Title page for ETD etd-06072011-165413


Type of Document Dissertation
Author Russell, Ryan Damion
URN etd-06072011-165413
Title Examination of Metabolism in Diabetic Offspring
Degree Doctor of Philosophy (Ph.D.)
Department Kinesiology
Advisory Committee
Advisor Name Title
Nelson, Arnold Committee Chair
Hondzinski, Jan Committee Member
Kraemer, Robert Committee Member
Reeve, T. Gilmour Committee Member
Constant, David Dean's Representative
Keywords
  • metabolic flexibility
  • lipotoxicity
  • diabetic offspring
  • diabetes metabolism
Date of Defense 2011-04-06
Availability unrestricted
Abstract
The purpose of this study was to categorize aberrant metabolic function in diabetic offspring (FH+). This study examined metabolic flexibility (MF), and changes in fasting blood-glucose concentrations and markers of lipotoxicity with resistance training in college age FH+ and FH-. Results are significant at p = 0.05. MF testing indicate no baseline differences in RMR, VO2, REE, fat or CHO use were noted between T2D, FH+, or FH-. Passive stretching caused increased metabolism overall, however the T2D group temporarily displayed increased CHO use during passive stretching, which quickly returned to pre-stretched levels during recovery as compared with FH-. Both T2D and FH+ display impaired MF as compared with FH- via indirect calorimetry as noted by the change in RER. With training, changes in glucose: lactate ratios were no different between groups, but increased immediately after exercise with training, and decreased at five and ten minutes post-exercise with training. Lastly, there were no differences between FH- and FH+ in pre-training strength, BMI, or in markers measured in plasma before or after exercise. Strength increased from pre to post training similarly. However, changes in NEFA and insulin were noted in weight loss subjects vs non-weight loss. Negative correlations exist between weight loss and: TG, NEFA, insulin and HOMA, and strength, and positive correlations with blood glucose AUC.

Though there are differences metabolic flexibility and recovery kinetics between groups with and without a family history of diabetes, this study does not reveal any such differences in glucoregulatory function, or markers of lipotoxicity. Resistance training did not affect FH+ differently than FH-, however there were differences in these markers when groups were re-categorized by weight loss. We were unable to isolate specific factors likely to contribute to the development of IR or T2D within the confines of the current study. However, further research, such as lipid tracers and MRI studies are needed to determine factors leading to more aberrant metabolic function in order to better understand what factors lead to the development of IR and T2D.

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