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Factors influencing glucose homeostasis in a rat model with mutated ATP synthase Open Access


Other title
mitochondrial diabetes
glucose tolerance
Type of item
Degree grantor
University of Alberta
Author or creator
Harasym, Anne C.
Supervisor and department
Chan, Catherine B. (Agricultural, Food, & Nutritional Sciences/ Physiology)
Wright, David C. (Human Health & Nutritional Sciences, University of Guelph)
Examining committee member and department
Cheeseman, Chris (Physiology)
Farmer, Anna (Agricultural, Food, & Nutritional Sciences)
Department of Agricultural, Food, and Nutritional Science
Nutrition & Metabolism
Date accepted
Graduation date
Master of Science
Degree level
This study examined glucose homeostasis mechanisms involved in the BHE/cdb rat model of mitochondrial diabetes with a mutated Fo subunit of ATP synthase. Twenty-one-week old male BHE/cdb rats exhibited enhanced glucose tolerance despite impaired insulin secretion. Whole body in vivo characterization showed that BHE/cdb rats had enhanced insulin sensitivity compared to controls, along with moderately increased (p<0.01) respiratory exchange ratios, oxygen consumption, carbon dioxide production and heat production, despite similar relative body composition, physical activity, food and water consumption. In vitro markers of insulin-dependent and insulin-independent signaling pathways were similar in BHE/cdb rats and controls. Phosphoenolpyruvate carboxykinase expression in liver (p<0.05), liver glycogen storage (p<0.05), and epitrochlearis muscle glycogen (p<0.01) were increased in BHE/cdb rats. Additionally, in vivo pyruvate-stimulated gluconeogenesis was attenuated in BHE/cdb rats (p<0.01). Results indicate that increased glucose oxidation, increased thermogenesis, and reduced hepatic glucose output mediate glucose tolerance in the BHE/cdb model.
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