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Metabolic evidence was sought to explain the reduced body fat and increased body protein observed in Atlantic salmon fed diets supplemented with L-carnitine. By stimulating fatty acid oxidation, dietary carnitine might increase flux through pyruvate carboxylase and decrease flux through the branched-chain alpha-keto acid dehydrogenase complex, by increasing regulatory ratios of acetyl CoA:free enzyme A (CoA-SH) and ATP:ADP. Such changes could conserve nitrogen by providing more carbon for amino acid biosynthesis and by blocking oxidative loss of the branched-chain amino acids. Consistent with this hypothesis, salmon fed carnitine (23 mmol/kg diet) for 9 wk exhibited greater metabolic rates than cohorts fed a carnitine-free diet (P < 0.05) for the following: 1) 1-[14C] palmitate oxidation by liver cubes (48%) and by isolated hepatocytes (151%), 2) pyruvate-dependent [14 CO2]-fixation by isolated mitochondria (81%), 3) incorporation of 1-[14C] lactate into glucose by liver cubes (120%) and by isolated hepatocytes (210%), and 4) incorporation of [35S]-methionine into the acid-insoluble fraction of liver cubes (59%) and isolated hepatocytes (89%). Hepatic concentrations of seven amino acids, including the branched-chain amino acids, were greater (7-112%), as were the plasma concentrations of three of these (45-130%). However, 230% more enzyme in the mitochondria of carnitine-fed fish, and not a difference in the ratios of acetyl CoA:CoA-SH or ATP:ADP, appeared to account for accelerated flux through pyruvate carboxylase; flux through the dehydrogenase complex was unchanged. These results implicate induction of pyruvate carboxylase (or a reduction in turnover) and enhanced protein synthesis in the mechanism for carnitine-induced changes in gluconeogenesis and nitrogen metabolism.

Ovariectomised mice were treated with sesame seed oil, oestradiol, or one of three different levels of the insecticide chlordecone (1, 1a, 3, 3a, 4, 5, 5a, 6-decachloro-octahydro-1, 3, 4-metheno-2H-cyclobuta[cd] pentalen-2-one). After 9 days of treatment, the uteri were injected with (35)S-methionine and radiolabelled proteins were flushed from uteri 4 h later. Reproductive tract weights and the total amount of radioactivity in uterine flushings were measured. Reproductive tract weights increased significantly only in animals treated with the highest dose of chlordecone tested and oestradiol-treated animals. Trichloroacetic acid (TCA) precipitated radioactivity was increased by all doses of insecticide chlordecone tested but increases were significant only at one level. The greatest stimulation of (35)S-methionine incorporation occurred in ovariectomised animals treated with oestradiol. Radioactive proteins were analysed by fluorography of two-dimensional gels. The fluorograms showed that the proteinaceous uterine secretions, as influenced by chlordecone, were greatly reduced in number as compared with those secreted under the influence of oestradiol. Chlordecone appears to cause the secretion of proteinaceous material from the uteri of mice in a qualitatively different manner than does oestradiol.