Improving estimates of trophic shift in Nile tilapia, Oreochromis niloticus (L.), using measurements of lipogenic enzyme activities in the liver.

To test whether the measurement of selected enzyme activities could be used to estimate more precisely the trophic shift of C isotopes, Nile tilapia (Oreochromis niloticus) were fed semi-synthetic diets differing in their lipid contents (1.7%, 5.0%, 10.8% and 20.0%). The diets were formulated to contain the same amount of nitrogen and metabolizable energy and were made from casein, wheat starch, corn germ oil supplemented with vitamins, minerals and L-arginine. The influence of the different diets on the activity of two lipogenic enzymes, ATP-citrate lyase and malic enzyme, on delta13C values in the whole fish, the liver and their correlation was investigated. There was a strong positive correlation between delta13C values in the lipids of whole fish and those of their livers. The activities of lipogenic enzymes increased significantly with increasing trophic shift of C isotopes (Deltadelta13Cdiet-fish values) in the lipids. If the relationship between trophic shift and enzyme activity can be confirmed in situations where feed quantity and quality are not known, the determination of enzyme activities would enable better estimates of the trophic shift to be made thus significantly improving back-calculation of diets from stable isotope data.

Nickel deficiency alters liver lipid metabolism in rats.

The present investigation was designed to examine the effect of nickel deficiency on lipid metabolism in liver and serum lipoproteins of rats. Therefore, a study over two generations was conducted feeding a nickel-deficient diet containing 13 microg/kg nickel or a nickel-adequate diet supplemented with 1 mg/kg nickel. Male 7-wk-old pups from the second offspring were studied. Pups fed a diet poor in nickel tended to have lower weight gains (P < 0.15), nickel concentrations in liver (P < or = 0.1) and iron levels in serum (P < 0.1) than nickel-adequate rats. They were classified as nickel-deficient on the basis of significantly lower erythrocyte counts, hemoglobin concentrations, hematocrits and nickel concentrations in kidney compared with nickel-adequate rats. Nickel deficiency caused a significant triacylglycerol accumulation in liver, with greater concentrations of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids than nickel-adequate rats. Nickel deficiency had slight but significant effects on the fatty acid composition of liver total lipids and phosphatidylcholine and phosphatidylethanolamine. Moreover, nickel-deficient rats had significantly lower activities of the lipogenic enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malic enzyme and fatty acid synthase than nickel-adequate rats. Nickel-depleted pups had significantly higher concentrations of triacylglycerols and phospholipids in serum VLDL, and cholesterol in serum LDL than nickel-adequate pups. Most of these alterations in lipid metabolism are similar to those obtained in several iron-deficiency studies. Because nickel deficiency also slightly compromised iron status, it is possible that at least some of the observed alterations are due to the moderate iron deficiency.

Polyunsaturated fatty acid-mediated suppression of insulin-dependent gene expression of lipogenic enzymes in rat liver.

The effects of dietary polyunsaturated fat on insulin-dependent gene expression of lipogenic enzymes and a possible mechanism for PUFA-mediated suppression of the gene expression have been investigated in rat livers. When diabetic rats were injected with insulin, the insulin dose-dependent induction of lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil. On the other hand, the PUFA-mediated suppression of the mRNA concentrations was partially restored by treatment with pioglitazone, a candidate for increasing insulin receptor phosphorylation. Moreover, insulin binding to receptors of liver, receptor autophosphorylation, and kinase activity toward exogenous substrate were lower in the corn oil diet group than in the hydrogenated fat group. The PUFA-mediated suppression of insulin binding was somewhat restored by pioglitazone, and the suppression of insulin receptor phosphorylation was significantly restored. It is suggested that the PUFA-mediated suppression of insulin-dependent gene expression of lipogenic enzymes can be ascribed to a decrease in insulin receptor binding primarily and also to receptor phosphorylation. Thus, PUFA appears to suppress the lipogenic enzyme gene expression stimulated by insulin.