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Brominated vegetable oil myopathy: inhibition at multiple sites
Abstract:
Skeletal muscle lipid storage was induced by feeding rats brominated vegetable oil (BVO). The defect was examined by measuring radioactive substrate oxidation, intermediates of fatty acid oxidation, and activities of oxidative enzymes. One- and U-[14C] palmitate and 1-[14C] pyruvate oxidation were reduced in muscle after four doses of BVO. Inhibition of U-[14C] palmitate oxidation occurred after two doses. Short chain acylcoenzyme A(CoA) derivatives accumulated in the muscle. Several enzymes of beta-oxidation were significantly reduced, with the greatest reduction in 3-ketoacyl-CoA thiolase. The inhibition probably affected multiple sites of CoA and CoA-derivative metabolism.
Insights
Brominated vegetable oil (BVO) induces skeletal muscle lipid storage in rats. This impairs fatty acid oxidation by reducing key enzymes, affecting energy metabolism.
Area of Science:
- Biochemistry
- Cellular Biology
- Toxicology
Background:
- Skeletal muscle's role in lipid metabolism is crucial for energy homeostasis.
- Understanding the impact of exogenous substances on muscle lipid processing is vital.
Purpose of the Study:
- To investigate the effects of brominated vegetable oil (BVO) on skeletal muscle lipid metabolism in rats.
- To identify specific defects in fatty acid oxidation and related enzyme activities.
Main Methods:
- Rats were fed brominated vegetable oil (BVO) to induce lipid storage.
- Radioactive substrate oxidation (palmitate, pyruvate) and enzyme activities were measured.
- Accumulation of acylcoenzyme A (CoA) derivatives was analyzed.
Main Results:
- BVO administration reduced palmitate and pyruvate oxidation in skeletal muscle.
- Inhibition of palmitate oxidation was observed after two BVO doses.
- Key beta-oxidation enzymes, particularly 3-ketoacyl-CoA thiolase, were significantly reduced.
- Short-chain acyl-CoA derivatives accumulated in muscle tissue.
Conclusions:
- Brominated vegetable oil (BVO) disrupts skeletal muscle lipid metabolism.
- The observed defects likely result from impaired fatty acid oxidation due to reduced enzyme activity.
- These disruptions may affect multiple sites within CoA and CoA-derivative metabolism.