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Regulation of apolipoprotein A1 synthesis in lymph drained rats

The effect of lymph diversion on plasma apolipoprotein A-I levels was studied. In lymph fistula rats apolipoprotein A-I levels in plasma stayed constant in spite of a loss of an equivalent of one-half plasma pool of apolipoprotein A-I per day through the lymph fistula. This indicates that synthesis of apolipoprotein A-I increases or that catabolism of apolipoprotein A-I decreases in a compensatoryThe effect of lymph diversion on plasma apolipoprotein A-I levels was studied. In lymph fistula rats apolipoprotein A-I levels in plasma stayed constant in spite of a loss of an equivalent of one-half plasma pool of apolipoprotein A-I per day through the lymph fistula. This indicates that synthesis of apolipoprotein A-I increases or that catabolism of apolipoprotein A-I decreases in a compensatory

200 ka of glacial events in NW Svalbard: an emergence cycle facies model and regional correlations

Late Quaternary sedimentary units at Kongsfjordhallet, NW Svalbard, represent five cycles of glaciations and subsequent deglaciations during high relative sea levels. The high sea level events are interpreted as glacioisostatically induced and imply preceding regional glaciations, which we constrain in time by luminescence and radiocarbon ages to just prior to ~ 195, ~ 130, ~ 85, ~ 60, and ~ 15 ka

Cell density dependent release of hepatic lipase in cultured hepatocytes

Cultured rat hepatocytes release the enzyme hepatic lipase. In this study we investigated the effect of cell density on this metabolic function under a variety of experimental conditions. The release of hepatic lipase from cultured rat hepatocytes exhibits a cell-density dependence, the secretion per mg cell protein being increased with increasing cell density. When cell density dependence was tak

Lipoprotein deficient serum stimulates the uptake of chylomicron remnants in cultured hepatocytes

Rat hepatocyte monolayers were cultured in the presence of 1-10% lipoprotein-deficient foetal calf serum. This increased the uptake and degradation of chylomicron remnant cholesteryl ester significantly. The increase occurred at all cell densities, i.e. also with less dense cultures where the basal rate of uptake per mg protein was highest. This indicates that tissue culture medium content of lipo

Insulin stimulates the uptake of chylomicron remnants in cultured rat hepatocytes

The effects of insulin (10-1000 microU ml-1) on chylomicron remnant uptake and degradation were studied in hepatocyte monolayer cultures. Both uptake and degradation were stimulated by insulin. The degree of stimulation was influenced by cell density, being most pronounced in sparse cultures. The uptake was stimulated in a dose-dependent fashion and was noticed already at a physiological insulin l

Cell density dependent uptake of chylomicron remnants in rat hepatocyte monolaayers. Effects of compactin and mevalonic acid.

In rat hepatocytes cultured in lipoprotein-deficient serum, the uptake and degradation of chylomicron remnant cholesteryl ester per mg cell protein varies inversely with cell density. Compactin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme-A reductase, stimulates the uptake at all cell densities. Mevalonic acid, on the other hand, can suppress a significant part of the remnant up

Cell density dependent uptake of LDL in cultured hepatocytes

An inverse relationship between low-density lipoprotein uptake and cell density was observed in rat hepatocyte monolayers incubated with lipoprotein-deficient serum. This was also true for cell association, binding and degradation of low-density lipoproteins. Compactin stimulated cell association and degradation of low-density lipoproteins both at low and high concentrations. Insulin, on the other