Assoc Prof Christopher J Nolan. Author links open the author workspace. FRACP
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Opens the author workspace a. Numbers and letters correspond to the affiliation list. Click to expose these in author workspace Prof Peter Damm. Author links open the author workspace. DMSc b. Numbers and letters correspond to the affiliation list. Click to expose these in author workspace Prof Marc Prentki. Author links open the author workspace. PhD c. Numbers and letters correspond to the affiliation list. Click to expose these in author workspace a Department of Endocrinology, Canberra Hospital and Australian National University Medical School, Canberra, ACT, Australia b Centre for Pregnant Women with Diabetes, Department of Obstetrics, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark c CRCHUM and Montreal Diabetes Research Center and Department of Nutrition and Department of Biochemistry, University of Montreal, QC, Canada
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.
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