Arias G, Asins G, Hegardt F G, Serra D
Department of Biochemistry, School of Pharmacy, University of Barcelona, Spain.
Mol Cell Biochem. 1998 Jan;178(1-2):325-33. doi: 10.1023/a:1006875716407.
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 and enzyme activity of the two genes responsible for regulation of ketogenesis: carnitine palmitoyl transferase I (CPT I) and mitochondrial HMG-CoA synthase. Dexamethasone produced a 2 fold increase in mRNA and activity of CPT I in intestine, but led to a decrease in mit. HMG-CoA synthase. In liver the mRNA levels and activity of both CPT I 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 ketone 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 CPT I in liver or intestine. While mRNA levels for mit. HMG-CoA synthase changed little, the enzyme activity is decreased in both tissues.
通过测定负责生酮调节的两个基因（肉碱棕榈酰转移酶I（CPT I）和线粒体HMG-CoA合酶）的mRNA水平和酶活性，研究了地塞米松注射对12日龄乳鼠肠道和肝脏中生酮作用的影响。地塞米松使肠道中CPT I的mRNA和活性增加了2倍，但导致线粒体HMG-CoA合酶减少。在肝脏中，CPT I和线粒体HMG-CoA合酶的mRNA水平和活性均降低。将这些值与地塞米松处理后两个组织的生酮率进行比较表明，线粒体HMG-CoA合酶可能是负责调节乳鼠生酮作用的主要基因。地塞米松引起的血清酮体变化，其特征与肝脏而非肠道中的生酮率更相似，表明肝脏对乳鼠酮体合成的贡献更大。地塞米松治疗两天对肝脏或肠道中CPT I的mRNA或活性水平没有影响。虽然线粒体HMG-CoA合酶的mRNA水平变化不大，但两个组织中的酶活性均降低。
