Role of Hepatic L- -Glycerophosphate and Triglyceride Synthesis in Production of Fatty Liver by Ethanol.

Abstract

4). In the uterus of the rat glycogen synthesis is catalyzed by phosphorylase from G-1-P and not through the UDPG pathway. Since the morphology and physiology of smooth muscle and skeletal muscle are not the same the difference in the metabolic pathway for synthesis of glycogen is not surprising. It is possible that smooth muscle cells of organs that are not stimulated by ovarian hormones can behave in a different way from the smooth muscle cells of the uterus.Summary. UDPG-glycogen synthetase was not demonstrated in the uterus of the ovariectomized or in the ovariectomized-hormone treated rats. However, in the tongue the enzyme was present. The results show that glycogen of the rat uterus is not synthesized through the UDPG pathway. The results also demonstrate a difference in glycogen synthesis between the smooth muscle of the uterus and skeletal muscle of the tongue.The authors are grateful to Dr. Warren N. Dannenburg, Dept. of Obstetrics and Gynecology Research, for helpful discussions during the investigation.1. Stetten, D., Stetten, M., Physiol. Rev., 1960, v40, 505.

Multiple biochemical effects in the pathogenesis of alcoholic fatty liver

“…In the liver, the actions of alcohol dehydrogenase followed by aldehyde dehydrogenase result in the production of NADH [11], which could in turn lead to an increased rate of esterification [12]. However, in animal studies, addition European Journal of Clinical Investigation (1997) 27, 719-722 of oxidants to the diet does not prevent alcoholic fatty liver [13] and hepatic redox changes are attenuated to levels seen in control animals after some months of alcohol feeding without a concomitant lowering of triglyceride levels [14].…”

“…In the early stages of alcohol feeding, the acute shift in the cytsolic NAD þ / NADH ratio enhances hepatic triacylgycerol formation via the ratio [glycerol-3-phosphate]/[dihydroxyacetone phosphate] [11] and inhibition of b-oxidation by lowered intramitochondrial NAD þ /NADH ratio [10], together leading to steatosis, as observed in acute moderate alcohol intake [42]. If excessive alcohol intake is continued, however, then the shift in the cytosolic NAD/ NADH ratio becomes attenuated [12], so that if it were the only cause of hepatic alcoholic steatosis, then the steatosis would also become attenuated.…”

The effect of acute and chronic ethanol intake on hepatic glycerolipid biosynthesis in the hamster.

“…The mechanism of the increase in hepatic triglyceride biosynthesis during ethanol ingestion is not clear. Elevated hepatic levels of fatty acids (3,10,16) and sn-glycerol-3-phosphate (3,7,9,17,18) during ethanol consumption may contribute to the rise in hepatic glycerolipid biosynthesis. Alternatively, A preliminary report of this research was presented on 4 April 1977 in Chicago, Ill., at the annual meeting of the Federation of American Societies for Experimental Biology.…”

Paradoxical effect of ethanol on liver lipogenesis in the genetically-obese Zucker rat

“…1985), hepatic triacylglycerol levels were found to be lower for the fu/fu rats given diet E. Although it was not significant, the decrease in hepatic glycerol kinase activity for these rats given diet E supports this suggestion. These changes are, therefore, the reverse of those described for the normal rat (Nikkila & Ojala, 1963;Joly et ul. 1973;Lamb & Fallon, 1974), for which ethanol increases both the quantity of glycerol kinase metabolites (a-glycerophosphate; Nikkila & Ojala, 1963) and the activities of enzymes (such as glycerol kinase) implicated in glycero-lipid synthesis (glycerophosphate acyltransferase (EC 2.3. l .15; Joly et ul.…”

“…These changes are, therefore, the reverse of those described for the normal rat (Nikkila & Ojala, 1963;Joly et ul. 1973;Lamb & Fallon, 1974), for which ethanol increases both the quantity of glycerol kinase metabolites (a-glycerophosphate; Nikkila & Ojala, 1963) and the activities of enzymes (such as glycerol kinase) implicated in glycero-lipid synthesis (glycerophosphate acyltransferase (EC 2.3. l .15; Joly et ul. 1973) and phosphatidate phosphatase (EC 3.1 .3.4; Lamb & Fallon, 1974)).…”