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Impaired 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. We investigated whether oral administration of pure LA improves wound healing in streptozotocin-induced diabetic rats. Dorsal 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. LA 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). Oral administration of LA hastened wound closure in diabetic rats by improving the inflammatory phase and angiogenesis.

[This corrects the article DOI: 10.1371/journal.pone.0165115.].

Protein depletion is associated with hepatic steatosis and decreased circulating triacylglycerol (TAG). Since conjugated linoleic acid (CLA) increases lean body mass, protects against muscle catabolism, and modulates lipid metabolism, the aim of this work was to investigate the effects of CLA with two different amounts of dietary fat on the regulation of plasma and hepatic TAG concentration, and its possible connections with changes in fatty acid (FA) profile in plasma, liver and adipose tissue and hepatic oxidative status during protein repletion. Rats were fed a low protein diet (14 days) and then a protein repletion diet (30 days), supplemented or not with CLA, containing 7% (w/w) or 20% (w/w) of fat. Hepatic TAG secretion and removal by muscle and adipose tissue lipoprotein lipase, FA profile and liver oxidative status were evaluated. Protein depletion affected hepatic TAG secretion and peripheral removal, decreasing plasma and increasing liver TAG concentration, whereas protein repletion with CLA improved these abnormalities independently of the amount of dietary fat by increasing hepatic TAG secretion. This prevention in the absence of CLA was not observed. CLA was incorporated in plasma and tissues (adipose > liver > plasma, and c9,t11-CLA > t10,c12-CLA), accompanied by alterations in FA composition, mainly in adipose tissue. The hepatic oxidative stress was overcome by protein repletion. CLA had a beneficial impact on TAG metabolism in protein repleted animals, preventing hepatic steatosis through higher hepatic TAG secretion.

Our aim was to investigate the effects of dietary conjugated linoleic acid (CLA) at high-fat (HF) levels on parameters related to triacylglycerol (TG) regulation and some potential impacts on liver damage. Growing mice were fed a control diet (7% corn oil), an HF diet containing 20% corn oil, or an HF diet containing 3% CLA (HF + CLA) for 30 d. Tissue and organ weights, plasma and tissue TG levels, and parameters related to their regulation were evaluated. Liver oxidative status was also assessed. Dietary CLA showed detrimental and beneficial effects. CLA added to the HF diet caused hepatomegaly (+32%) and exacerbated the hepatic TG accumulation (+168%) observed with the HF diet without inducing liver damage; however, it significantly reduced plasma TG concentrations (−37%) and normalized muscular TG content. An increase in glutathione was associated with total normalization of liver lipid peroxidation. In addition, HF + CLA caused dystrophy of epididymal fat pads, even when the HF diet had increased the adipose tissue mass (30%). The biochemical mechanisms involved in the regulation of lipid levels were related to reduced (−20%) hepatic very low-density lipoprotein-TG secretion and decreased muscle (−35%) and adipose (−49%) tissue contributions to the removal of plasma TG by lipoprotein lipase enzymes. Examination of CLA at HF levels showed hepatomegaly and exacerbation of lipid accretion as a negative impact; however, some positive aspects such as hypotriglyceridemia and protection against oxidative stress were also induced. Even the fat reduction is nutritionally important for weight control; the biochemical mechanisms whereby CLA mediates the potential effects could produce undesirable metabolic alterations.

Conjugated linoleic acid (CLA) might regulate the lipid depots in liver and adipose tissue. As there is an association between maternal nutrition, fat depots and risk of offspring chronic disease, the aim was to investigate the effect of maternal CLA consumption on TAG regulation and some inflammatory parameters in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed control (C) or CLA-supplemented (1 %, w/w) diets during 4 weeks before and throughout pregnancy and lactation. After weaning, male offspring of CLA rats were fed C or CLA diets (CLA/C and CLA/CLA groups, respectively), whereas C male rat offspring were fed a C diet (C/C group) for 9 weeks. Serum TAG levels were increased in the CLA/CLA and CLA/C groups, associated with a reduction of lipoprotein lipase activity and weights of adipose tissue. The liver TAG levels were decreased in the CLA/CLA group, related to a significant reduction of fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) and glucose-6-phosphate dehydrogenase enzyme activities, as well as to the mRNA levels of FAS, ACC, stearoyl-CoA desaturase-1 and sterol regulatory element-binding protein-1c. Even though normal TAG levels were found in the liver of CLA/C rats, a reduction of lipogenesis was also observed. Thus, these results demonstrated a programming effect of CLA on the lipid metabolic pathways leading to a preventive effect on the TAG accretion in adipose tissue and the liver of male rat offspring. This knowledge could be important to develop some dietary strategies leading to a reduced incidence of obesity and fatty acid liver disease in humans.

Protein depletion is associated with decreased body weight gain, low nitrogen balance, intrahepatic lipid accumulation, and hypoalbuminemia. Because conjugated linoleic acid (CLA) can increase lean body mass, enhance feed efficiency, and modulate lipid metabolism, this study investigated the effects of CLA at two levels of dietary fat on energy efficiency, nitrogen retention, and plasmatic and hepatic lipid levels in rats during dietary protein repletion. The animals were subjected to a moderate protein restriction for 14 d. After that, they were fed a protein repletion diet for 30 d, supplemented or not with CLA at recommended and high-fat levels. Energy efficiency, nitrogen balance, and nutritional parameters in serum and tissues were evaluated. Protein repletion improved most of the nutritional parameters evaluated independently of CLA supplementation at both fat levels. At recommended fat levels, CLA did not have any effect. At high-fat levels, energy efficiency increased more than 20% by fat accumulation in carcasses and epididymal pads, serum cholesterol increased (two-fold), and liver triacylglycerol accumulation remained elevated. However, at high-fat levels, CLA prevented lipid accumulation in liver and adipose tissue. Protein repletion improved the nutritional status of protein-restricted rats with minor effects of CLA at both dietary fat levels. However, when high-fat diets were given, CLA-enriched oil showed preventive effects on liver and adipose tissue lipid accumulation and no deleterious effects were observed. Because there are no studies dealing with CLA effects on protein repletion, this experimental model could improve nutritional interventions to overcome the protein-deficit stage.

The di(2-ethylhexyl) phthalate (DEHP) is an ubiquitous environmental chemical with detrimental health effects. The present work was designed to asses some potential mechanisms by which DEHP causes, among others, a reduced body fat retention. Since this effect could be related to an alteration of adipocyte triacylglycerol (TG) metabolism, we evaluated the effects of dietary DEHP in adipose tissues upon (1) the number and size of fat cells; (2) the basal and stimulated lipolysis and (3) the lipoprotein lipase (LPL) activity. Groups of male Wistar rats were fed for 21 days a control diet alone (control group) or the same control diet supplemented with 2% (w/w) of DEHP (DEHP group). The LPL activity of DEHP-fed rats was increased in lumbar and epididymal adipose tissues. These rats had significantly reduced weight in epididymal and lumbar tissues, together with reduced size of epididymal adipocytes. These alterations do not seem to be associated with higher lipid mobility because neither basal lipolysis nor ‘in vitro’ stimulated lipolysis by noradrenaline (NA) showed to be modified by DEHP. Based on these results, we concluded that the adipose tissue size reduction induced by DEHP intake is not due to changes in lipolysis nor to a decreased LPL activity. More research is needed to achieve a comprehensive understanding of the potential mechanisms by which DEHP causes, among others, a reduced body fat retention.

Aim: Our aim was to investigate the effects of trans-fatty acids (TFA) on liver lipid metabolism in mice fed on experimental diets rich in either oleic or linoleic acid. Methods: Twenty-two male CF1 mice (22.0 ± 0.1 g) were fed with diets rich in corn oil or olive oil, supplemented or not with TFA (0.75 g TFA/100 g diet), for 4 weeks. Changes in triacylglycerol content, the activity and expression of enzymes involved in lipogenesis and fatty acid oxidation were measured. Results: Supplementation of an olive oil-rich diet with TFA increased liver triacylglycerols, the activity and expression of lipogenic enzymes and sterol regulatory element-binding protein SREBP-1a expression. By contrast, when TFA were added to a corn oil-rich diet, they did not modify these parameters. No significant differences were observed among the experimental groups in the activity and expression of carnitine palmitoyltransferase-Ia, body and liver weights or serum triacylglycerol concentrations. Conclusions: The effect of TFA on liver fat accumulation depends on the dietary fatty acid composition. Steatosis induced by TFA when included in an olive oil diet (but not in a corn oil diet) was associated with an increased lipogenesis but not with a decreased fatty acid oxidation in animals fed on the olive oil diet. This metabolic change is mediated by SREBP-1a but not by SREBP-1c, and seems to be independent of insulin.

The chronic exposure to Aluminum (Al) may compromise different liver functions, mainly during the hepatic regeneration. The aim of this study is to investigate the interactions between the chronic i.p. exposure to Al and hepatic regeneration (HR) on bile flow and organic anion transport in experimental animals. For this purpose, we studied bile flow and fractional transfer rates for the transport of hepatic organic anions (hepatic uptake, sinusoidal efflux, and canalicular excretion), as well as parameters related with the oxidative stress (OS), on rats chronically treated with Al at 0 and 2 days of HR. The Al treatment and time of HR caused a decrease in the biliary flow and in the hepatic uptake and canalicular excretion constants. In addition, Al and HR increased the lipoperoxidation associated with a reduction of the glutathione content and glutathione peroxidase and catalase enzyme's activities. Since the effects of Al and HR on biliary flow and transport systems were additive, but not on the oxidative status, different mechanisms might be involved on these alterations. Even though the OS may play a key role on the hepatic deleterious effects, there is no unique cause-effect relationship between OS and liver dysfunction in this experimental animal model.

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.