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