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School of Biological Sciences

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Substrate-level control of glucose metabolism in C2C12 myotubes

2016-03-30 , Hsu, Chia

Metabolic flexibility is critical for muscle to maintain proper function and overall health. Muscle adapts to metabolic stress with increasing ATP synthesis by enhancing the rate of glycolysis and mitochondrial respiration. The control of that rate is mediated by several glucose metabolites. This project is based on the conceptual model that AMP indicates the balance of ATP synthesis and degradation, and NADH indicates the balance of glucose delivery to oxygen delivery. AMP signaling facilitates all aspects of glucose metabolism, and NAD+ signaling facilitates oxidative metabolism and inhibits reductive metabolism. The overall hypothesis is that the distribution of glucose depends on AMP and NAD+ generated during energetic stress. The results suggest that glucose metabolism is highly sensitive to ATP homeostasis via AMPK activity. NADH oxidation alone is not sufficient to influence glucose oxidation, but require co-activation of AMPK. AMP and NAD+ signaling work independently in metabolic gene expression. The overall conclusion is that glucose metabolism depends on AMP signaling, but NAD signaling is unable to alter glucose disposal. AMP and NAD independently induced metabolic and differentiation adaptation. These findings suggest that other molecule may represent an additional gauge of aerobic and anaerobic metabolism.

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Mechanical and metabolic stresses contribute to high force contraction signaling

2012-03-27 , Rahnert, Jill Anne

Force production by a muscle is critical to maintaining proper function and overall health of a human or animal. Muscle adapts to increased loading with hypertrophy by activating a number of intracellular signaling cascades that regulate protein synthesis. The overall hypothesis is that force-dependent processes acutely activate growth-related signaling during active force generation. This project took two approaches. The first employed a general survey of muscles in which age-dependent changes in muscle activity differed. No conclusive activity-dependent signaling emerged however coordinated signaling among kinases broke down with age. The second approach utilized an in situ muscle preparation in which force production or metabolic costs were specifically controlled. Similar sub-maximal force levels generated by different methods found that force, per se, is not a primary modulator of growth-related signaling but that ERK phosphorylation is dependent on fiber-activation. Prolonging the duration of electrical stimulation applied to the nerve or increasing the frequency at which stimulations are applied was expected to increase the metabolic stress associated with contraction. Several growth-related kinases correlated with markers of metabolic stress, i.e. increased AMPK activity and decreased glycogen content, which were decoupled from force decline. This suggests energy depletion, specific to stimulation pattern, strongly influences the immediate response to high force contraction signaling. The overall conclusion is that signaling molecules previously implicated in force-dependent signaling lie much too downstream to relay strict force-dependent signaling.

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