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Biomedical subjects

G Pascal

Publications and source records attributed to G Pascal.

At least 55 records · Page 3Linked to original sources

Dietary alpha-linolenic acid deficiency in the rat. I. Effects on reproduction and postnatal growth.

The effects of a dietary alpha-linolenic acid (18 : 3 n-3) deficiency on reproduction and postnatal growth in rats were studied during 3 successive gestations and 4 successive generations. Female rats received respectively a semi-synthetic diet in which the lipids were incorporated either as sunflower oil at 1.5% (deficient diet) or as soya oil at 1.87% (control diet). Both diets supplied the same amount of linoleic acid (18 : 2 n-6) (940 mg/100 g of diet), but the sunflower oil supplied 22 times less alpha-linolenic acid than the soya diet (6 mg vs 130 mg/100 g of diet). The results showed that, in our experimental conditions, the alpha-linolenic acid deficiency had no effect on fecundity (% of pregnant females), fertility (number of pups/litter), pup birth weight, food intake and weight of pregnant or lactating females, or pup growth during suckling. However, this deficiency did cause abnormally high rates of perinatal mortality from birth to postpartum day 3, namely on the average, for successive gestations: 18.5% in deficient pups vs 5.2% in the controls, and for successive generations: 16.6% in deficient pups vs 5.3% in the controls. Rat n-3 PUFA requirement during reproduction has been discussed; it appears to be more than 100 mg/100 g of feed. But this need should also be estimated in relation to n-6 PUFA supply; for female rats during reproduction, the ratio n-6: n-3 should be less than 10.

Aging↗

Recovery of altered fatty acid composition induced by a diet devoid of n-3 fatty acids in myelin, synaptosomes, mitochondria, and microsomes of developing rat brain.

Rats were fed a semisynthetic diet containing either sunflower oil or soya oil. Half the litter fed with sunflower oil diet was changed to a soya oil diet when the pups were 15 days old (during active myelination). Fatty acid analysis was then performed on subcellular fractions of the animals fed (a) soya oil, (b) sunflower oil, and (c) soya oil replacing sunflower oil from the 15th day, to determine the speed of the recovery. All material from animals fed sunflower oil showed an important reduction in docosahexaenoic acid (22:6 n-3), compensated by an increase in docosapentaenoic acid (22:5 n-6), whereas arachidonic acid (20:4 n-6) was not affected. In all fractions examined, when sunflower oil was replaced by soya oil in 15-day-old pups the recovery started from the very first day but lasted more than 2 months (this recovery was determined by the increase of 22:6 n-3 up to the normal value and decrease of the 22:5 n-6). In addition a delay was found for myelin recovery, starting only from the 25th day.

Animals↗

[Choledochoduodenal anastomoses in biliary lithiasis].

In choledocholithiasis, after opening the common bile duct, we used to perform choledochoduodenostomy in old patients. The aim of this study was to evaluate our results in 77 patients. The mean age of the patients was 75 years. Twenty-two patients were operated for angiocholitis, 19 had jaundice, and 36 had gallstones without angiocholitis or jaundice. There was two hospital deaths (2.6 p. cent). All the patients but two could be traced. The mean follow-up was 6.7 years. Two patients had had transients episodes of angiocholitis. Twenty-five patients have dead. Expected mortality in french population corresponding in age and sex was 29 deaths. Our results suggest that choledochoduodenostomy is a safe and effective procedure in the management of calculous biliary tract disease for old patients.

Aged↗

Choledochoduodenostomy for calculous biliary tract disease.

After the opening of the common bile duct, several controversial procedures may be used. In choledocholithiasis, our preference is to perform choledochoduodenostomy in older patients. We report the results in 77 consecutive patients with a mean age of 75 years. There were two hospital deaths (2.6%). Follow-up ranged from six months to 15 years, with an average of 6.7 years. Fifty patients are alive and well. Twenty-five patients have died. Only two patients were unavailable for follow-up. Expected mortality in the French population corresponding in age and sex was 29 deaths and the overall survival is not different, including the two postoperative deaths. Delicate technique allows anastomoses to ducts of any size, with no difference in long-term survival compared with a French population similar in age and sex.

Aged↗

Comparative changes in the lipogenic enzyme activities and in the in vivo fatty acid synthesis in liver and adipose tissues during the post-weaning growth of male rats.

Changes in the specific activities of acetyl-CoA-carboxylase (ACX), malic enzyme (ME) and glucose-6-phosphate dehydrogenase (G-6-PD) were compared to changes in de novo lipogenesis measured by in vivo incorporation of [3H] of tritiated water into fatty acids of liver and of perirenal and dorsal subcutaneous adipose tissues. In the adipose tissues, the specific activities of the three enzymes rather closely followed fluctuations in the rate of fatty acid synthesis. In the liver, ACX and especially ME activities were satisfactory indicators of de novo lipogenesis; G-6-PD activity did not depend on de novo lipogenesis.

Acetyl-CoA Carboxylase↗

[Adipose tissue cellularity in the piglet as a function of the level of energy supply of the maternal diet and the number of young per litter].

Adipose tissue cellularity has been evaluated in piglets at birth and at weaning at 35 days in relation with the energy supply of the maternal diet during gestation (group B: 3 000 KcalED/day: group N; 6 500 KcalED/day; group H: 10 000 Kcal/day) and with the number of piglets per litter during suckling. This approximation was obtained by simultaneously measuring piglet carcass triglyceride content and the mean diameter of the lipid inclusions of the fat cell population. At birth there were no significant differences between N and H piglets. However, B piglets weighed less and had lower lipid stores than the piglets of the other two groups. This lower adiposity was due to the smaller number of fat cells (about--25%). A weaning piglet weight and adiposity depended on both the energy supply of the maternal diet during gestation and the number of piglets per litter. These differences were due to the number of fat cells; this number was usually greater when the maternal diet during gestation had a higher energy level and the number of piglets per litter was smaller. Between birth and weaning the number of fat cells increased by a factor related with the number of piglets per litter; this factor was 1.9 or 2.5, depending on whether the sow suckled 4 or 8 piglets.

Adipose Tissue↗

[Specific contribution of dietary polyunsaturated fatty acids of the n-3 series to the development of nervous system membranes].

Polyunsaturated fatty acids, especially omega 3 fatty acids, made a specific contribution to the nervous tissue. Retarded intrauterine growth caused a twofold reduction in the oligodendrocyte ratio of omega 3/omega 6 while the same ratio increased by more than twofold in the neurons. A fatty acid-poor diet composed of arachid or sunflower oil dramatically altered the composition of cells and subcellular particles when compared with a soya or rapeseed oil diet containing omega 3 fatty acids; phosphatidylethanolamine was particularly affected. Nerve cell culture showed that brain essential fatty acids are probably docosahexaenoic acid and arachidonic acid.

Animals↗

Alterations in the fatty acid composition of rat brain cells (neurons, astrocytes, and oligodendrocytes) and of subcellular fractions (myelin and synaptosomes) induced by a diet devoid of n-3 fatty acids.

Rats were fed through four generations with a semisynthetic diet containing 1.0% sunflower oil (6.7 mg/g n-6 fatty acids, 0.04 mg/g n-3 fatty acids). Ten days before mating, half of the animals received a diet in which sunflower was replaced by soya oil (6.6 mg/g n-6 fatty acids, 0.8 mg/g n-3 fatty acids) and analyses were performed on their pups. Fatty acid analysis in isolated cellular and subcellular material from sunflower-fed animals showed that the total amount of unsaturated fatty acids was not reduced in any cellular or subcellular fraction (except in 60-day-old rat neurons). All material from animals fed with sunflower oil showed an important reduction in the docosahexaenoic acid content, compensated (except in 60-day-old rat neurons) by an increase in the n-6 fatty acids (mainly C22:5 n-6). When comparing 60-day-old animals fed with soya oil or sunflower oil, the n-3/n-6 fatty acid ratio was reduced 16-fold in oligodendrocytes, 12-fold in myelin, twofold in neurons, sixfold in synaptosomes, and threefold in astrocytes. No trienes were detected. Saturated and monounsaturated fatty acids were hardly affected. This study provides data on the fatty acid composition of isolated brain cells.

Animals↗

Relative contribution of the main tissues and organs to body fatty acid synthesis in the rat.

Tritiated water was used to measure the rate of fatty acid synthesis in the main tissues and organs of 7-week old Wistar male rats in order to determine the relative contribution of each tissue to body fatty acid synthesis. We reached the following conclusions: (a) the liver is the main site of fatty acid synthesis, it alone synthesizes 42% of the newly synthesized fatty acids in the body. (b) The dissectable white adipose tissues synthesize 27% of the fatty acids in the body. This group of tissues is heterogeneous because the mesenteric adipose tissue alone contains 40% of the labeled fatty acids present in the white adipose tissues. (c) Besides the intestines, organs other than the liver play a negligible role (2% of the total) in fatty acid synthesis. (d) The skin contributes 7% of the body fatty acid synthesis. (e) The rest of the carcass, essentially composed of the musculature and the skeleton, contributes 18% of body fatty acid synthesis and accounts for 33% of the extrahepatic tissue fatty acid synthesis.

Adipose Tissue↗

Lipogenic capacity and relative contribution of the different tissues and organs to lipid synthesis in male rat.

The rates of 3H2O incorporation into total lipids and fatty acids were measured in vivo in the different organs and tissues of 7-week old male Wistar rats to compare the lipogenic capacity of those organs and tissues and to determine their relative contributions to body lipid synthesis. Our results were the following; (1) liver was the major site of the synthesis of total lipids and fatty acids (37 and 42%, respectively, of body synthesis); (2) white adipose tissues synthesized about 24% of the total lipids; mesenteric adipose tissue alone synthesizing 40% of the fatty acids produced in dissectable white adipose tissues; (3) skin showed low lipid synthesis but played an appreciable role in that synthesis (8% of the total) due to its large contribution to total body weight; (4) other organs (excluding liver) showed low lipid synthesis; however, that of the small intestine was 1-2% of body synthesis; (5) the rest of the carcass (mainly musculature and skeleton) contributed 25% to body lipid synthesis. The putative roles of the different tissues and organs in adipose tissue development have been discussed.

Adipose Tissue↗

In vivo changes in the rates of total lipid and fatty acid synthesis in liver and white adipose tissues of male rats during postweaning growth.

1. In suckling rats, lipid synthesis is low in liver and adipose tissues. The rest of carcass is the major site of body lipogenesis. 2. After weaning, lipid synthesis (per g of wet wt) strongly increases in liver, perirenal and subcutaneous adipose tissues, and rest of carcass. The relative contributions of liver and both adipose tissues to body lipogenesis are about 35-40 and 6-9% respectively, but the rest of the carcass is still the main site of lipogenesis up to the age of 50 days. 3. In adult rats, lipid synthesis (per g of wet wt) remains high in liver but is strongly reduced in adipose tissues and carcass. Liver becomes the principal site of body lipogenesis.

Adipose Tissue↗

[De novo lipogenesis: kinetics of in vivo incorporation of tritiated water 3H into fatty acids and total lipids of the liver, plasma, adipose tissue and carcass of the male rat].

Tritiated water 3H, injected by intraperitoneal route into 7-week old male Rats, was incorporated into lipids synthesized de novo. The Rats were killed 0, 3, 7, 10, 15, 30, 60 and 120 min. after tracer injection. The results show that an optimal interval of about 10 min. between tracer injection and animal sacrifice was necessary to obtain a correct estimate of lipogenesis de novo by avoiding intertissue exchanges.

Adipose Tissue↗

Cellularity of adipose tissue in fetal pig.

Adipose tissue cellularity was studied in the 85-day-old Large-White pig fetus. The aim of this work was to count the adipose cells of forming tissue in an animal species which could be a possible model for studying adipose tissue in humans. Using a morphometric method with electron microscopy, mean triglyceride volume per cell was determined independently of mean cell volume. This method is suitable for counting adipose cells in the early stage of differentiation whatever their size and lipid inclusion volume. Site-by-site dissection of adipose tissue was not feasible in the 85-day old fetus and adipose cell number was computed by dividing total carcass triglyceride volume by mean triglyceride volume per cell. The carcass triglyceride seemed to originate only from adipose cells. The mean total carcass triglyceride volume per fetus (1.84 g) was low but, owing to the low mean triglyceride volume per cell (180.28 microns3), the adipose cell number (11.15 X 10(9)) was relatively important, as it represented about 27% of the extramuscular adipose cell number in the Large-White adult pig (41 X 10(9)).

Adipose Tissue↗

[Effects of ingestion of an antioxidant, BHT, on the metabolism of ascorbic acid and vitamin A in rats].

The antioxidant foor additive, BHT, was fed to male rat for 28 days at a 0.5% concentration in a diet containing ascorbic acid or not. BHT intake had no effect on ascorbic and dehydroascorbic acid contents in the adrenals, spleen or liver, whether or not the diet contained ascorbic acid. When the ration included 100 mg/kg of ascorbic acid, BHT intake caused a sharp rise in urinary excretion of this compound. This data confirm the work of other authors studying an ascorbic acid-poor diet. These results indicate that BHT intake leads to increased synthesis of ascorbic acid. This augmentation would be the result of stimulating the biosynthesis pathway of uridyl-di-phospho-glucuronic acid, which is necessary to the elimination of BHT in the form of glucuroconjugate. BHT intake in an ascorbic acid-rich diet reduces hepatic vitamin A concentration by 44 p. 100 and the hepatic reserve of this vitamin by 22 p. 100. BHT detoxication, as that of other exogenous compounds, thus seems to cause increased vitamin A utilization.

Adrenal Glands↗

[Treatment of hypercholesterolemia in the male rat by introduction of soya oil supplemented or not with sardine oil in the diet].

Substituting soya oil for lard considerably reduced hypercholesterolemia in the male rat with induced hypercholesterolemia due to a dietary overlead of cholesterol and sodium deoxycholate. The decrement was more marked when a mixture of 80 p. 100 soya oil + 20 p. 100 sardine oil replaced the lard. This improvement of the hypocholesterolemic effect by adding sardine oil to soya oil was due to the long-chain fatty acids (mainly C20:5 and/or C22:5 n-3 in the fish oil).

Animals↗