Effects of starvation on the tissular lipogenic rate in the obese Zucker rat.

The lipogenic rate of the obese rats was significantly higher than that of the lean rats in liver, white adipose tissue, skeletal muscle, heart and carcass. In the lean rats, a 24 h starvation period caused a significant decrease in the lipogenic rate of white adipose tissue and skeletal muscle while it increased that of heart, brain and brown adipose tissue. In the obese rats, starvation decreased the lipogenic rate in liver, skeletal muscle, white adipose tissue, brown adipose tissue and carcass. In spite of this, liver and skeletal muscle showed higher rates of lipid synthesis than the corresponding fed lean. It is concluded that starvation induces a qualitatively similar response in the obese versus the lean rat although the total lipogenic capacity of the animal is still higher.     

Effect of progesterone on rat plasma and liver lipid levels (author's transl)

The effect of progesterone upon several lipidic parameters on rat liver and plasma was studied. Progesterone administration led to a significant increase in the hepatic triacylglyceride and cholesterol esterified levels and to a decrease in the phospholipid content. After progesterone treatment decreases in plasma total lipids, phospholipids, cholesterol and cholesterol esterified were observed, whereas plasma triacylglyceride and free fatty acid levels increased. The hormonal treatment altered the lipoprotein pattern, which significantly reduced the beta-lipoprotein fraction.     

Effect of dietary nucleotides and orotate on the blood levels of prostacyclin (PGI2) and thromboxane (TXA2) in the weanling rat

Dietary nucleotides affect the maintenance of immune responses, tissue repair and polyunsaturated fatty acid metabolism. Orotate, a pyrimidine nucleotide precursor, induces fatty livers by impairing VLDL hepatic secretion. The aim of this study was to evaluate the changes in the blood levels of fatty acids and prostacyclin (PGI2) and thromboxane (TXA2) in the weanling rat caused by the dietary intake of nucleotides and orotate. Three groups of rats at weaning were fed a control diet, an orotate supplemented diet (O-50) and a nucleotide supplemented diet (N-50) during 4 weeks, respectively. Absolute values of plasma polyunsaturated fatty acids greater than 18 carbon atoms of the n-6 and n-3 series were increased in the N-50 group and decreased in O-50 with regard to the control. However, the relative fatty acid composition of plasma lipid fractions was mostly unaffected. Plasma 6-keto-PGF1 alpha showed a trend to be increased in N-50 and serum TXB2 was significantly increased in that group. Both eicosanoids were unchanged by dietary orotate intake. These results may be explained because of the increased plasma 20:4n-6 found in rats fed a supplemented nucleotide diet. Thus, nucleotides present in foods appear to modulate PUFA conversion and eicosanoids synthesis in early life.     

Effect of dietary fat on pancreatic lipase levels in the rat

The effect of dietary fat on levels of lipase and other enzymes in rat pancreas has been studied. It was possible to raise levels of lipase in animals by supplementing their commercial chow diet with added fat or by raising the level of fat in semipurified diets from 4% to 22%. Pancreatic amylase levels decreased in rats fed the high fat diets, whereas levels of chymotrypsinogen and trypsinogen were unaffected. The type of carbohydrate in the semipurified diets made no difference. Thus, the levels of enzymes in rats fed dextrose-containing diets or cornstarch-containing diets were similar. On the basis of the present data, and results of others, it would appear that levels of pancreatic lipase are increased when the fat content of the diet is raised from about 5% to 15-22%, but that little or no additional increase in lipase levels can be attained by any further increase in the amount of dietary fat.     

Effect of buspirone on glutathione hepatic levels in rat

The effect of oral administration of buspirone (0.5-1.0 and 2.0 mg/Kg) on GSH levels was studied in rat liver. The modulating activity of buspirone on hepatic content of this tripeptide is clearly opposite to that of DAZ, put into evidence by us in previous works. Thus our observations let us hypothesize a different mechanism of action for buspirone than that for benzodiazepines.     

Effect of ethanol on cyclic AMP levels in the rat brain

Ethanol decreased in a dose-dependent manner the cyclic AMP level in the rat brain and separation of the brain into several parts showed that this decrease was limited to the cerebellum. High doses of ethanol (4–6 g/kg) blocked the rise of cyclic AMP levels induced by decapitation in all brain areas studied. Pentobarbital treatment which produced central depression similar to that caused by a high dose of ethanol, also decreased the cyclic AMP level in the cerebellum but it prevented the postdecapitation rise only in the pons and medulla oblongata. Lower doses of ethanol (1–2 g/kg) enhanced the decapitation-induced rise of cyclic AMP levels in the pons and medulla oblongata.     

Effect of quipazine on rat plasma prolactin levels

Quipazine (2-(1-piperazinyl) quinoline maleate), a serotonin agonist which also has other effects on serotonin metabolism, in doses from 2.5 – 20 mg/kg, i.p., was found to markedly increase plasma prolactin levels in male rats. This increase was blocked by the serotonin antagonists methysergide and brom-lysergic acid diethylamide and potentiated by para-chlorophenylalanine, an inhibitor of serotonin synthesis. These findings suggest that the increase in plasma prolactin levels is due to the serotonin agonist properties of quipazine. Apomorphine and 2-Br-α-ergocryptine pretreatment blocked the effect on plasma prolactin of quipazine, while apomorphine given 15 min after quipazine brought about a rapid decline in the elevated plasma prolactin levels produced by quipazine.     

Effect of monofluoromethyldopa (MFMD) on trace amine levels

The concentrations of the trace amines, m-tyramine, p-tyramine, phenylethylamine and tryptamine, were measured in the striatum of the brain and in the kidney of adult rats treated with alpha-monofluoromethyldopa (MFMD), an inhibitor of aromatic amino acid decarboxylase. While MFMD decreased the levels of all four amines in the kidney, only phenylethylamine and tryptamine levels were decreased in the striatum compared to control. Striatal p-tyramine levels were not affected, while striatal m-tyramine levels were increased by MFMD. When the rats were injected with a monoamine oxidase (MAO) inhibitor before MFMD administration, similar changes in striatal and kidney trace amine levels were observed compared to MFMD alone.     

Effect of iron deficiency on phosphoinositide levels in rat brain

Adult rats raised on 90% iron deficient diet for 6 weeks showed a decrease in the levels of brain phosphatidylinositol (60%), phosphatidylinositol 4-phosphate (25%) and phosphatidylinositol 4,5-bisphosphate (30%), the precursors for the second messengers, diacylglycerol and inositol phosphates. Rehabilitation to normal diet for 24 days was found to restore the levels to control values. The data suggests that iron deficiency could lead to alterations in the functions related to phosphoinositide-linked receptor system(s).     

Effect of corticosterone on CART peptide levels in rat blood

We have recently demonstrated that CART peptides display a diurnal rhythm in blood that depends partly on glucocorticoids levels. This study extends previous findings by directly testing the effects of acute administration of corticosterone and metyrapone on CART peptide levels in blood. Acute treatment with corticosterone augmented CART levels, while metyrapone administration prevented the increase in CART in the evening hours. These results further support the hypothesis that glucocorticoids play a role in the regulation of CART levels in blood.     

Effect of chronic hyperglycemia on crystallin levels in rat lens

Crystallins are the major structural proteins in the vertebrate eye lens that contribute to lens transparency. Although cataract, including diabetic cataract, is thought to be a result of the accumulation of crystallins with various modifications, the effect of hyperglycemia on status of crystallin levels has not been investigated. This study evaluated the effect of chronic hyperglycemia on crystallin levels in diabetic cataractous rat lens. Diabetes was induced in rats by injecting streptozotocin and maintained on hyperglycemia for a period of 10 weeks. At the end, levels of α-, β-, γ-crystallins and phosphoforms of αB-crystallins (αBC) were analyzed by immunoblotting. Further, solubility of crystallins and phosphoforms of αBC was analyzed by detergent soluble assay. Chronic diabetes significantly decreased the protein levels of α-, β- and αA-crystallins (αAC) in both soluble and insoluble fraction of lens. Whereas γ-crystallin levels were decreased and αBC levels were increased in lens soluble fraction with no change in insoluble fraction in diabetic rat lens. Although, diabetes activated the p38MAPK signaling cascade by increasing the p-p38MAPK in lens, the phosphoforms of αBC were decreased in soluble fraction with a concomitant increase in insoluble fraction of diabetic lens when compared to the controls. Moreover, diabetes strongly enhances the degradation of crystallins and phosphoforms of αBC in lens. Taken together, the decreased levels of crystallins and insolubilization of phosphoforms of αBC under chronic hyperglycemia could be one of the underlying factors in the development of diabetic cataract.