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Vitamin A is a known regulator of adipose tissue growth. In this paper, we report the possible role of dietary vitamin A supplementation in the regulation of adipose tissue mass, using a novel obese rat model of the WNIN/Ob strain developed at the National Centre for Laboratory Animal Sciences of the National Institute of Nutrition, India. Twenty-four male lean and obese rats of the WNIN/Ob strain were broadly divided into two groups at 7 months of age; each group was subdivided into two subgroups consisting of six lean and six obese rats and they were given diets containing either 2·6 mg or 129 mg vitamin A/kg diet for 2 months. Feeding a high but non-toxic dose of vitamin A (129 mg/kg diet) resulted in a significant reduction in the adiposity index and retroperitoneal white adipose tissue (RPWAT) weight in obese rats while a marginal reduction was observed in lean rats. Further, this treatment resulted in a significantly increased RPWAT apoptotic index and Bax protein expression and a decreased expression of Bcl2 in the lean rats. However, no such changes were observed in the RPWAT of the obese rats subjected to identical treatment. Thus, our data suggests that chronic dietary vitamin A supplementation at a high dose effectively regulates adipose tissue mass both in the lean and obese phenotypes of the WNIN/Ob rat strain, perhaps through different mechanisms.

PUFA of the n-6 and n-3 series have beneficial effects on key risk factors of coronary heart disease (CHD). Our earlier studies on the intake of FA and on the FA composition of plasma and platelet phospholipids suggested the need to improve the n-3 PUFA nutritional status in the Indian population. The present long-term study was conducted on 80 middle-aged Indian subjects (40 men and 40 women) using the subjects' own home-prepared diets to evaluate the effects of dietary n-3 PUFA on biochemical indices of CHD risk. Substitution of Blend G (equal proportions of groundnut and canola oils) for groundnut oil or substitution of Blend S (equal proportions of sunflower and canola oils) for sunflower oil increased alpha-linolenic acid (ALNA) fourfold and decreased the linoleic acid (LA)/ALNA ratio from 35 to 6 and 65 to 9, respectively. Twelve subjects (six men and six women) who received Blend G were switched back to groundnut oil and were administered 0.3 g daily of long-chain (LC) n-3 PUFA from fish oil. At the end of the trial period for both blends in both sexes, plasma lipid and apolipoprotein levels had not changed, and ADP-induced aggregation had decreased. In plasma and platelet phospholipids, LA as well as LCn-3 PUFA had increased, suggesting competition between LA and ALNA for metabolism into the respective LC-PUFA. Fish oil supplementation increased LCn-3 PUFA in plasma and platelet phospholipids, decreased ADP-induced platelet aggregation, and increased plasma cholesterol. On the basis of the increased LCn-3 PUFA in plasma phospholipids, it was calculated that 0.75% energy (en%) (2.2 g) ALNA (from vegetable oils) may be required to increase LCn-3 PUFA to about the same extent as 0.1 en% (0.3 g) LCn-3 PUFA (from fish oils). Since both n-6 and n-3 PUFA play a critical role in fetal growth and development and in the programming of diet-related chronic diseases in adults, an improvement in the n-3 PUFA nutritional status in cereal-based diets through long-term use of cooking oils containing 25-40% LA and 4% ALNA may contribute to the prevention of CHD in Indians.