Polyunsaturated fatty acid-rich diets: effect on adipose tissue metabolism in rats.

The aim of the present study was to evaluate the effect of diets rich in n-6 and n-3 fatty acids on adipose tissue metabolism. Starting at weaning, male Wistar rats were fed ad libitum, for 8 weeks with one of the following diets: C, rat chow; S, rat chow containing 15 % (w/w) soyabean oil; F, rat chow containing 15 % (w/w) fish oil; SF, rat chow containing 15 % (w/w) soyabean and fish oil (5:1, w/w). Casein was added to the fat diets to achieve the same 20 % (w/w) protein content as in the control chow. Food intake and body weight were measured weekly. The rats were killed by decapitation and the retroperitoneal (RET) and epididymal (EPI) white adipose tissues were removed and weighed. Tissue lipid and protein content, in vivo lipogenesis rate, uptake of diet-derived lipids, in vitro lipolytic rate, adipocyte area, lipoprotein lipase, ATP citrate lyase, and malic enzyme activities were evaluated. Carcass lipid and protein contents were also measured. Energy intake was reduced while carcass lipid content was increased in the three fat-fed groups. However, carcass protein and body weight gains were elevated only with diets F and SF. Lipolysis rate was diminished by diets F and SF, while the uptake of diet-derived lipids was elevated by the diet S in both RET and EPI tissues. These metabolic alterations may have contributed to the increase in in vivo lipogenesis rate in the presence of decreased ATP citrate lyase and malic enzyme activities induced by the three lipid diets. These results indicate that enrichment of the diet with polyunsaturated fatty acids causes changes in adipose tissue metabolism that favour fat deposition. Different metabolic pathways were preferentially affected by each type of fatty acid used.

Ethanol intake during lactation. I. Effects On dams' metabolism and pups' body weight gain.

Wistar lactating rats (8 pups per dam) had free access to either tap water (control group, C) or one of three concentrations of ethanol (E) in the drinking water: 5% (E5), 10% (E10), and 20% (E20). All animals received normal rat chow ad libitum and were killed on day 12 of lactation. Intake of both 10% and 20% ethanol solutions decreased food intake, dams' body weight, and pups' body weight gain as compared with findings in the C group. The relative weights (g/100g b.w.) of the mammary glands (MG) and of the parametrial white adipose tissue depot were decreased only in E20 as compared with findings in the C group. Protein and lipid content of these tissues were not altered in any of the ethanol groups. In comparison with the C group, the lipogenesis rate was increased in the MG (135. 6%) and liver (120.2%) in E5 and the MG (58.1%) and parametrial white adipose tissue depot (147.0%) in E20. No modifications in lipogenesis rate were noted in E10. The malic enzyme activity was decreased in the MG in E10 (25.3%) and E20 (26.4%) and in the liver in E20 (45.7%). In E5, however, it was increased in the liver (23. 9%). The activity of ATP-citrate lyase in the liver was decreased in E20 (56.7%), while it was increased by 37.5% in E5 and 34.2% in E10. Blood glucose concentration of dams was not affected by ethanol ingestion. However, plasma triacylglycerol concentration was higher in E10 (17.9%) and E20 (13.3%) than in the C group, and plasma protein was lower in E20 (15.7%) than in C. We concluded that alcohol intake during lactation increased the MG lipogenesis rate; although at the highest dose, this metabolic alteration was not enough to allow normal pups' growth. However, the low dose of ethanol (5%), despite having altered dams' metabolism, did not affect pups' body weight gain.

Ethanol intake during lactation. II. Effects On pups' liver and brain metabolism.

Lactating rats, with litters adjusted to 8 pups on day 1, were divided into 4 groups: control animals (C), which received water and Nuvilab chow ad libitum, and ethanol animals (E), which received 20% (E20), 10% (E10), or 5% (E5) ethanol diluted in the drinking water and Nuvilab chow ad libitum. On day 12 of life, the pups were weighed and decapitated. The intake of 10% and 20% ethanol solutions by the lactating rats decreased the pups' body weight and liver weight. The pups' liver ATP-citrate lyase activity was decreased in all ethanol groups. The pups' brain weight decreased in E20 only. Glucose metabolism and lactate production were studied in the pups' brain slices, which were incubated at 37 degrees C in Krebs-Henseleit buffer under carbogen in the presence of glucose (5 mM) plus 14C-glucose (0.04 microCi) with or without beta-hydroxybutyrate or insulin. Study of the incubated pups' brain slices showed that the intake of the 20% ethanol solution by the dams increased glucose consumption, oxidation, lactate production, and lipogenesis rate from glucose in all media studied, as compared with findings in the C group. In the pups' brain slices, the lactate production and lipogenesis rate from glucose were higher in E10 than in the C group. The addition of beta-hydroxybutyrate to the incubation medium caused a decrease in glucose oxidation in C, E5, and E20 and an increase in glucose consumption in E10. Ingestion of the 5% ethanol solution by dams decreased the pups' brain lipogenesis rate from glucose in all media studied. We concluded that the effects of maternal alcohol intake on the pups' development and metabolism are dose-dependent. High amounts of ethanol intake (10% or 20%) caused a great impairment in the pups' growth, as well as their liver and brain metabolism. The low dose (5%) did not affect the pups' body weight gain or their brain and liver weight, but it did alter brain glucose metabolism.

Effect of adrenalectomy and glucocorticoid therapy on lipid metabolism of lactating rats.

Although adrenal glucocorticoids were known to be important for adequate milk production, little is known about their effects on the metabolism of mammary glands during lactation. In this study, lactating Wistar rats on the 12th day of lactation were divided in the following groups: sham-operated (SO) and adrenalectomized (ADX) receiving no treatment; SO and ADX starved for 24 h and refed intragastrically with 2.5 ml of 50% glucose solution, 2 h before the experiment (SOR and ADXR) and ADX receiving substitute therapy with dexamethasone (ADX + DEX). Sacrifices were performed 2 days after surgery. Weight, lipid content and in vivo lipogenesis rate were evaluated in mammary gland (M.GLAND), liver, parametrial white adipose tissue (PARA) and interescapular brown adipose tissue (BAT). ATP citrate lyase activity was measured in M.GLAND, liver and PARA of SO, ADX and ADX + DEX. The rate of lipogenesis and 14CO2 production from 14C-glucose by isolated acini from M.GLAND and plasma glucose were also determined. In ADX rats, food intake, lipid content, in vivo lipogenesis rate and ATP citrate lyase activity in M.GLAND were significantly lower than those in SO rats. The M.GLAND lipogenesis rate of SOR group was similar to the value found in SO rats. In ADXR rats, the M.GLAND lipogenesis rate was not normalized. However, the therapy with DEX elevated lipid content, in vivo lipogenesis rate and ATP citrate lyase activity to levels similar to those in SO. These results suggest that the glucocorticoids are essential for the occurrence of normal lipid synthesis in M.GLAND during lactation.