Feeding rats a purified diet containing peanut oil with a low a-linolenic acid (18:3(n-3)j content resulted in lower amounts of (n-3) polyunsaturated fatty acids, mainly docosahexaenoic acid (22:6(n-3)|, greater amounts of docosapentaenoic acid (22:5(n-6)j in uterus phospholipids, and altered postnatal uterus development when compared with rats fed a diet containing peanut and rapeseed oils. Maximaldifferences in uterine growth, as measured by uterine weight, protein and DNA con tent, occurred between d 24 and 30 postpartum and disappeared near the end of sexual development (d 40). The induction of the progesterone receptor was not af fected, and serum estradici concentrations were not sig nificantly reduced in deficient animals. Moreover,growth response of the uterus to low doses of 17ß-estradiol (<5 |ig/kg) was significantly reduced in ovariectomized animals fed the diet containing only peanut oil. However, the maximal response of the uterus, observed with higher 17ß-estradiol doses (5-50 ng/kg), was not af fected. Because the two diets used differed in the content of a-linolenic acid, it is likely that a-linolenic acid deficiency in animals fed the diet containing only peanut oil was the cause of the affected uterine development. J. Nutr. 122: 1529-1535, 1992.

The fatty acid composition of serum total lipids, of phospholipids of various organs (liver, heart, kidney), and of nervous structures (brain, retina, sciatic nerve, myelin, synaptosomes) have been compared in lean (Fa/-) and genetically obese (fa/fa) Zucker female rats. Both received a standard commercial diet including 37% of 18:2n-6 and 5% of n-3 polyunsaturated fatty acids (PUFA), 1.7% of which were in the form of 20:5n-3 and 22:6n-3. In comparison with lean rats, the results for the obese rats pointed out (i) no difference in the fatty acid composition of nervous structures; (ii) a decrease of 18:2n-6 (from -8% to -35%) and of 20:4n-6 (from -9% to -49%) in serum, liver and in kidney; this was compensated for by an increase in 20:3n-6 (from +30% to +320%) and in total n-3 PUFA (from +68% to +76%); (iii) a decrease of 20:4n-6 (-18%) and of 22:6n-3 (-24%) in heart compensated for by an increase in 18:2n-6 (+39%) and in 20:3n-6 (+233%); and (iv) constant levels of total PUFA (n-6 and n-3) in the various fractions studied, except in serum where this level decreased (-23%). Finally, except for the nervous structures, tissue phospholipids of obese rats included a lower proportion of 20:4n-6 and a higher proportion of 20:3n-6. This resulted in a significant reduction in the 20:4n-6/20:3n-6 ratio; by contrast, the 20:3n-6/18:2n-6 ratio increased. The results suggest that in Zucker rats, the obese character (fa/fa) affects the desaturation-elongation process of 18:2n-6 to 20:4n-6 by specifically decreasing delta 5-desaturase activity.

Feeding rats a purified diet containing peanut oil with a low α-linolenic acid [18:3(n-3)] content resulted in lower amounts of (n-3) polyunsaturated fatty acids, mainly docosahexaenoic acid [22:6(n-3)], greater amounts of docosapentaenoic acid [22:5(n-6)] in uterus phospholipids, and altered postnatal uterus development when compared with rats fed a diet containing peanut and rapeseed oils. Maximal differences in uterine growth, as measured by uterine weight, protein and DNA content, occurred between d 24 and 30 postpartum and disappeared near the end of sexual development (d 40). The induction of the progesterone receptor was not affected, and serum estradiol concentrations were not significantly reduced in deficient animals. Moreover, growth response of the uterus to low doses of 17β-estradiol (<5 μg/kg) was significantly reduced in ovariectomized animals fed the diet containing only peanut oil. However, the maximal response of the uterus, observed with higher 17β-estradiol doses (5–50 μg/kg), was not affected. Because the two diets used differed in the content of α-linolenic acid, it is likely that α-linolenic acid deficiency in animals fed the diet containing only peanut oil was the cause of the affected uterine development.

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The combined effects of age and dietary n-6 and n-3 fatty acids were studied in 3-, 6- and 9-month-old rats. At each age, two groups were fed diets containing 5% (w/w) of vegetable oils rich in either 18:3n-6 (borage group) or 18:3n-6 plus 18:4n-3 (black currant group), for a period increasing with age. A control group was fed the essential fatty acids 18:2n-6 and 18:3n-3 only. For each group, delta 6, delta 5 and delta 9 desaturase activities were measured in liver microsomes, and fatty acid composition was determined in microsomal phospholipids. Desaturase activity varied as a function of age and dietary lipids. delta 6 Desaturation of 18:3n-3 was more sensitive to these factors while delta 6 desaturation of 18:2n-6 and delta 9 desaturation were more dependent on season than the other two. Desaturase activity was influenced more by the black currant than by the borage diet, especially at 6 and 9 months of age. A large proportion of arachidonic acid was maintained in the microsomes independent of the diet. Changes in the fatty acid composition did not strictly reflect the differences in desaturase activities. The effects of the two factors (age and diet) on the activities of the desaturases are complex, suggesting that the enzymes are susceptible to other factors as well.

Previous studies have shown that rats exposed to 3,3′,4,4′-tetrachlorobiphenyl (TCB) exhibit decreased liver vitamin A stores. The activity of retinyl ester hydrolase (REH), the enzyme responsible for the hydrolysis of the storage form of vitamin A (retinyl esters) into free retinol, may therefore be altered by TCB. This study was carried out to investigate the effect of TCB on vitamin A distribution and on REH activity in the rat. REH activity was measured in liver homogenates and microsomes (650 μg protein), in Tris-maleate buffer 0.1 M at pH 7.2 in the presence of 150 mM CHAPS and 1.5 mM retinyl palmitate dispersed in Triton X-100 0.2%. Using these conditions, the kinetic parameters of the enzyme were determined and the inter-animal variation coefficient (10%) allowed statistical comparisons between experimental groups. Male Wistar rats of sufficient or deficient vitamin A status were treated IP with 340 fimol of TCB/kg. Vitamin A levels were significantly depressed in liver. REH activity was decreased about 20%, and serum retinol was decreased about 50%, independent of the initial vitamin A status of the animals. Vitamin A levels in lungs and testes were also decreased, suggesting that TCB could interfere with vitamin A delivery to target organs. The negative effect of TCB on REH activity in vivo was also observed when TCB was added in vitro to the incubation medium at concentrations near to those expected after in vivo treatment. TCB is a non-competitive inhibitor of retinyl palmitate hydrolase.

Liver nuclei, prepared from normal and vitamin A‐deficient rats, were incubated in the presence of GDP‐(14C)mannose or UDP‐N‐acetyl(14C)glucosamine and the labelled glycoproteins analysed by SDS PAGE. Fluorographic analysis has shown that (14C) mannose labelling is enhanced by vitamin A deficiency whereas N‐acetyl(14C)glucosamine transfer remains approximately at the same level regardless of the vitamin A status; we did not notice any modification when the proteins were monitored by Coomassie blue or by silver nitrate.

Liver nuclei, prepared from normal and vitamin A-deficient rats, were incubated in the presence of GDP-(14C)mannose or UDP-N-acetyl(14C)glucosamine and the labelled glycoproteins analysed by SDS PAGE. Fluorographic analysis has shown that (14C) mannose labelling is enhanced by vitamin A deficiency whereas N-acetyl(14C)glucosamine transfer remains approximately at the same level regardless of the vitamin A status; we did not notice any modification when the proteins were monitored by Coomassie blue or by silver nitrate.

Mature male Sprague-Dawley rats received a single IP injection of either 2,2',4,4',5,5'-hexachlorobiphenyl (HCB), 3,3',4,4'-tetrachlorobiphenyl (TCB) (300 microm/kg) in corn oil (10 ml/kg) or the corn oil vehicle alone, and were killed four days later after having been fasted overnight. The vehicle control group consisted of rats which were allowed free access to feed as well as pair-fed animals. Lipid analyses were conducted on liver, hepatic microsomes and serum. TCB- (but no HCB-) treatment resulted in a statistically significant increase in total liver lipids and triglycerides. Liver phospholipids remained unchanged. Both PCBs increased the cholesterol and phospholipids content of the liver microsomal fraction. Serum lipids measured were not statistically different from control values. While HCB had little effect on the fatty acid composition of liver lipids, TCB caused an increase in C 18:1 (n-9) and a decrease in C 20:4 (n-6). Both PCBs increased C 18:0 in the hepatic microsomal fraction, but TCB also decreased C 16:0. Neither PCB altered the fatty acid composition of serum total lipids. These data are consistent with the concept that specific alterations in lipid metabolism are dependent on the structure of the PCB.

The sciatic nerve of rats fed sunflower oil (6 mg 18∶3n−3/100 g of diet) presented dramatic alterations in the long chain polyunsaturated fatty acids in comparison with those fed soy oil (130 mg 18∶3n−3/100 g of diet). In both 15-day-old and 60-day-old animals fed sunflower oil, 22∶6n−3 (cervonic acid) was fourfold less, 22∶5n−6 was 10-fold greater; adrenic acid (22∶4n−6) was slightly greater and arachidonic acid (20∶4n−6) was close to that in rats fed soy oil. The percentage distribution of total polyunsaturated fatty acids as well as the individual saturated and monounsaturated fatty acids were the same in both groups.

Study by electron spin resonance (ESR) of N (3,5-diterbutyl-4 hydroxybenzyl) 4 amino 2,2,6,6-tetramethylpiperidinyl oxy: ‘BHT-amino TEMPO’, a paramagnetic analog of BHT, incorporated into the usual compound of rigid polyvinyl chloride (PVC) revealed that after contact of the labelled polymer with aqueous media (water, 3% acetic acid, 20% ethanol) the BHT-amino TEMPO migrated and that the structure of the polymer was altered after 10 days of immersion at 50°C. This modification was assigned to the penetration of the aqueous media into the PVC. The ESR spectrum of the modified polymer consisted of two superimposed signals, the first one corresponding to BHT-amino TEMPO highly immobilized in the plastic material and the second to the same molecule moving more freely in spaces probably occupied by the solvent. Estimates of BHT-amino TEMPO levels in the immersion media seemed to indicate that they were of the same order of magnitude as the losses of the freer markers in the PVC after 10 days of immersion at 50°C.

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.

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.

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.

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.