Liver failure carbohydrate metabolism

Because the liver is a major processor of dietary and endogenous carbohydrates, liver disease affects carbohydrate metabolism in a variety of ways (see Chapter 25). However, none of the conventional modes of evaluating carbohydrate metabolism have value in the diagnosis of liver disease. Because the liver is the major site of both glycogen storage and gluconeogenesis, hypoglycemia is a common complication in certain liver diseases, particularly Reye s syndrome, fulminant hepatic failure, advanced cirrhosis, and hepatocellular carcinoma. 

Liver Trovafloxacin was withdrawn from the European market because of Uver toxicity and acute liver failure in 1999, but it is still available under very strong restrictions in the USA. In experiments in isolated human hepatocytes trovafloxacin inhibited expression of hepatic nuclear factor-4a (HNF-4ot), which in turn suppressed the function of a network of genes that govern major metabolic processes, lipid and carbohydrate metabolism, and mitochondrial biol-ogy [78 ]. The author concluded that this is the probable underlying mechanism of trovafloxacin-induced hepatotoxicity. 

No specific antidote has been shown to be effective in treating 1,2-dibromoethane intoxication once absorption into the bloodstream has occurred (Ellenhorn and Barceloux 1988). Intravenous infusions of glucose may limit the hepatotoxicity of 1,2-dibromoethane (ERA 1989b). During the recovery phase, a diet rich in vitamin B and carbohydrates may limit liver damage (Dreisbach and Robertson 1987 Lawrence and Michaels 1984). Hemodialysis may be needed to regulate extracellular fluid and electrolyte balance and to remove metabolic waste products if renal failure occurs (ERA 1989b). 

The liver is responsible for synthesis of cholesterol, high-density lipoproteins, and very-low-density lipoproteins. The enzymes lipoprotein lipase and lecithin-cholesterol acyltransferase also are synthesized in this organ. Increased serum triglyceride and FFA concentrations are encountered in patients with hepatic failure, primarily due to the increased lipolysis. The significant insulin resistance that can be seen in cirrhosis causes a shift to lipids as a fuel source. Whereas only 35% of total calories are derived from fat in normal patients after an overnight fast, this can increase to 75% in patients with cirrhosis. Incorporation of late evening snacks in patients with liver cirrhosis may correct abnormal substrate metabolism, increase carbohydrate, and decrease fat oxidation rates. ... 

Thyroid hormone effects on metabolism arc diverse. The rates of protein and carbohydrate synthesis and catabolism are inlluenced. An example of the effect of thyroid hormones on lipid metabolism is the observation of a high serum cholesterol in some hypothyroid patients. This is a consequence of a reduction in cholesterol metabolism due to down regulation of low-density lipoprotein (LDL) receptors on liver cell membranes, with a subsequent failure of sterol excretion via the gut. 

Diabetes and Insulin. In 1944, Stetten and co-workers - concluded, from experiments carried out with deuterium, that the failure to utilize glucose for fatty acid synthesis is a major metabolic defect in diabetes, and more recently this conclusion has been amply confirmed in studies with C -labeled glucose and acetate. - Table XI shows the utilization of acetate-C and glucose-C for fatty acid formation by the livers of two types of rats (1) normal, and (2) alloxan diabetic. For several days before the animals were sacrificed they were fed a high carbohydrate diet (see below). The liver slices prepared from diabetic rats lost, to a considerable extent, the capacity to incorporate the isotope of glucose or acetate into fatty acids. The dramatic action of injected insulin in... 

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