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Biomedical subjects

J Dupont

Publications and source records attributed to J Dupont.

At least 109 records · Page 6Linked to original sources
PubMed1987

Essential fatty acids and prostaglandins.

The World Health Organization's recommendation for dietary intake of essential fatty acids is 3% of energy (en%) of linoleate. Evidence from rat studies suggests that more than 3 en% is desirable for the regulation of eicosanoid metabolism. With such a low level of available linoleate, humans tend to synthesize more prostanoids than they do with 6% or more energy from linoleate. High rates of prostanoid synthesis probably are deleterious, so that the lower rate commensurate with 6-12 en% of linoleate probably is desirable. The amount of linoleate needed for normal function is influenced by the dietary content of other fatty acids, particularly saturated fats and those of the n-3 family. Vitamin E is necessary for normal metabolism of polyunsaturated fatty acids. In a diet providing sufficient available total energy with 30% as fat, the lower range of linoleate (6-8 en%) probably is sufficient if the saturated fatty acid content is 10% or less. With a greater proportion of saturated fatty acids, more linoleate is needed to maintain a polyunsaturated to saturated fatty acid ratio of 0.7 to 1.0. Some n-3 fatty acids probably are required, and more than a minimal amount may be beneficial. Current recommendations are for 0.5-1.0 en% in a diet containing 5-6 en% of linoleate.

Adolescent↗
PubMed1986

Translocation (2;3) in hematologic malignancies.

Cytogenetic studies have revealed nonrandom involvement of some chromosomes in specific structural abnormalities in human neoplasias. In this report we present three patients with t(2;3) associated with hematologic malignancies, and review the pertinent literature. These findings lead us to regard the region between 3q26 and 3q29 as implicated in chromosomal changes in these disorders, whereas, no vulnerable point has been observed in chromosome #2. We suggest that these translocations may activate genes on chromosome #3 related to these neoplasias.

Acute Disease↗
PubMed1986

Gender differences in prostacyclin and prostaglandin E2 synthesis by human endothelial cells.

The incidence of atherosclerosis and thrombosis is higher in males than in females. Gender differences in prostacyclin synthesis by rat aortic rings have been described. In this paper, sex differences in prostacyclin (PGI2, measured as 6-keto PGF1 alpha) and prostaglandin E2 (PGE2) synthesis by human endothelial cells isolated from the vein of umbilical cords are reported. Cells isolated from cords from male babies synthesized more prostacyclin and PGE2 than cells isolated from those from female babies when the cells were stimulated with 0.125 units of thrombin. The difference in PGI2 was eliminated by incubation with 0.5 units of thrombin. PGE2 synthesis was higher in males than in females using both 0.125 and 0.5 units of thrombin. Incubation of the cells with culture medium containing 20% heat inactivated plasma from either male or female subjects did not have an effect upon prostaglandin synthesis. Our results support previous evidence obtained using rat aortas and show a higher response of male cells to thrombin stimulation than that of female cells.

Cells, Cultured↗
PubMed1985

Quantitative relationships between dietary linoleate and prostaglandin (eicosanoid) biosynthesis.

Essential fatty acid deficiency consistently depresses eicosanoid (prostaglandin E2, F2, and I2 and thromboxane) biosynthesis independent of sampling protocols. Tissue fatty acid analyses support the hypothesis that the decrease is due in part to depression of arachidonate and accumulation of eicosatrienoate (n-9). Research on the alteration of eicosanoid biosynthesis by dietary linoleate supplementation is reviewed extensively. Responses of whole blood, lung, liver and heart eicosanoid synthesis to feeding eight concentrations of dietary linoleate between 0 and 27 energy percent are reported. It is concluded that stimulation, depression and no change in eicosanoid production could be equally well documented as a response to linoleate supplementation. Evidence for the obvious mechanism that alterations in precursor fatty acid composition are a possible explanation is fragmentary and inconsistent. The appropriate sampling techniques appear not to be established at this time and most likely are species, gender and tissue specific.

Animals↗
PubMed1985

Cholesterol metabolism in relation to aging and dietary fat in rats and humans.

A review of research in the authors' laboratories regarding effects of dietary fat polyunsaturation upon longevity in rats and some aspects of the regulation of cholesterol metabolism with regard to age of rats and humans is presented. The longevity of the rat was found to be enhanced by consumption of dietary fat providing a polyunsaturated to saturated fatty acid (P/S) ratio of 0.3 to 1, corresponding to about 5-12% of energy (en%) as linoleate, compared with less or more polyunsaturated fat. Mechanisms of the effects of the fats upon cholesterol metabolism were studied. With advancing age, there seems to be a decline in the rate of catabolism of cholesterol, resulting in longer retention in the body of the rat. In the human, there seems to be a decline in regulation of uptake of cholesterol by leukocytes and, therefore, perhaps other tissues, resulting in increased synthesis of cholesterol by the peripheral tissues. Moderate rather than high dietary consumption of polyunsaturated fat seems to be favorable to metabolic processes contributing to longevity.

Aging↗
PubMed1985

Portacaval shunt as treatment for hypercholesterolemia. Metabolic and morphological effects in a swine model.

Since 1973 the portacaval shunt has been used as a treatment for homozygous familial hypercholesterolemia. Favorable results have been reported, but the mechanism or reduction of cholesterol is not clear. The objective of this research was to evaluate mechanisms of lipid alterations after portacaval shunting in Yucatan miniature swine. The animals were fed a high-fat diet, similar in composition to the average American diet, with or without added cholesterol. Controls were fed the atherogenic diet (+ cholesterol) for 8 months. Pigs were fed atherogenic or American diets for 8 months, then surgery (shunt or sham) was performed. They were continued on the diets for another 8 months. The vascular system was examined for the distribution and severity of atherosclerotic disease. Blood lipids and numerous biochemical indices were measured. Progression of atherosclerosis was slowed by portacaval shunting. Low density lipoprotein (LDL) concentrations were positively and high density lipoprotein (HDL) concentrations were negatively correlated with severity of atherosclerosis. Serum insulin concentrations were positively correlated with atherosclerosis. Cholesterol synthesis was increased by the shunting and decreased by cholesterol feeding. The cholesterol-fed swine is not an adequate model for familial hypercholesterolemia, but the results are consistent with inhibition of the atherosclerotic process and the involvement of lipoproteins and insulin in the mechanisms.

Animals↗
PubMed1983

Oxidative interactions between fatty acid peroxy radicals and quinones: possible involvement in cyanide-resistant electron transport in plant mitochondria.

The interactions between duroquinol, linoleic acid, and lipoxygenase have been followed spectrophotometrically in the uv (210-340 nm) in a simple reaction medium (5 mM [4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid] buffer, pH 6.0). Duroquinol is oxidized by reacting with the peroxy radicals of linoleic acid generated in the presence of lipoxygenase. This oxidation is insensitive to cyanide but is sensitive to salicylhydroxamic acid, propylgallate, and disulfiram, the known inhibitors of lipoxygenase and of the cyanide-resistant electron transport pathway of plant mitochondria. This reaction is proposed as a model for the functioning of this pathway in plant mitochondria.

Benzoquinones↗
PubMed1983

Lipoprotein lipid and protein responses to dietary fat and diabetes in rats.

Dietary and insulin-deficiency types of hyperlipidemia were compared in adult normal and streptozotocin-induced diabetic male breeder rats. High beef tallow, high corn oil or low fat diets (BT, CO and LF, respectively) were fed ad libitum for 2 months. Glucose and insulin were measured in plasma and total cholesterol, free cholesterol, cholesteryl ester, triglycerides and apoproteins in very low density, low density and high density lipoproteins (VLDL, LDL and HDL, respectively). Diet did not affect plasma glucose or insulin levels. LDL-triglycerides were higher in BT and diabetic than in CO and LF rats. HDL-free cholesterol levels were higher in CO- and LF-than in BT-fed rats. Diabetes resulted in a decrease in HDL-cholesterol. Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. VLDL-triglycerides were higher in diabetic than in normal rats, with no dietary differences in normal rats. In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. Diabetes resulted in an increase in LDL-apoB but a decrease in LDL-apoE. HDL-apoE levels were higher, although HDL-apoA-I levels were lower in LF than in high fat-fed rats. The results related to lipoprotein composition supported the hypothesis that excess intake of a diet high in saturated fat may contribute to a metabolic pattern that resembles that of a diabetic state.

Animals↗
PubMed1983

Effects of prostaglandin modifiers and zinc deficiency on possibly related functions in rats.

Experiments were conducted to investigate the role of prostaglandins (PG) in zinc absorption and biological functions (food intake and weight gain, alkaline phosphatase activity, T-cell-mediated immune response). PG levels were modified by administering an inhibitor of their synthesis, aspirin or indomethacin in the diet. Zinc level was modified by controlling the dietary concentration. Weanling rats were fed the assigned diets for 1 month after which they were anesthetized with ether. Samples of blood, gut contents and mucosa, liver, lung and tibia were collected for zinc, PG, lymphocyte stimulation with T-cell mitogen, and alkaline phosphatase assays. There was more than 50% inhibition of PG synthesis by indomethacin and aspirin. This inhibition of PG synthesis, however, did not affect the zinc status of the rats as measured by general appearance, food intake, weight gain, organ weight, zinc concentration in different organs, serum alkaline phosphatase activity, and cell-mediated immune response to T-cell mitogens. It is concluded that under physiological conditions inhibitors of PG synthesis do not alter these zinc metabolic functions.

Alkaline Phosphatase↗
PubMed1983

[Desynchronization of the circadian rhythm of oral temperature in young human subjects with poor tolerance for night work].

15 night workers (mean age, 28 years; mean seniority 1.5 years) volunteered to measure their oral temperature (clinical thermometers 0.05 degrees C precision) 5 times/24 hrs. during a 21 day span. Time series were analyzed individually according to 3 methods. 11 of the subjects with a good tolerance had (with one exception) their prominent circadian period tau equal to 24 hrs. as well as a relatively large circadian amplitude (A from 0.19 to 0.42 degrees C). By contrast, subjects with a poor tolerance (sleep disorders, persisting fatigue, psychological troubles, etc.) had a tau value ranging from 24.9 to 25.7 hrs. associated with a relatively small rhythm amplitude (A from 0.04 to 0.13 degrees C). These results support the hypothesis that a desynchronisation of circadian rhythms help to explain why certain subjects do not tolerate shiftwork.

Adult↗
PubMed1982

Effects of diet composition and fasting on glucose turnover in lean and polygenic obese mice.

Effects of high beef tallow (BT), high corn oil (CO) or low-fat (LF) diets upon the outcome of genetic obesity were investigated. Diets were instituted ad libitum at the time of weaning. When mice were six months of age, blood samples were taken 1, 5, 15, 30, and 60 minutes after intravenous injection of glucose-U-14C. Within dietary treatments, obese and lean mice showed similar plasma glucose-U-14C disappearance patterns. Plasma glucose disappearance always tended to be faster in ad libitum-fed mice relative to 24-hour fasted mice. Body glucose pool sizes tended to be larger in fed obese BT and LF mice compared to their lean counterparts. This pattern was not seen in non-fasted CO mice. Fasting caused a decrease in body glucose pool sizes in all mice. In contrast to CO and LF mice, lean BT mice appeared to conserve glucose during fasting the same as the obese line. Since the glucose disappearance curves can be described by a two-exponential decay function, at least a two-component or two-pool system must be involved in plasma glucose turnover. Calculated rate constants were used to express interchanges of carbon molecules between the glucose and glycogen pool and the net movement of glucose carbon to a carbon pool representing "irreversible end products". The data indicate that differences in glucose metabolism, in part, explain the possibility that dietary energy source can overcome the genetic tendency to leanness.

Animals↗
PubMed1982

Effect of zinc deficiency on prostaglandin synthesis in different organs of the rat.

Zinc has been implicated in regulation of some aspects of prostaglandin (PG) metabolism. Effects of zinc deficiency, on PG synthesis and secretion were examined. Weanling rats were fed a control (adequate in zinc) or a zinc-deficient diet for 30 days. A third group was pair-fed to the zinc-deficient group with the control diet. The rats were anesthetized with ether, and tissues were excised for analysis. Zinc concentrations were measured in plasma, gut contents, gut mucosa, liver, lung and tibia. Prostaglandins F2alpha, E1, E2, thromboxane B2 (TXB2), 6-keto PGF1alpha (metabolite of PGI2, met I2) and 13, 14-dihydro-15 keto PGF2alpha (met F2alpha) were measured by radioimmunoassay. The results indicate that, with the exception of gut contents, in most organs studied and for most PG measured, food restriction is as effective in reducing PG level as zinc deficiency. In the gut contents, however, there was a positive correlation between zinc and PGE1 concentrations, and zinc deficiency decreased PGE1, PGF2alpha and PGI2 metabolite levels beyond food restriction. The decrease in PG concentrations of gut contents without any change in their mucosal concentrations suggests an active process of PG secretion involving zinc. In addition, in serum from clotted blood, zinc deficiency increased the level of met F2alpha (p less than 0.05), suggesting that zinc might be involved in control of PG levels by changing PG degradation rate.

Alprostadil↗
PubMed1982

Linoleic acid absorption in children with cystic fibrosis.

When safflower oil (triglyceride) was consumed without pancreatic enzymes by children with cystic fibrosis (CF), there was no rise in mean plasma linoleic acid levels over the next 4 h. When linoleic acid monoglyceride (LAM) was consumed, the increase in plasma linoleic acid levels was significantly greater than for safflower oil at 2 (p less than 0.02), 3 (p less than 0.01), and 4 h (p less than 0.01). When free fatty acid (hydrolyzed safflower oil) was ingested, there was almost no increase in plasma linoleic acid levels in CF or control children. The absorption of linoleic acid from triglyceride, but not from LAM, was greater when the CF children also took pancreatic enzymes. Three children with CF had greater increases in plasma linoleic acid levels following ingestion of safflower oil when they took antacid and cimetidine with their pancreatic capsules, compared to when they only took the pancreatic capsules.

Antacids↗
PubMed1982

Interaction between Mitochondrial Cytochromes and Linoleic Acid Hydroperoxide: POSSIBLE CONFUSION WITH LIPOXYGENASE AND ALTERNATIVE PATHWAY.

O(2) uptake by tissue extracts in the presence of linoleic acid is generally ascribed to lipoxygenase. Such an O(2) uptake can be observed not only with mitochondria of Solanum tuberosum L. and Arum maculatum L. and pure lipoxygenase but also with cytochrome c. However, the rate of oxidation is highly dependent on the procedure used to prepare the solutions of linoleic acid. Unless special care is taken to prevent contact between linoleic acid and O(2), it appears that linoleic acid hydroperoxide is readily formed. This derivative can be readily oxidized by mitochondria or cytochrome c. On the other hand, the use of a rapid and specific enzymic procedure to estimate the disappearance of linoleic acid demonstrates that linoleic acid itself is not consumed at any appreciable rate by mitochondria or cytochrome c, the true substrate being linoleic acid hydroperoxide. During the reaction, the heme nucleus of added cytochrome c or of mitochondrial cytochromes undergoes deep alterations. Therefore, caution should be exerted when equating an O(2) uptake observed in the presence of linoleic acid to a lipoxygenase activity. The same holds true for the similarity of reaction towards specific inhibitors between lipoxygenase and the cyanide-insensitive pathway oxidase.

Journal Article↗