceptibility is acquired early in life, probably owing to fetal or neonatal programming via epigenetic phenomena. Maternal and early childhood health might, therefore, be crucial to the development of effective...[Show more]
dc.contributor.author | Nolan, Christopher | |
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dc.contributor.author | Damm, Peter | |
dc.contributor.author | Prentki, Marc | |
dc.date.accessioned | 2015-12-08T22:20:37Z | |
dc.identifier.issn | 0140-6736 | |
dc.identifier.uri | http://hdl.handle.net/1885/32072 | |
dc.description.abstract | Type 2 diabetes is now a pandemic and shows no signs of abatement. In this Seminar we review the pathophysiology of this disorder, with particular attention to epidemiology, genetics, epigenetics, and molecular cell biology. Evidence is emerging that a substantial part of diabetes susceptibility is acquired early in life, probably owing to fetal or neonatal programming via epigenetic phenomena. Maternal and early childhood health might, therefore, be crucial to the development of effective prevention strategies. Diabetes develops because of inadequate islet β-cell and adipose-tissue responses to chronic fuel excess, which results in so-called nutrient spillover, insulin resistance, and metabolic stress. The latter damages multiple organs. Insulin resistance, while forcing β cells to work harder, might also have an important defensive role against nutrient-related toxic effects in tissues such as the heart. Reversal of overnutrition, healing of the β cells, and lessening of adipose tissue defects should be treatment priorities. | |
dc.publisher | Lancet Publishing Group | |
dc.source | Lancet, The (UK edition) | |
dc.subject | Keywords: 2,4 thiazolidinedione derivative; cyclin dependent kinase inhibitor 2A; cyclin dependent kinase inhibitor 2B; folic acid; glucagon like peptide 1; glucose; glucose transporter 2; hemoglobin A1c; hepatocyte nuclear factor 1beta; incretin; insulin receptor | |
dc.title | Type 2 diabetes across generations: from pathophysiology to prevention and management | |
dc.type | Journal article | |
local.description.notes | Imported from ARIES | |
local.identifier.citationvolume | 378 | |
dc.date.issued | 2011 | |
local.identifier.absfor | 110306 - Endocrinology | |
local.identifier.ariespublication | u4971216xPUB88 | |
local.type.status | Published Version | |
local.contributor.affiliation | Nolan, Christopher, College of Medicine, Biology and Environment, ANU | |
local.contributor.affiliation | Damm, Peter, University of Copenhagen | |
local.contributor.affiliation | Prentki, Marc, University of Montreal | |
local.description.embargo | 2037-12-31 | |
local.bibliographicCitation.issue | 9786 | |
local.bibliographicCitation.startpage | 169 | |
local.bibliographicCitation.lastpage | 181 | |
local.identifier.doi | 10.1016/S0140-6736(11)60614-4 | |
local.identifier.absseo | 970111 - Expanding Knowledge in the Medical and Health Sciences | |
dc.date.updated | 2016-02-24T11:32:15Z | |
local.identifier.scopusID | 2-s2.0-79960202841 | |
Collections | ANU Research Publications |
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