Detail of "9012-31-1"

Reference

Coordinate repression of cholesterol biosynthesis and cytoplasmic 3-hydroxy-3-methylglutaryl coenzyme A synthase by glucocorticoids in HeLa cells

Coordinate repression of cholesterol biosynthesis and cytoplasmic 3-hydroxy-3-methylglutaryl coenzyme A synthase by glucocorticoids in HeLa cells. Ramachandran, Chittoor K.; Gray, Susan L.; Melnykovych, George (Dep. Microbiol., Univ. Kansas Med. Cent., Kansas City, Kans., USA). Arch. Biochem. Biophys., 189(1), 205-11 (English) 1978. CODEN: ABBIA4. ISSN: 0003-9861. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) The increase in cholesterol (I) [57-88-5] synthesis from acetate after serum removal from the medium was partially suppressed by dexamethasone (II) [50-02-2]. However, this suppression was not accompanied by an expected decrease in activity of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase (EC 1.1.1.34) [9028-35-7] the enzyme identified as the rate-limiting step in the biosynthetic sequence from acetate to I. Instead, HMG-CoA reductase activity became higher in response to II treatment. I-induced inhibition of sterol synthesis was not accompanied by any significant alteration in fatty acid synthesis. Acetyl-CoA synthetase (EC 6.2.1.1) [9012-31-1] and cytosolic acetoacetyl-CoA thiolase (EC 2.3.1.9) [9027-46-7] activities were also unchanged. In contrast, activity of cytosolic 3-hydroxy-3-methylglutaryl CoA-synthase (EC 4.1.3.5) [9027-44-5] decreased in parallel to the inhibition of sterol synthesis by II. A concn.-dependent inhibition of this enzyme by II and a correlation with the 11b,1ma,21-trihydroxy structure of C21 steroids were demonstrated. These results suggest that HMG-CoA synthase is controlling the rate of cholesterogenesis when I synthesis is partially suppressed by glucocorticoids.

Effect of prolonged ethanol ingestion on hepatic lipogenesis and related enzyme activities

Effect of prolonged ethanol ingestion on hepatic lipogenesis and related enzyme activities. Savolainen, Markku J.; Hiltunen, J. Kalervo; Hassinen, Ilmo E. (Dep. Med. Biochem., Univ. Oulu, Oulu, Finland). Biochem. J., 164(1), 169-77 (English) 1977. CODEN: BIJOAK. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) In rats fed for 21 days on low-, medium-, and high-fat liq. diets contg. EtOH [64-17-5] (36% of total energy of diet), the rate of hepatic fatty acid synthesis was slower than in rats fed corresponding diets contg. carbohydrate instead of EtOH; when the fat/carbohydrate ratio was kept the same in EtOH-fed and control rats, EtOH ingestion did not affect the rate of fatty acid synthesis. Hepatic glucose 6-phosphate dehydrogenase (EC 1.1.1.49) [9001-40-5] activity was lower in EtOH-fed rats; malic enzyme (EC 1.1.1.40) [9028-47-1] activity was not affected by EtOH ingestion if the fat/carbohydrate ratio was kept unchanged. ATP citrate lyase (EC 4.1.3.8) [9027-95-6] and acetyl-CoA synthetase (EC 6.2.1.1) [9012-31-1] activities in the liver were decreased in EtOH-fed rats on all diets. The hepatic concn. of the active form of pyruvate dehydrogenase (EC 1.2.4.1) [9014-20-4] was lower in EtOH-fed rats. Thus, hepatic fatty acid synthesis does not play a major role in EtOH-induced triacylglycerol accumulation.