This study was conducted to examine the effect of insulin on lipid metabolism of adipocytes during pregnancy and lactation in ewes. During the first 3 mo of pregnancy, metabolism of adipocytes from omental adipose tissue was characterized by a high rate of de novo lipogenesis (90 to 125 nmol of acetate incorporated into lipids.2 h-1.10(6) cells-1) and a 38% reduction in response to beta-lipolytic stimulus (isoproterenol 10(-6) M). Simultaneously, there was a rise in the number of high-affinity insulin receptors (Kd = .2 nM), and insulin binding characteristics showed a decrease in the negative cooperativity phenomenon. Moreover, lipogenesis stimulated by insulin (1 mU/ml) increased in comparison with observations in nonpregnant ewes. The last third of pregnancy and early lactation were characterized by a marked fall in lipogenesis and a simultaneous increase in isoproterenol-stimulated lipolysis. During lactation, the number of total insulin receptors was decreased by 62% and insulin stimulation of lipogenesis became inefficient. Results suggest that insulin plays a direct role in adipose tissue metabolism during pregnancy.

In this paper, in Table 4, the values for 20:3n-6 for kidney should read 1.0 _+ 0.2 for lean rats and 1.3 _+ 0.25 for obese rats (rather than 0.5 + 0.2 and 0.3 +_ 0.1), and for heart 0.3 _+ 0.1 for lean rats and 0.7-+ 0.2 c for obese rats (rather than 0.7 _+ 0.2 and 0.5 +_ 0.1). In Table 6, the obese/lean ratios for brain for the A6-desaturase index should be 1.25 (and not 0.80), and for the A5-desaturase index 0.75 (and not 1.32). Study on the Lipid Composition of Aging Fisher-344 Rat Lymphoid Cells: Effect of Long-Term Calorie Restriction Serge Laganiere and Gabriel Fernandes Lipicls 26, 472-478 (1991) In Table 2 of this paper, the value for 20:4 for long-term calorie restricted rats (LCR) at 12 months should be 17.98 _+ 0.61 (rather than 7.98 _+ 0.61). Similarly in Figure 3, upper right panel, the shaded LCR bar at 12 m for 20:4 should extend to 17.98 _+ 0.61 (rather than to 7.98 _+ 0.61).

Summary. The effects of a dietary a-linolenic acid (18 : 3 n-3) deficiency on lipid fatty acid composition of the liver and serum of lactating rats have been studied during three gestations and over three generations. These females were compared to corresponding females which remained sterile.

Summary. The effects of a dietary a-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 a-linolenic acid than the soya diet (6 mg vs 130 mg/100 g of diet).The results showed that, in our experimental conditions, the a-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.

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.