Acta physiologica latino americana最新文献

The effect of clofibrate and ethanol in the rat was studied on the following aspects of lipid composition and metabolism: liver delta 5, delta 6 and delta 9 fatty acid desaturases, fatty acid synthetase and fatty acid desaturase microsomal electron transport chain activity and serum cholesterol, triacylglycerols and high (HDL), low (LDL) and very low density lipoprotein (VLDL) levels. Clofibrate administered for 9 days (0.3% W/W) did not modify the relative composition of liver phospholipids and cholesterol, but did diminish triacylglycerol levels increased by ethanol. This effect could be explained by the possible beta-adrenergic blocking properties of clofibrate or by an increased activity of peroxisomal beta-oxidation. Clofibrate also promoted a decrease in serum cholesterol and triacylglycerol levels, delta 6 desaturase activity and a suppression of the electron transport chain as measured by NADH cytochrome b5 reductase and NADH cytochrome c reductase. The drug increased delta 9 desaturase activity and fatty acid synthetase, while no effect could be found in delta 5 desaturase activity. The hypocholesterolenic effect of clofibrate can not be explained through the delta 6 desaturase inhibition, or the fatty acid synthetase enhancement. Ethanol increased the HDL and VLDL and lowered LDL serum concentrations, while clofibrate reversed these results. Considering that clofibrate could have antiatherosclerotic effect in the rat, it is difficult to explain it through these changes in lipoprotein levels, since according to Miller and Miller low HDL levels are predictive of coronary heart disease.

The effects of vitamin D3 and the aqueous extract of Solanum malacoxylon on intestinal alkaline phosphatase and tissue phosphate content were studied on rachitic chicks treated with large doses of ethane-1-hydroxy-1,1 diphosphonate (EHDP). The EHDP treatment blocks the increase of intestinal calcium or phosphate absorption induced by the vitamin D3, while it has no effects on the rise of intestinal alkaline phosphatase activity or the increment in tissue phosphate content. The lack of correlation between the increment of alkaline phosphatase and that of Ca or phosphate absorption in vitamin D3 plus EHDP treated chicks excludes a participation of the alkaline phosphatase in the mechanism of Ca or P intestinal absorption. The Ca or phosphorus absorption are elicited specifically by 1,25-(OH)2-D3, while alkaline phosphatase activity and phosphate tissue concentration respond to a broader spectrum of stimuli.

Pork insulin was labeled by the chloramine T technique (phosphate buffer 0.25 M; pH 7.5; EDTA 0.001 M; chloramine T: 0.2625 mg/ml; sodium metabisulfite 2.4 mg/ml) in a reaction volume of 50 microliters, adding chloramine T every 30 seconds twice (2.1 micrograms in 1 minute) and halting the reaction with 5 microliters metabisulfite. Three fractions were separated in preparative starch gel: F1 (mono-125I-insulin contaminated with cold insulin), F2 (mono-125I-insulin free from cold insulin), and F3 (di-125I-insulin). Insulins with low and high specific activity (iodine/insulin ratios 0.1/1 and 1/1 respectively) were prepared for study purposes, and quality was assessed by means of dose-response curves with antibodies and with liver cells. Specific activity of F2 as obtained from dose-response curves utilizing Scatchard's plot was 323 and 382 mCi/mg. Specific activity of F1 varied according to the extent of contamination with cold insulin. A reduction in the F2 B/F ratio was observed upon iodination with iodine/insulin ratios of 1/1 or in the neighborhood. The mass and immunoreactivity of F3, as well as its B/F ratios were constant, regardless of specific activity. The behavior with antibodies was ratified upon observations on uptake by liver cells and glucose consumption by isolated fat cells. In conclusion, F2 labeled with 0.1/1 iodine/insulin ratios was separated from cold insulin in preparative starch gel, thus increasing its specific activity (360 mCi/mg approximately) without alteration of its immunologic or biologic properties.

The release and metabolism of 3H-noradrenaline (3H-NA) produced by d-amphetamine was studied in the superior cervical ganglion of the cat (cell bodies) and in the nictitating membrane (nerve endings). Exposure of the nictitating membrane to 10 microM d-amphetamine, resulted in the release of 5.1% of the total radioactivity. This was mainly collected as 3H-normetanephrine (3H-NMN) and as 3H-NA; 3H-3,4-dihydroxyphenylglycol (3H-DOPEG) did not contribute to the drug-induced outflow of radioactivity. In contrast, exposure of ganglionic cell bodies to 10 microM d-amphetamine for 10 min released only 1.74% of the total tissue radioactivity and 3H-DOPEG represented the most important fraction of the released radioactivity. When ganglia were exposed to 30 microM d-amphetamine, the radioactivity released was 5.2%; the proportion of 3H-NA and 3H-NMN increased and 3H-DOPEG was reduced. These results show that: a) d-amphetamine releases 3H-NA from prelabeled cell bodies and nerve endings; b) the potency of d-amphetamine was higher in nerve terminals than in cell bodies, and c) at low concentrations of d-amphetamine, the metabolism of the released neurotransmitter differed between both parts of the adrenergic neuron.

Two enriched plasma membrane subfractions were obtained from syncytiotrophoblast isolated from human placenta. They were isolated from a "crude" plasma membrane fraction at the buffer-24% and 24-30% (w/w) sucrose interfaces of a sucrose gradient; another enriched plasma membrane fraction was isolated from the microsomal fraction at buffer-24% (w/w) sucrose interface and was similar to that isolated from the "crude" plasma membrane fraction at the same sucrose density. Although all three subfractions contain a high specific activity in 5'-nucleotidase and alkaline phosphatase, the specific activity was twofold higher in the lighter than in the heavier subfractions. The activities of succinate dehydrogenase, monoamine oxidase, acid phosphatase and glucose-6-phosphatase indicated very low contamination with other organelles. Polyacrylamide-gel electrophoresis resolved the polypeptides of the plasma membrane subfractions into about 14 major protein bands; no differences were observed in the patterns of the two enriched plasma membrane subfractions derived from the "crude" plasma membrane fraction.

The injection of a bolus of insulin (40 millimicrons) in the coeliac trunk in anesthetized rabbits elicits an immediate rapid rise of arterial IRI. Inferior vena cava and jugular glucose levels drop precipitously 2 min after insulin injection, increasing the A-V glucose difference. The same amount of insulin injected via the coeliac trunk in abdominal-vagotomized rabbits, failed to induce any significant changes in venous glucose concentration and A-V glucose, although there was a similar rise of IRI concentration in arterial plasma. Electrical stimulation of the central stump of the abdominal vagi does not alter the IRI levels in arterial plasma, however, arterial blood glucose increases suddenly, venous blood glucose drops in the first 2 min of stimulation and the A-V glucose difference increases; there are no significant changes in blood flow, arterial pressure and oxygen saturation in cephalic circulation. These data suggest that small amounts of insulin injected or secreted in a zone irrigated by the coeliac trunk, trigger a hypoglycemic reflex. Evidence is provided to suggest that this is by causing a rapid increase in glucose both by the brain and leg muscle mass.