The influence of the injection of dexamethasone on ketogenesis in 12 day old suckling rats was studied in intestine and liver by determining mRNA levels anti enzyme activity of the two genes responsible for regulation of ketogenesis: carnitine palmitoyl transferase I (CPTI) and mitochondrial HMG-CoA synthase. Dexamethasone produced a 2 fold increase in mRNA and activity of CPTI in intestine, but led to a decrease in mit. HMG-CoA synthase. In liver the mRNA levels and activity of both CPTI and mit. HMG-CoA synthase decreased. Comparison of these values with the ketogenic rate of both tissues following dexamethasone treatment suggests that mit. HMG-CoA synthase could be the main gene responsible for the regulation of ketogenesis in suckling rats. The changes produced in serum kerone bodies by dexamethasone, with a profile that is more similar to the ketogenic rate in the liver than that in the intestine, indicate that liver contributes more to ketone body synthesis in suckling rats. Two day treatment with dexamethasone produced no change in mRNA or activity levels for CPTI in liver or intestine. While mRNA levels for mit. HMG-CoA synthase changed little, the enzyme activity is decreased in both tissues.
Bibliographical noteFunding Information:
This work was supported by the Grants PB92-0544 and PB95-0012 from the Comisión Interministerial de Ciencia y Tecno-logia, and from the Generalitat de Catalunya. We thank Robin Rycroft from the Language Service for his editorial help.
- Carnitine palmitoyl transferase I
- Mitochondrial HMG-CoA synthase
- Suckling rats