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Hepatic mitochondrial function in lean and obese Zucker rats
The American Journal of Physiology
|September 1, 1983
Summary
Obesity and starvation do not alter mitochondrial fatty acid oxidation or keto acid production capacity in rats. Differences in liver tissue may stem from reduced mitochondrial protein per liver weight in obese rats.
Area of Science:
- Metabolic research
- Mitochondrial biology
- Obesity research
Background:
- Hepatic mitochondrial function is crucial for energy metabolism.
- Obesity and starvation significantly impact metabolic processes.
- Understanding these impacts at the mitochondrial level is key.
Purpose of the Study:
- To investigate hepatic mitochondrial function in lean and obese Zucker rats.
- To assess the effects of starvation on mitochondrial oxidative capacity.
- To determine how obesity and starvation influence fatty acid oxidation and keto acid production.
Main Methods:
- Studied mitochondrial function in fed and starved lean and obese Zucker rats.
- Measured state 3 mitochondrial oxidative rates and palmitoylcarnitine utilization.
- Assessed acetoacetate and citrate production and carnitine palmitoyltransferase activity.
Main Results:
- No significant differences in state 3 mitochondrial oxidative rates due to obesity or starvation.
- Palmitoylcarnitine utilization per milligram mitochondrial protein was equivalent between lean and obese rats.
- Obese rats showed higher overall liver rates but lower rates per gram liver for fatty acid oxidation and keto acid production.
Conclusions:
- Mitochondrial capacity for fatty acid oxidation and keto acid production is unaffected by genetic obesity or starvation.
- Observed differences in whole-organism studies may be due to reduced mitochondrial protein per unit liver weight in obese rats.
- This suggests a normalization of mitochondrial function on a per-protein basis despite obesity.