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The effects of chronic intake of di(2-ethylhexyl)phthalate (DEHP) on the main intermediate glycolytic metabolites in liver and gastrocnemius muscle were investigated in experimental animals. Male Wistar rats (90 -100 g) were fed for 21 days either with a standard chow or the same diet supplemented with 2% (w/w) of DEHP. The DEHP-fed rats had an altered in vivo glucose tolerance associated with abnormal glucose intermediate metabolite contents in liver and skeletal muscle. In these rats, the hepatic content of glucose-6 -phosphate (G-6 -P), fructose-6 -phosphate, pyruvate, lactate, glucose-1 -phosphate and glycogen decreased. At the same time, the G-6 -P content decreased while the pyruvate and lactate levels increased in skeletal muscle. These data, along with the high plasma glucose concentration and the normal lactate blood levels of this group, could indicate that DEHP-fed rats could present a deficiency in muscle glucose and lactate transport, a reduction of the flux through muscle hexokinase and hepatic glucokinase, and a reduction in glycogen synthesis.

IntroductionImpaired wound healing has been widely reported in diabetes. Linoleic acid (LA) accelerates the skin wound healing process in non-diabetic rats. However, LA has not been tested in diabetic animals.ObjectivesWe investigated whether oral administration of pure LA improves wound healing in streptozotocin-induced diabetic rats.MethodsDorsal wounds were induced in streptozotocin-induced type-1 diabetic rats treated or not with LA (0.22 g/kg b.w.) for 10 days. Wound closure was daily assessed for two weeks. Wound tissues were collected at specific time-points and used to measure fatty acid composition, and contents of cytokines, growth factors and eicosanoids. Histological and qPCR analyses were employed to examine the dynamics of cell migration during the healing process.ResultsLA reduced the wound area 14 days after wound induction. LA also increased the concentrations of cytokine-induced neutrophil chemotaxis (CINC-2αβ), tumor necrosis factor-α (TNF-α) and leukotriene B4 (LTB4), and reduced the expression of macrophage chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1). These results together with the histological analysis, which showed accumulation of leukocytes in the wound early in the healing process, indicate that LA brought forward the inflammatory phase and improved wound healing in diabetic rats. Angiogenesis was induced by LA through elevation in tissue content of key mediators of this process: vascular-endothelial growth factor (VEGF) and angiopoietin-2 (ANGPT-2).ConclusionsOral administration of LA hastened wound closure in diabetic rats by improving the inflammatory phase and angiogenesis.

The aim of the present study was to investigate the potential nutritional and metabolic impact of trans (t) fatty acids (FA) on an appropriate experimental dietary model. Since previously reported experimental designs have been matter of concern, we developed a dietary model to compare the effect of t isomers and/or the saturation of FA independently of other variables. Wistar rats were fed diets containing identical amounts of nutrients and high levels of dietary fats (200 g/kg) for 30 d. Dietary fat rich in t-FA was compared with fat rich in saturated (s) FA or rich in cis (c) FA, maintaining the same length of C chain of the FA. The fats were obtained through isomerization or hydrogenation of the c-FA present in the control fat. Apparent fat absorption, energy efficiency and triacylglycerol levels in serum and liver were different in rats fed t-FA or s-FA than c-FA. The apparent fat absorption was (%): s-FA 85·7 (SD 3·4), t-FA 93·1 (SD 0·4),c-FA 96·7 (SD 1·1) (P, 0·05). The efficiency of energy utilization was lower in t-FA (11·7 %) and s-FA (18·5 %) diets, reaching statistical significance only between s-FA and c-FA. A striking finding was the change in the lipid profile in serum and liver. Serum and hepatic triacylglycerol levels were greater for t-FA and s-FA diets than in c-FA; however, the increases on serum triacylglycerol concentrations were greater with the s-FA diet and the increases on hepatic triacylglycerol content were greater with t-FA. Knowledge of the t-FA effects on this kind of experimental dietary model could contribute to determine the potential risk of t-FA intake for man. Trans fatty acids: Isomerized fat: Hydrogenated fat: Dietary fatTrans (t) fatty acids (FA) are geometrical isomers of FA present in variable and important amounts in margarine, shortenings and baked products, reaching up to 50 % of total t-FA (Aro et al. 1998). The main source of t-FA for man's intake is through the partial hydrogenation of vegetable oils (Katan et al. 1995): they are undesirably produced at the same time as saturated (s) FA are generated. However, the physicochemical properties of t-FA are different from the natural cis (c) isomer and from the s-FA, even though from the structural view-point t-FA resemble s-FA. Louheranta et al. (1999) have suggested that t-FA resemble their s-FA counterparts with regard to some biochemical and metabolic effects. Studies of the influence of t-FA intake on plasma lipid profiles have yielded conflicting results. Most of the studies on human subjects have shown that dietary t-FA increased the plasma LDL-cholesterol, and contradictory effects have been observed on plasma HDL-cholesterol and on plasma lipoprotein

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We have shown that aluminum (Al) induces cholestasis associated with multiple alterations in hepatocellular transporters involved in bile secretory function, like Mrp2. This work aims to investigate whether these harmful effects are mediated by the oxidative stress caused by the metal. For this purpose, the capability of the antioxidant agent, vitamin E, to counteract these alterations was studied in male Wistar rats. Aluminum hydroxide (or saline in controls) was administered ip (27 mg/kg body weight, three times a week, for 90 d). Vitamin E (600 mg/kg body weight) was coadministered, sc. Al increased lipid peroxidation (+50%) and decreased hepatic glutation levels (-43%) and the activity of glutation peroxidase (-50%) and catalase (-88%). Vitamin E counteracted these effects total or partially. Both plasma and hepatic Al levels reached at the end of the treatment were significantly reduced by vitamin E (-40% and -44%, respectively; p<0.05). Al increased 4 times the hepatic apoptotic index, and this effect was fully counteracted by vitamin E. Bile flow was decreased in Altreated rats (-37%) and restored to normality by vitamin E. The antioxidant normalized the hepatic handling of the Mrp2 substrates, rose bengal, and dinitrophenyl-S-glutathione, which was causally associated with restoration of Mrp2 expression. Our data indicate that oxidative stress has a crucial role in cholestasis, apoptotic/necrotic hepatocellular damage, and the impairment in liver transport function induced by Al and that vitamin E counteracts these harmful effects not only by preventing free-radical formation but also by favoring Al disposal.

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