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Antihyperlipidemic activity of saccharin analogues in rodents.

Saccharin analogues were observed to be potent antihyperlipidemic agents at 20 mg/kg/day in rodents, significantly reducing both serum cholesterol and triglyceride levels in both normal and atherogenic mice. The saccharin analogues suppressed in vitro and in vivo liver enzymatic activity of acetyl-CoA synthetase, citrate lyase, and mitochondrial citrate exchange leading to a reduction of available cytoplasmic acetyl-CoA, which is required for the synthesis of cholesterol and fatty acids. Liver acetyl-CoA carboxylase, phosphatidate phosphohydralase, and glycerol-3-phosphate acyl transferase activities were markedly reduced by the saccharin analogues. Suppression of these enzymes would lead to a reduction of triglyceride synthesis. The saccharin analogues accelerated bile excretion of cholesterol metabolites and increased the fecal excretion of the cholesterol, triglycerides, neutral lipids, and phospholipids. The liver and plasma lipoprotein lipid content (including cholesterol, triglycerides, and neutral lipids) was markedly reduced by the saccharin analogues, whereas phospholipid content was elevated. The reduction of lipid content of serum chylomicron, very low-density, low-density, and high-density lipoprotein fractions by the saccharin analogues indicates that these agents may be useful in controlling hyperlipidemic diseases where specific lipoprotein fractions are elevated.