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1 Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
2 Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pharmacology, Jilin University, Changchun, Jilin, China
3 Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada
* To whom correspondence should be addressed. E-mail: bnyomba{at}cc.umanitoba.ca.
Rat offspring exposed to ethanol (EtOH-rats) during pregnancy are insulin resistant, but it is unknown if they have increased gluconeogenesis. To address this issue, we determined blood glucose and liver gluconeogenic genes, proteins and enzyme activities before and after insulin administration in juvenile and adult EtOH-rats and submitted adult EtOH-rats to a pyruvate challenge. In juvenile rats, basal glucose, peroxisome proliferator-activated receptor-coactivator (PGC)-1
protein and mRNA, and phosphoenolpyruvate carboxykinase (PEPCK) enzyme activity, protein and mRNA were similar between groups. After insulin injection, these parameters failed to decrease in EtOH-rats, but glucose decreased by 30% and gluconeogenic enzymes, proteins and mRNAs decreased by 50-70% in control rats. In adult offspring, basal PGC-1 protein and mRNA levels were 40-80% higher in EtOH-rats than in controls. Similarly, basal PEPCK activity, protein and mRNA were ~1.8-fold greater in EtOH-rats than in controls. These parameters decreased by ~50% after insulin injection in control rats, but they remained unchanged in EtOH-rats. After insulin injection in the adult rats, glucose decreased by 60% in controls, but did not decrease significantly in EtOH-rats. A subset of adult EtOH-rats had fasting hyperglycemia and an exaggerated glycemic response to pyruvate compared with controls. The data indicate that, after prenatal EtOH exposure, the expression of gluconeogenic genes is exaggerated in adult rat offspring and is insulin resistant in both juvenile and adult rats, explaining increased gluconeogenesis. These alterations persist through adulthood and may contribute to the pathogenesis of type 2 diabetes after exposure to EtOH in utero.
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