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Biomedical subjects

M M Mathias

Publications and source records attributed to M M Mathias.

At least 37 records · Page 2Linked to original sources
PubMed1982

Eicosanoid production in rat blood as affected by fasting and dietary fat.

The effects of fasting and dietary linoleate on eicosanoid production in clotting rat blood incubated 10 minutes at 37 degrees C was studied. Fasting increased eicosanoid synthesis. Dietary manipulation of eicosanoid levels was best demonstrated in the fed rat model. TXB2, PGE2, F2 alpha, and E1 synthesis increased when dietary linoleate increased from 0.0 to 0.4% calories; from 0.4 to 29% linoleate calories there was no change in PG synthesis, but a decrease in TXB2 production was apparent.

Animals↗
PubMed1982

Effect of dietary fat on pulmonary enzymes and toxicity during normobaric hyperoxia.

Weanling male rats were fed a semi-purified diet containing 10, 20, 40 or 60% of calories as fat having a constant polyunsaturated/saturated fatty acid ratio of 0.7. After 21-28 d of feeding, animals from each treatment group were exposed to pure oxygen at one atmosphere absolute for up to 72 h. Some animals were sacrificed after 0 or 48 h of oxygen exposure and lung tissue analyzed for the activities of the hexose monophosphate shunt and prostaglandin dehydrogenase/reductase. Other animals were exposed to hyperoxia until death. With increasing dietary fat content, the pre-exposure activities of the two enzymes decreased and oxygen-induced mortality increased. There was no dietary effect on enzyme activities after 48 h of hyperoxia. We concluded that both dietary fat content and the pre-exposure activity of prostaglandin dehydrogenase/reductase influenced the relative susceptibility to pulmonary oxygen poisoning.

Animals↗
PubMed1981

Fatty acid and cholesterol synthesis from specifically labeled leucine by isolated rat hepatocytes.

Hepatocytes isolated from female rats meal-fed a high-glucose diet were incubated in Krebs-Henseleit bicarbonate medium containing 16.5 mM glucose, 3H2O, and 14C-labeled amino acids (-)-Hydroxycitrate depressed the incorporation of 3H2O and [14C] alanine into fatty acids and cholesterol. Incorporation of [U-14C]leucine into lipids was not affected but incorporation of 3H2O into lipids was decreased significantly by (-)-hydroxycitrate. (-)-Hydroxycitrate depressed the incorporation of radioactivity from [2-14C]leucine into fatty acids and cholesterol by 61 and 38%, respectively, and stimulated the incorporation of radioactivity from [4,5-3H]leucine 35 and 28%. As [2-14C]leucine labels the acetyl-CoA pool and [4,5-3H]leucine labels the acetoacetate pool, it was concluded that mitochondrial 3-hydroxy-3-methylglutaryl-CoA is not incorporated intact into cholesterol, and that acetoacetate can be activated effectively in the liver cytosol for support of cholesterol and fatty acid synthesis.

Acetoacetates↗
PubMed1981

Pulmonary prostaglandin metabolism during normobaric hyperoxia.

Prostaglandin metabolism by rat lung tissue was measured following exposures of 6, 24 and 48 hours to either pure oxygen or air at one atmosphere. Tissue concentrations of PGE1, PGE2 and PGF2 alpha were not altered by oxygen exposures. Prostaglandin synthetase activity decreased between 24 and 48 hours but was not significantly different from control at 48 hours. Combined prostaglandin dehydrogenase/reductase activity decreased between 24 and 48 hours to 13% of control values and was significantly lower than in air at 48 hours. The plasma concentration of 13, 14 dihydro-15-keto PGF2 alpha, a catabolite of PGF2 alpha, was significantly lower in oxygen-exposed rats at 24 and 48 hours. We conclude that endogenous pulmonary prostaglandin concentrations are maintained during hyperoxia but that catabolism of prostaglandins by the lungs may be impaired.

15-Oxoprostaglandin 13-Reductase↗
PubMed1981

Vitamin E and aspirin depress prostaglandins in protection of chickens against Escherichia coli infection.

The hypothesis was tested that vitamin E protects chickens from a lethal Escherichia coli infection by inhibiting the biosynthesis of prostaglandins, thereby activating humoral immunity and phagocytosis. When chickens were fed supplement vitamin E at the level of 300 mg/kg diet, which is six times the presently used dietary level, endogenous PGE1, PGE2, and PGF2 alpha levels decreased in the immunopoietic organs, bursa, and spleen. Antibody titers to E. coli lipopolysaccharide and phagocytosis increased at the same time. Infection slightly increased prostaglandin levels and vitamin E appeared to compensate for this increase. Aspirin, a known prostaglandin inhibitor acted synergistically with vitamin E in depressing endogenous PG levels in bursa and decreasing mortality from E. coli infection.

Animals↗
PubMed1981

Rat platelet prostaglandin, cyclic AMP and lipid response to variations in dietary fat.

Diets supplying 20 or 40% of the calories as fat with linoleate to saturated fatty acid ratios of 0.4, 0.8 and 5.5 were fed to male weanling rats for 8 and 11 weeks. Recalcification clotting time was not affected by dietary treatment. Concentration of cAMP in the platelets was significantly elevated at the highest level of dietary linoleate. Cyclic AMP was negatively correlated with concentration of dihomo-gamma-linolenic acid in platelet phospholipids and positively correlated with prostaglandin E1, suggesting that dihomo-gamma-linolenic acid is rapidly converted to prostaglandin E1 causing a rise of cAMP due to stimulation of adenylate cyclase. Dietary treatment did not markedly change the composition of the platelet phospholipid fatty acids and, therefore, resulted in no change in synthesis of the proaggregatory prostaglandin by platelets during clotting. Although the fatty acid composition of the platelet phospholipids remained constant, dietary treatment did affect the total amount of phospholipid fatty acid present in the platelet. Serum concentrations of cholesterol were significantly higher in rats fed the 20% fat diet than in rats fed the 40% fat diet. Platelet cholesterol followed the same trend as serum cholesterol indicating that the cholesterol content of platelets appears to reflect the lipid environment of the plasma.

Animals↗
PubMed1980

Effects of dietary essential fatty acid concentration upon prostanoid synthesis in rats.

The effects of dietary linoleate as zero to 27% of energy, fed to female rats for 6 months, in relation to ability of whole blood to synthesize PG during clotting at 37 degrees was studied. Synthesis of PGE1, PGE2, PGF2 apha and TXB2 after 10 or 40 minutes of incubation of whole blood was determined by assay of serum concentration by radioimmunoassay. Fatty acid composition of serum phospholipids, cholesteryl esters and acyl glycerides was determined. PG synthesis increased with linoleate as zero to 2% of kcal; from 2% up to 7% there was a decrease of PG synthesis; from 7% to 27% there was a linear increase. There was no pattern to PGF2 alpha maximum concentration. PGE2 had a linear increase from 0 to 30% linoleate. PGE1 decreased with 0 to 2% linoleate, then increased between 2 and 7% and maintained a plateau through 27%. The concentration of TXB2 was found to be about 20-40 times that of PGE2 and PGF2 alpha. The decline of PGE1 synthesis with 2-7% linoleate calories was correlated with 20:3n-6 concentration and PGE2 and PGF2 alpha production with 20:4. With dietary linoleate concentrations greater than 7.4% PG synthesis had a linear increase up to 27% of kilocalories, not correlated with fatty acids.

Animals↗
PubMed1979

The relationship of dietary fats to prostaglandin biosynthesis.

The direct and indirect evidence that the fatty acid composition of dietary fat is involved in the regulation of prostaglandin biosynthesis was reviewed. Direct evidence included effects of essential fatty acid deficiencies and excesses on endogenous tissue levels and production rates of prostaglandins by several tissues. Indirect evidence included lipolytic, platelet aggregatory, hypertensive, inflammatory and immune responses. In general, composition of dietary fat did not affect prostaglandin biosynthesis unless a biochemical essential fatty acid deficiency was induced or the linoleate to saturated fatty acids ratio of the dietary fat was greater than 5. Most results were interpreted in light of changing fatty acid composition; however, very few direct measurements have been made.

Adipose Tissue↗
PubMed1978

Prostaglandin production and lipolysis in isolated rat adipocytes as affected by dietary fat.

The influence of dietary fat on prostaglandin production and lipolysis was tested in basal and norepinephrine stimulated adipocytes isolated from the epididymal fat pads of fasted rats. Seven diets varying in fat calories and polyunsaturation were utilized. No basal differences were noted for prostaglandin E2 production or lipolysis. Norepinephrine stimulated prostaglandin E2 and F2alpha production was significantly (P less than 0.01) increased with greater polyunsaturation of fat, but not by increased fat calories. Norepinephrine stimulated lipolysis was depressed by an increase in fat calories but was unaffected by the degree of polyunsaturation of fat. This is in vitro evidence against the concept that prostaglandins play a feedback regulator role in fat cell lipolysis since no correlation could be made between the two parameters.

Adipose Tissue↗
PubMed1978

Dietary fat type and ambient oxygen tension influence pulmonary prostaglandin synthetic potential.

Chronic hyperoxia produces pathological changes in lung which can be fatal. With an interest in delineating dietary factors which might affect the pulmonary response to hyperoxia, we fed rats a semi-synthetic diet containing polyunsaturated fatty acids (PUFA) as either 5% or 78% of the fat complement. The rats were exposed to pure oxygen at one atmosphere. Half the animals in each diet group were injected with aspirin during the hyperoxic exposure. Radioimmunoassay of lung prostaglandins (PG) F2alpha, E2 and E1 were performed at 0, 24, 48 and 72 hours. The major findings were: (1) Feeding the high PUFA diet elevated lung PG synthetic potential tenfold over that of low PUFA-fed animals. There was no effect of diet on mortality. (2) Hyperoxia significantly increased F2alpha-synthetic potential during the first 24 hours of hyperoxia and moderately increased the synthetic potential of E2 and E1. (3) Aspirin significantly depressed synthetic potential of all three PG prior to oxygen exposure but its effect was overcome during hyperoxia. Aspirin-injected rats showed 80% mortality in oxygen vs. 50% for saline controls.

Animals↗
PubMed1975

Linoleate enrichment of diet and prostaglandin metabolism in rats.

Evidence that biosynthesis of prostaglandins (PG) in tissues of animals deficient in essential fatty acids is dependent on the availability of their precursors has been demonstrated. The purpose of this study was to determine the following: (1) effects of dietary linoleate enrichment on PG biosynthesis in rats; (2) effects of exogenous PGE2 and dietary linoleate on plasma free fatty acids and serum cholesterol in fed and fasted rats. Rats were fed three different concentrations of dietary linoleate as beef tallow, hydrogenated vegetable fat, or corn oil. The concentrations of PGE1 and PGF2a measured by radioimmunoassay were higher in rats fed the fed the beef tallow diet independent of energy status. A decrease in the concentration of PG between fasted and fed rats receiving hydrogenated vegetable fat is discussed in respect to the possible influence of trans isomers of unsaturated fatty acids on the biosynthesis of PG. There were significant effects of fasting on serum cholesterol concentration regardless of diet and significant interactions among effects of PGE2, fasting, and diet, suggesting regulatory effects of PGE2 on serum cholesterol concentration. The increase in plasma free fatty acids associated with fasting was prevented by PGE2 for all diets, but had the most marked effect on rats fed hydrogenated vegetable fat.

Animal Nutritional Physiological Phenomena↗