The metabolic syndrome of fructose-fed rats: Effects of long-chain polyunsaturated ω3 and ω6 fatty acids. I. Intraperitoneal glucose tolerance test

Abstract

Abstract. The present series of experiments aim mainly at investigating the possible influence of changes in the com position of dietary lipids (sunflower oil, salmon oil, safflower oil) upon the metabolic syndrome found in rats exposed to a fructose-rich diet. For purpose of comparison, a control group of rats received the sunflower oil diet with substitution of fructose by starch. An intraperitoneal glucose tolerance test, performed after overnight starvation fifty days after the start of the experiments at the 6th week after birth, indicated, as expected, impaired tolerance to glucose and deterioration of insulin sensitivity (HOMA index), without changes in the insulinogenic index, when comparing the fructose-fed rats to the starch-fed rats both exposed to the sunflower oil diet. In the fructose-fed rats, enrichment of the diet by long-chain polyunsaturated ω3 fatty acids supplied by salmon oil, a modest improvement of insulin sensitivity was opposed, in term of glucose homeostasis, by a decreased secretory response to glucose of insulin-producing cells. Last, in the fructose-fed rats, the partial substitution of sunflower oil by safflower oil rich in long-chain polyunsaturated ω6 fatty acids further deteriorated glucose homeostasis, with a higher mean HOMA index and a severe decrease of the insulinogenic index. These findings justify further investigations on such items as the time course for changes in metabolic and hormonal variables and both the metabolic and secretory responses of isolated pancreatic islets to selected nutrient secretagogues. IntroductionA metabolic syndrome with insulin resistance, hyperinsulinemia and hypertension is known to prevail in rats exposed to a high dietary supply of D-fructose (1). Attention was recently drawn to both the comparison between rats exposed to either a fructose-enriched diet or fructose-enriched drinking water, as well as the reversibility of the fructose-induced metabolic perturbations (2).Rats deprived of a dietary supply of long-chain polyunsaturated ω3 fatty acids also develop a metabolic syndrome with liver steatosis, visceral obesity, insulin resistance, hypertension and resulting cardiac hypertrophy (3-8).The present experiments aim mainly at exploring the effects of long-chain polyunsaturated ω3 and ω6 fatty acids in rats exposed from the 8th week after birth and for the ensuing 8 weeks to a fructose-enriched diet. More precisely, a first comparison deals with rats fed a sunflower oil diet and given access to either a control diet or a fructose-enriched diet obtained by substitution of starch by D-fructose. In this first comparison, the two diets contained 5.0% (w/w) sunflower oil, containing <0.1% of its total fatty acid content as long-chain polyunsaturated ω3 fatty acids. In the second set of com parisons, the just-mentioned rats exposed to the fructose-rich and sunflower oil-containing diet served as the control fructose-fed rats. In another group of rats, part of the sunflower oil (1.6%, w/w) in the fructose-rich diet was replaced by an equal amount...

Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats

“…However, Sprague-Dawley rats are known to be more sensitive towards the development of T2D and are therefore less representative of human population [7, 13]. The majority of studies on fructose effects were performed over a period between 8 and 12 weeks long [6, 7, 14–17], using mainly high quantity of fructose (60–66% of fructose in the chow) [7, 8, 17]. Recently, some authors had begun to define more realistic diets using Sprague-Dawley rats [18] as well as Wistar rats [19].…”