Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 124, Issue 2, Pages 139-148Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/13813455.2017.1369549
Keywords
Combined oral contraceptives; glycogen synthase kinase-3; insulin resistance; nicotine; pancreatic beta-cell function
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Context: Cigarette smoking is considered to be a major risk factor for the development of diabetes and cardiovascular disease. Oestrogen-progestin combined oral contraceptive (COC) use has been associated with adverse cardiometabolic events. Objective: We hypothesized that nicotine would ameliorate insulin resistance (IR) that is accompanied by decreased cardiac glycogen synthase kinase-3 (GSK-3) and plasminogen activator inhibitor-1 (PAI-1). Methods: Female Wistar rats received (po) low-(0.1 mg/kg) or high-nicotine (1.0 mg/kg) with or without COC containing 5.0 mu g levonorgestrel plus 1.0 mu g ethinylestradiol daily for 8 weeks. Results: Data showed that COC treatment or nicotine exposure led to IR, glucose deregulation, atherogenic dyslipidemia, increased corticosterone, aldosterone, cardiac and circulating GSK-3 values and PAI-1. However, these effects with the exception of corticosterone and aldosterone were ameliorated in COC + nicotine-exposed rats. Conclusion: Amelioration of IR induced by COC treatment is accompanied by decreased circulating PAI-1, cardiac PAI-1 and GSK-3 instead of circulating aldosterone and corticosterone.
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