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High dietary fat selectively increases catalase expression within cardiac mitochondria
Paul M Rindler1, Scott M Plafker, Luke I Szweda
1Free Radical Biology and Aging Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
The Journal of Biological Chemistry
|December 4, 2012
Summary
Obesity and fasting increase the antioxidant enzyme catalase in heart mitochondria. This catalase upregulation helps manage oxidative stress from increased fat metabolism, suggesting a key metabolic regulatory process.
Area of Science:
- Biochemistry
- Metabolic research
- Cardiovascular science
Background:
- Obesity is linked to diabetes and cardiovascular disease, often involving dyslipidemia and high triglycerides.
- Oxidative stress from lipid utilization is implicated in these diseases.
- The antioxidant enzyme network's response to high fat utilization is not well understood.
Purpose of the Study:
- To investigate the response of antioxidant enzymes in heart tissue to diet-induced obesity.
- To determine the role and localization of catalase during high fat utilization.
- To examine if catalase upregulation is a conserved response to conditions increasing lipid oxidation.
Main Methods:
- Utilized a multiplexed quantitative proteomics method to measure antioxidant enzyme expression in mouse heart tissue.
- Assessed catalase protein, activity, and mRNA levels.
- Compared antioxidant expression in diet-induced obese mice and fasted mice.
Main Results:
- Diet-induced obesity rapidly and specifically upregulated catalase protein, activity, and mRNA in heart tissue.
- Catalase was found in cardiac mitochondria, with increased content and activity during high fat feeding.
- A similar specific catalase increase was observed in mice fasted for 24 hours.
Conclusions:
- Increased catalase in cardiac mitochondria helps consume excess hydrogen peroxide (H2O2) produced by increased fat metabolism.
- Catalase expression is regulated to prevent damage while sensing diet composition via H2O2.
- This process may adjust insulin sensitivity to prioritize lipid metabolism for complete utilization.