dinoprost and Nutrition-Disorders

We examined the effects of undernutrition on lipid metabolism in reindeer (<1 year) during mid-winter and spring, with particular focus on the proportions of polyunsaturated fatty acids (PUFAs) in major serum lipids. The reindeer (n=8) were fed their winter feed, lichen, ad libitum for 5 weeks, followed by 40% restriction of energy for 8 weeks and refeeding to normal for 6 weeks. The concentrations of major serum lipids, cholesterol and phospholipids decreased significantly during the ad libitum period (by 50 and 44%, respectively). The proportion of major PUFA, linoleic acid in serum cholesteryl esters, decreased from 48.2 to 38.4% during the ad libitum period (P < 0.01), and to 29.2% during the restriction period (P < 0.001). The proportion of linoleic acid in phospholipids decreased from 27.9 to 15.6% during the ad libitum period (P < 0. 001), and to 13.0% during the restriction (P < 0.01). Also alpha-linolenic acid in the major lipids decreased significantly during the ad libitum and restriction periods. The decreases in the major lipids and linoleic acid were reversed during the refeeding. The control group (n=8) which was fed high-quality concentrates ad libitum gained weight most of the spring but showed similar although slower decreases in the major serum lipids and PUFAs than the lichen group. Our results indicate that feeding reindeer on lichen during winter leads to the retardation of growth and reductions in major serum lipids and their principal C18-PUFA proportions. The decreased proportions of the principal PUFAs most probably reflect their low dietary intake but may have been modified also by seasonal factors.

Topics: Animals; Blood Glucose; Body Weight; Cholesterol Esters; Diet; Dinoprost; Eating; Fatty Acids, Unsaturated; Lipids; Male; Nutrition Disorders; Reindeer; Seasons

Zinc has been implicated in regulation of some aspects of prostaglandin (PG) metabolism. Effects of zinc deficiency, on PG synthesis and secretion were examined. Weanling rats were fed a control (adequate in zinc) or a zinc-deficient diet for 30 days. A third group was pair-fed to the zinc-deficient group with the control diet. The rats were anesthetized with ether, and tissues were excised for analysis. Zinc concentrations were measured in plasma, gut contents, gut mucosa, liver, lung and tibia. Prostaglandins F2alpha, E1, E2, thromboxane B2 (TXB2), 6-keto PGF1alpha (metabolite of PGI2, met I2) and 13, 14-dihydro-15 keto PGF2alpha (met F2alpha) were measured by radioimmunoassay. The results indicate that, with the exception of gut contents, in most organs studied and for most PG measured, food restriction is as effective in reducing PG level as zinc deficiency. In the gut contents, however, there was a positive correlation between zinc and PGE1 concentrations, and zinc deficiency decreased PGE1, PGF2alpha and PGI2 metabolite levels beyond food restriction. The decrease in PG concentrations of gut contents without any change in their mucosal concentrations suggests an active process of PG secretion involving zinc. In addition, in serum from clotted blood, zinc deficiency increased the level of met F2alpha (p less than 0.05), suggesting that zinc might be involved in control of PG levels by changing PG degradation rate.

Topics: Alprostadil; Animals; Dinoprost; Dinoprostone; Epoprostenol; Male; Nutrition Disorders; Organ Specificity; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Thromboxane B2; Tissue Distribution; Zinc