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J P Poisson

Publications and source records attributed to J P Poisson.

65 records · Page 4Linked to original sources
PubMed1983

[Effect of supplementation with gamma-linolenic acid on the fatty acid composition of lipids from the liver and plasma in the diabetic rat].

The main difference between normal and streptozotocic rat fed a diet, supplied during 35 days, including (as 1.5 g oil for 100 g diet) either naudicelle oil (with gamma-linolenic acid), either sunflower oil (without gamma-linolenic acid), or naudicelle oil + peanut oil, is that there are more non esterified fatty acids in streptozotocic livers. This result supports the view that liver phospholipids are more labile or that there is an important release of fat, even if we do not observe an increase of streptozotocic rat plasmatic non esterified fatty acids. Comparing normal and streptozotocic rat we found interesting results about fatty acids liver lipids composition: non esterified fatty acids are particularly rich in polyunsaturated fatty acids, mainly in linoleic and arachidonic acids, in diabetic rat. These results contribute to explain, to some extent, the important catabolism of polyunsaturated fatty acids in the diabetic rat, as they may reveal an increased activity of phospholipase A2 in this kind of animal. Naudicelle oil in the diet is, in our experiment, without favourable results on the amount of different lipidic classes and their fatty-acids composition, into liver and plasma of the streptozotocic rat, comparatively to the rat administered with sunflower oil; this may be explain by the fact that gamma-linolenic acid was in restricted amount in the diet and that its own conversion was partially inhibited by diabetes.

Animals↗
PubMed1980

[Dietary alpha-linolenic acid and arterial pressure in the rat].

The effect of dietary alpha-linolenic acid (18: 3 n-3) upon the arterial pressure of rats has been studied. Three experiments were carried out on rats of different ages that were fed a diet containing alpoha-linolenic acid in the form of Primor oil (rapeseed oil low in erucic acid). Control animals were fed a peanut oil diet and a third group of rats was fed a low-lipid, commercial diet. The arterial pressure of the rats was periodically measured. After a two- or three-month period (depending on the experiment), the rats were killed. Some of the livers were taken out and their fatty acids analysed. Comparing the results obtained in the rats fed on the alpha-linolenic acid diet with those of the control rats, we found that: (1) Dietary alpha-linolenic acid brought about no noticeable effect upon arterial pressure. (2) The arachidonic: linoleic (w/w) ratio in the liver lipids was lowered in the animals that had received alpha-linolenic acid, indicating a partial inhibition of the biosynthesis of arachidonic acid in these rats. Two hypotheses have been tentatively proposed to explain the absence of hypertensive effect following the administration of alpha-linolenic acid, in spite of its inhibitory effect upon the conversion of linoleic acid into polyunsaturated fatty acids which are the precursors of prostaglandins in rats.

Animals↗
PubMed1979

[Effect of the streptozotocin diabetes upon the in vivo conversion of [I-14C] gamma-linolenic and dihomo-gamma-linolenic acids into arachidonic acid in rats (author's transl)].

Streptozotocin diabetic rats were administered the same tracer dose of either [1 14C] gamma-linolenic or [1 14C] dihomo-gamma-linolenic acid by stomach tube seven days after streptozotocin injection. They were killed 48 hours later and the radioactivity in individual fatty acids of the liver determined by radio-gas chromatography. Results were compared to those obtained in non diabetic rats similarly prepared. With either radioactive precursor, 14C radioactivity recovered in hepatic dihomo-gamma-linolenic acid was not significantly affected by the diabetic state. On the other hand, 14C radioactivity incorporated into arachidonic acid was considerably decreased in diabetic rats, compared with normal rats, when the weights of hepatic arachidonic acid were the same in the two groups of animals. These results suggest that streptozotocin diabetes causes a partial inhibition of the 5-desaturation of dihomo-gamma-linolenic acid in rat liver in vivo.

8,11,14-Eicosatrienoic Acid↗
PubMed1978

[Effect of dietary alpha-linolenic acid on the conversion of linoleic and gamma-linolenic acids (1-14C) into arachidonates in rats in vivo].

The effects of alpha-linolenic acid (9-12-15 octadecadienoic) upon the conversion in vivo of [1-14C] linoleic acid and of [1-14C] gamma-linolenic acid into arachidonate have been studied in adult rats. The two tracers have been administered by stomach tubing and the amounts of [14C]-radioactivity incorporated into arachidonate in the liver, kidneys and whole rat have been measured 48 h later. Three experiments have been carried out on rats fed on alpha-linolenic acid containing diets prior to the radioactive tubing. In these diets, alpha-linolenic acid was brought either as ethyl ester or in the form of Primor oil (erucic acid free rapeseed oil). In all of them, the ratio alpha-linolenic acid: linoleic acid did not exceed 0.45. Control animals were fed, in the same conditions, ethyl oleate or peanut oil respectively. Comparing the alpha-linolenic acid fed-rats to the control animals, we were able to observe the following results: (1) The exogenous supplies of alpha-linolenic acid used in the diets have not brought about any significant alteration in the amounts (weights) of arachidonic acid present in the liver, kidneys and whole animal. (2) Using [1-14C] linoleic acid as a precursor, the amounts of [14C]-radioactivity incorporated into arachidonate in the same organs as well as in the whole rat have been significantly lowered by dietary alpha-linolenate. (3) alpha-Linolenate, on the contrary, had no significant effect upon the amounts of radioactivity incorporated into hepatic, renal and whole body arachidonate following the administration of [1-14C] gamma-linolenic acid. These results lead to the conclusion that alpha-linolenic acid, when present in the diet of rats at a limited, phyisological level, partly inhibits the desaturation of linoleic acid in vivo but does not affect the subsequent reactions in the biosynthesis of arachidonic acid.

Animals↗
PubMed1975

[Metabolism of L-ascorbic, L-dehydroascorbic and 2,3-diketo-L-gulonic acids during a short duration fast in guinea pigs].

Tricolor variety of guinea-pigs, two or three months old, received, without sex distinction L(+)-ascorbic or L(+)-dehydroascorbic acids intraperitoneally injections as 20 mg p. 100 by weight, three or twenty-four hours after starting a forty-eight hours fast. Ascorbic, dehydroascorbic and 2,3 diceto-L-gulonic acids are estimated by the Roe, Mills, Oesterling and Damron differential 2,4-dinitrophenylhydrazin method in whole blood, urines, kidneys and liver. Food absorption during twenty-four hours after the end of the forty-eight hours fast is not suffisant for guinea-pigs regain first state, during this time, especially in their kidneys and liver. Three hours after the beginning of the fast, urinary excretion of the injected acid increases during the first twenty-four hours of fast; at the end of the forty-eight hours fast their kidneys are deficient in ascorbic acid. Twenty-four hours after the beginning of fast, urinary excretion of ascorbic, dehydroascorbic and 2,3-diceto-L-gulonic acids rises importantly, especially when L-ascorbic acid is injected; it is only the quantity of ascorbic acid which increases in their kidneys and liver, its level being higher in their liver. L-dehydroascorbic acid is utilized immediately. L-ascorbic acid is distributed slowly, stored in a reduced form and it prepares the animals to face a prolonged fast. When the animals are injected three hours after the fast begins, it will be protected for forty-eight hours; if it is injected twenty-four hours after the beginning of fast, the animal will be better prepared to face a prolonged state of stress or a fast lasting more than forty-eight hours.

2,3-Diketogulonic Acid↗
PubMedDate not supplied

Fatty acid metabolism, pharmacological nutrients and hypertension.

The purpose of the present study was to investigate the effect of a concentrated preparation (EPA 30) containing eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) on the limiting desaturation steps of the polyunsaturated fatty acid biosynthesis in spontaneously hypertensive rats (SHR). Adult SHR were divided into two groups: one group received a standard diet, and the experimental group the standard diet including 0.8% of EPA30 for 9 weeks. Blood pressure was measured at the end of the diets. The desaturase activities and fatty acid composition were determined in isolated hepatocytes. The blood pressure did not decrease in the experimental group. The desaturated products of the n-6 family (gamma-linolenic acid, 18:3 n-6 and arachidonic acid, 20:4 n-6) were lowered in the EPA30 group, when their respective substrates (18:2 n-6 and 20:3 n-6) were increased. EPA and DHA were higher in the experimental group delta 6 n-3, delta 6 n-6 and delta 5 n-6 desaturase activities were depressed approximately 20% in the EPA30 group. EPA30 being an active nutrient on the EFAs cascade, increasing the level of PG3 precursors and decreasing the level of PG2 precursors, favourable conditions have been established to reduce hypertension. The underlying mechanism related to the regulation of desaturase activities by these fatty nutrients remains to be elucidated.

Animals↗
PubMedDate not supplied

Spontaneous diabetes in bio-breeding rats: evidence for insulin dependent liver microsomal delta 9 stearic acid desaturation.

We studied liver microsomal delta 9 stearic acid desaturase activity and fatty acid composition of liver phospholipids and microsomal total lipids in the insulin-dependent spontaneously diabetic adult male Bio-Breeding rat. The diabetic Bio-Breeding rats (3 weeks of diabetes) were killed 48, 17 and 3 h after the last insulin injection (1.0 IU, 100 g body weight-1 day-1). Under these experimental conditions, delta 9 desaturase activity was defective during the normo- and hyper-glycaemic periods and restored during the hypoglycaemic period which followed the insulin injection to the diabetic rats. The fatty acid composition of diabetic rat liver phospholipids and microsomal total lipids were not consistent with delta 9 desaturase activity at the different periods of glycaemia and may be explained by factors other than disturbances of this desaturation.

Animals↗