Journal
DIABETES OBESITY & METABOLISM
Volume 10, Issue 9, Pages 763-771Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1463-1326.2007.00808.x
Keywords
beta-cell apoptosis; beta-cell mass; glucose homeostasis; nicotine; rosiglitazone; type 2 diabetes
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Funding
- GlaxoSmithKline
- Population Health Institute Chair in Diabetes Research (sponsored by Aventis)
- Canadian Institutes of Health Research (CIHR) Strategic Training Program
- Ontario Graduate Scholarship
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Aim: Interventions that preserve or increase beta-cell mass may also prevent type 2 diabetes. Rosiglitazone prevents diabetes in people with high glucose levels who have impaired glucose tolerance and/or impaired fasting glucose. The effect of this drug on both glucose levels and beta-cell mass was studied in a rat model of diabetes, characterized by reduced beta-cell mass at birth with normoglycaemia, and progression to dysglycaemia with age. Methods:Female Wistar rats were given either saline (vehicle) or nicotine during pregnancy and lactation. Offspring of saline-exposed dams were given vehicle and offspring of nicotine-exposed dams were randomized to receive either vehicle or rosiglitazone starting at weaning. Beta-cell mass, proliferation and apoptosis were determined at birth and at 4 and 26 weeks of age. Glucose homeostasis was examined following sequential oral glucose tolerance tests (OGTT). Results: Rosiglitazone treatment prevented the development of dysglycaemia in nicotine-exposed animals. The ability of rosiglitazone to preserve normoglycaemia appeared to be because of its ability to increase beta-cell mass through a combination of enhanced beta-cell proliferation and decreased beta-cell apoptosis. Conclusions: These results suggest that if rosiglitazone administration is started prior to the onset of glucometabolic abnormalities, it prevents the onset of dysglycaemia by partially restoring beta-cell mass in animals with reduced beta-cell mass at birth.
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