Visfatin was originally described as an adipokine with insulin mimetic effects. Recently, it was found that visfatin is identical with the Nampt (nicotinamide phosphoribosyltransferase) gene that codes for an intra- and extracellular NAD biosynthetic enzyme and is predominantly expressed outside the adipose tissue. In the current study, we found strong protein and mRNA expression of visfatin in rat heart, liver, kidney, and muscle, while the expression of visfatin in visceral fat was significantly lower and undetectable in subcutaneous fat. The insulin-mimetic effects of visfatin (extracellular form of Nampt or eNampt) are controversial and even less is known about autocrine effects of visfatin (intracellular form of Nampt or iNampt). Since liver plays a major role in glucose metabolism, we studied visfatin effects on insulin-stimulated cellular glucose uptake in Fao rat hepatocytes using RNA interference (RNAi). RNAi-mediated downregulation of visfatin expression in Fao cells was associated with significantly reduced NAD biosynthesis (0.3±0.01 vs. 0.5±0.01 mmol/h/g, P<0.05) and with significantly decreased incremental glucose uptake after stimulation with insulin when compared to controls with normal expression of visfatin (0.6±0.2 vs. 2.2±0.5 nnmol/g/2 h, P=0.02). These results provide evidence that visfatin exhibits important autocrine effects on sensitivity of liver cells to insulin action possibly through its effects on NAD biosynthesis.
Z������ J., S����� J., K������� K., K�������-K���� A., H���� T., Z���� V., F������� A. (2004): Effects of oxidised dietary cod liver oil on the reproductive functions of Wistar rat. Czech J. Food Sci., 22: 108-120.Weanling Wistar rats, males and females, were fed for 185 days with diets containing 15% of dietary fat in the form of a mixture of lard and partially oxidised cod liver oil. The proportion of cod liver oil in the dietary fat ranged from 0 to 100%, and the content of malondialdehyde from 0.3 to 19.6 mg/kg of the fat used. Animals fed with diets containing higher proportions of oxidised cod liver oil had higher concentrations of malondialdehyde in their livers. Serum lipid levels were lower in animals fed with higher proportions of cod liver oil than in animals fed control diets (milk fat or lard). The lowest concentration of serum lipid was found in the rats fed the diet containing half of its fat as fish oil. Increased intakes of cod liver oil resulted in lower body weight gains, weights of livers, kidneys, and weights of the reproductive organs. The relative weights of livers and kidneys/body weight were higher in the groups with higher intakes of cod liver oil. High intakes of cod liver oil led to a drastically impaired fertility of females, a decreased litter size, a higher postnatal mortality, and an increased incidence of morphologically abnormal spermatozoa in males.
In the current study, we tested a hypothesis that CD36 fatty acid (FA) transporter might affect insulin sensitivity by indirect effects on FA composition of adipose tissue. We examined the effects of CD36 downregulation by RNA interference in 3T3-L1 adipocytes on FA transport and composition and on sensitivity to insulin action. Transfected 3T3-L1 adipocytes, without detectable CD36 protein, showed reduced neutral lipid levels and significant differences in FA composition when levels of essential FA and their metabolites were lower or could not be detected including gamma linolenic (C18:3 n6), eicosadienic (C20:2 n6), dihomo-gamma linolenic (C20:3 n6), eicosapentaenoic (EPA) (C20:5 n3), docosapentaenoic (DPA) (C22:5 n3), and docosahexaenoic (DHA) (C22:6 n3) FA. Transfected 3T3-L1 adipocytes exhibited a significantly higher n6/n3 FA ratio, reduced 5-desaturase and higher 9-desaturase activities. These lipid profiles were associated with a significantly reduced insulin-stimulated glucose uptake (4.02+/-0.1 vs. 8.42+/-0.26 pmol.10(-3) cells, P=0.001). These findings provide evidence that CD36 regulates FA composition thereby affecting sensitivity to insulin action in 3T3-L1 adipocytes.
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