Effects of Different Vegetable Oils on the Nonalcoholic Fatty Liver Disease in C57/BL Mice.

Background: Nonalcoholic fatty liver disease (NAFLD) is the most common hepatic disorder, affecting 22-28% of the adult population and more than 50% of obese people all over the world. Modulation of the fatty acids in diet as a means of prevention against nonalcoholic fatty liver disease in animal models (NAFLD) remains unclear. The treatment of NAFLD has not been described in specific guidelines so far. Thus, the justification for the study is to check modifications in macronutrients composition, fatty acids, in particular, play a significant role in the treatment of NAFLD regardless of weight loss. Aim: To investigate different vegetable oils in prevention and progression of NAFLD in animal models. Methods: For the experiment were used fifty C57BL/6J mice male fed with high fat and fructose diet (HFD) to induce the NAFLD status and they received different commercial vegetable oils for 16 weeks to prevent steatosis. Liver steatosis and oxidative stress parameters were analyzed using biochemical and histological methods. Fatty acids profile in the oils and in the liver samples was obtained. Results: The high fat and fructose diet led to obesity and the vegetable oils offered were effective in maintaining body weight similar to the control group. At the end of the experiment (16 weeks), the HFHFr group had a greater body weight compared to control and treated groups (HFHFr: 44.20 ± 2.34 g/animal vs. control: 34.80 ± 3.45 g/animal; p < 0.001; HFHFr/OL: 35.40 ± 4.19 g/animal; HFHFr/C: 36.10 ± 3.92 g/animal; HFHFr/S: 36.25 ± 5.70 g/animal; p < 0.01). Furthermore, the HFD diet has caused an increase in total liver fat compared to control (p < 0.01). Among the treated groups, the animals receiving canola oil showed a reduction of hepatic and retroperitoneal fat (p < 0.05). These biochemical levels were positively correlated with the hepatic histology findings. Hepatic levels of omega-3 decreased in the olive oil and high fat diet groups compared to the control group, whereas these levels increased in the groups receiving canola and soybean oil compared to control and the high fat groups. Conclusion: In conclusion, the commercial vegetable oils either contributed to the prevention or reduction of induced nonalcoholic fatty liver with high fat and fructose diet, especially canola oil.

Plasma amino acids profile in first-episode psychosis, unaffected siblings and community-based controls.

Investigations of plasma amino acids in early psychosis and their unaffected siblings are rare. We measured plasma amino acids involved in the co-activation of dopaminergic, GABAergic, glutamatergic, and serotoninergic neurotransmitters in first-episode psychosis (FEP) patients (n = 166), unaffected siblings (n = 76), and community-based controls (n = 166) included in a cross-sectional study. Plasma levels of glutamic acid (GLU), glutamine, glycine, proline (PRO), tryptophan (TRP), tyrosine, serine and GABA were quantified by gas-chromatography-mass spectrometry. We used the generalized linear model adjusted by sex, age, and body mass index for group comparison and paired t-test for FEP-Sibling pairs. FEP had reduced GABA plasma levels compared to siblings and controls (p < 0.05 for both). Siblings had lower GLU, Glx and PRO (p < 0.05 for all) but increased TRP compared to patients and controls (p < 0.05 for both). FEP patients with longer duration of pharmacological treatment and medicated only with antipsychotics had increased GLU compared to FEP with shorter periods, or with those treated with a combination of medications (p < 0.05 for both). Finally, FEP patients treated only with antipsychotics presented higher Glx compared to those with mixed medications (p = 0.026). Our study suggests that FEP have low a GABA plasma profile. Unaffected siblings may be a possible risk group for metabolic abnormalities.

Antioxidant vitamin supplementation prevents oxidative stress but does not enhance performance in young football athletes.

OBJECTIVES: The aim of this study was to verify the effects of supplementation with antioxidants (vitamins C and E) on oxidative stress, delayed-onset muscle soreness (DOMS), and performance in football players during a recovery period after an exercise-induced oxidative stress protocol. METHODS: Twenty-one football athletes were randomly assigned to two groups: placebo and antioxidant-supplemented. Supplementation was performed in a double-blind, controlled manner using vitamin C (500 mg/d) and E (400 UI/d) for 15 d. After 7 d of supplementation, athletes were submitted to an exercise-induced oxidative stress protocol consisting of plyometric jumping and strength resistance sets to exhaustion. Blood samples, performance tests, and DOMS were determined before and 24, 48, and 72 h after exercise. RESULTS: Antioxidant supplementation was continued during the recuperation week and for a total of 15 d. Antioxidant supplementation caused a significant increase in plasma vitamins C and E. The antioxidant supplementation could inhibit oxidative stress characterized by elevated lipid peroxidation markers malondialdehyde and total lipid peroxidation as well as reduced ratio of glutathione to oxidized glutathione promoted by exercise. Antioxidant supplementation, however, did not significantly reduce the plasma creatine kinesis concentration or DOMS during the recovery days. Likewise, supplementation with vitamin C and E did not improve lower body power, agility, or anaerobic power, nor did it provide any indication of faster muscle recovery. CONCLUSION: Antioxidant supplementation does not attenuate elevated markers of muscle damage or muscle soreness promoted by acute exercise and do not exert any ergogenic effect on football performance of young athletes, although it reduced oxidative stress.

Dietary docosahexaenoic acid and eicosapentaenoic acid influence liver triacylglycerol and insulin resistance in rats fed a high-fructose diet.

This study aimed to examine the benefits of different amounts of omega-3 (n-3) polyunsaturated fatty acids from fish oil (FO) on lipid metabolism, insulin resistance and gene expression in rats fed a high-fructose diet. Male Wistar rats were separated into two groups: Control (C, n = 6) and Fructose (Fr, n = 32), the latter receiving a diet containing 63% by weight fructose for 60 days. After this period, 24 animals from Fr group were allocated to three groups: FrFO2 (n = 8) receiving 63% fructose and 2% FO plus 5% soybean oil; FrFO5 (n = 8) receiving 63% fructose and 5% FO plus 2% soybean oil; and FrFO7 (n = 8) receiving 63% fructose and 7% FO. Animals were fed these diets for 30 days. Fructose led to an increase in liver weight, hepatic and serum triacylglycerol, serum alanine aminotransferase and HOMA1-IR index. These alterations were reversed by 5% and 7% FO. FO had a dose-dependent effect on expression of genes related to hepatic ß-oxidation (increased) and hepatic lipogenesis (decreased). The group receiving the highest FO amount had increased markers of oxidative stress. It is concluded that n-3 fatty acids may be able to reverse the adverse metabolic effects induced by a high fructose diet.

The flavonols quercetin, myricetin, kaempferol, and galangin inhibit the net oxygen consumption by immune complex-stimulated human and rabbit neutrophils.

Stimulated human neutrophils exhibit increased net oxygen consumption (NOC) due to the conversion of O2 into the superoxide anion by the NADPH oxidase enzymatic complex during the respiratory burst. In several inflammatory diseases, overproduction of these oxidants causes tissue damage. The present study aims to: (a) optimize the experimental conditions used to measure the NOC in serum-opsonized zymosan (OZ)- and insoluble immune complex (i-IC)-stimulated human and rabbit neutrophils; and (b) compare the effect of four flavonols (quercetin, myricetin, kaempferol, and galangin) on this activity. We used a Clark-type oxygen electrode to measure the NOC of stimulated neutrophils. Eliciting the neutrophil respiratory burst with OZ and i-IC yielded similar maximum O2 uptake levels within the same species, but the human neutrophil NOC was almost four times higher than the rabbit neutrophil NOC. The optimal experimental conditions established for both cell types were 4 x 10(6) neutrophils mL(-1), 2 mg mL(-1) OZ, and 240 microg mL(-1) i-IC. Upon stimulation with OZ or i-IC, the tested flavonols reduced the human and rabbit neutrophil NOC in the same order of potency--quercetin and galangin were the most and the least potent, respectively. These compounds were around four times more effective in inhibiting the rabbit as compared to the human neutrophil NOC, respectively. The four flavonols were not toxic to human or rabbit neutrophils. The experimental conditions used are suitable for both the determination of human and rabbit neutrophil NOC and for the assessment of the modulatory effects of natural compounds on these activities. The relationship between the level of NOC and the inhibitory potency of the flavonols suggests that rabbit neutrophils can be useful experimental models to predict the effect of drugs on immune complex-stimulated human neutrophils.

Effects of α-tocopherol supplementation on liver of rats chronically exposed to ethanol.

BACKGROUND/AIMS: Chronic alcoholism is characterized by hepatotoxicity associated with antioxidant and redox status imbalance. Continuous ethanol intake induces free radical synthesis, resulting in the depletion of antioxidants, especially α-tocopherol, which has an important role in lipid peroxidation. This study aimed to evaluate if α-tocopherol supplementation can restore liver phenotype in rats chronically exposed to ethanol. METHODS: α-Tocopherol levels were determined and histologic analysis of liver was performed. Hepatic gene expression was analyzed through oligonucleotide microarray and real-time PCR. RESULTS: Alcohol exposure for 6 weeks did not decrease hepatic α-tocopherol levels; however, both groups exposed to ethanol (supplemented or not with α-tocopherol) displayed fatty liver. The antioxidant supplementation prevented Mallory bodies and inflammatory infiltration, but not apoptosis, in liver of the rats exposed to ethanol. Gene expression analysis showed evidence of adaptive response to chronic alcohol consumption, where antioxidant components were not regulated. Nevertheless, differentially expressed genes reflected the change in cellular homeostasis. CONCLUSION: The hepatic α-tocopherol content was coherent with the antioxidant gene expression in this study. Cells are likely to have adapted and restored their antioxidant status after long-term ethanol exposure, which might be the reason for such conflicting reports concerning α-tocopherol status in chronic alcoholism.

Vitamin E alters inflammatory gene expression in alcoholic chronic pancreatitis.

OBJECTIVE: To evaluate the effect of vitamin E supplementation on pancreatic gene expression of inflammatory markers in rats with alcoholic chronic pancreatitis. METHODS: Wistar rats were divided into 3 groups: control (1), alcoholic chronic pancreatitis without (2) and with (3) vitamin E supplementation. Pancreatitis was induced by a liquid diet containing ethanol, cyclosporin A and cerulein. α-tocopherol content in plasma and liver and pancreas histopathology were analyzed. Gene expression of inflammatory biomarkers was analyzed by the quantitative real-time PCR technique. RESULTS: The animals that received vitamin E supplementation had higher α-tocopherol amounts in plasma and liver. The pancreas in Group 1 showed normal histology, whereas in Groups 2 and 3, mild to moderate tissue destruction foci and mononuclear cell infiltration were detected. Real-time PCR analysis showed an increased expression of all genes in Groups 2 and 3 compared to Group 1. Vitamin E supplementation decreased the transcript number of 5 genes (α-SMA, COX-2, IL-6, MIP-3α and TNF-α) and increased the transcript number of 1 gene (Pap). CONCLUSION: Vitamin E supplementation had anti-inflammatory and beneficial effects on the pancreatic gene expression of some inflammatory biomarkers in rats with alcoholic chronic pancreatitis, confirming its participation in the inflammatory response mechanisms in the pancreas.

Creatine supplementation reduces increased homocysteine concentration induced by acute exercise in rats.

The aim of this study was to evaluate the effect of creatine supplementation on homocysteine (Hcy) metabolism after acute aerobic and anaerobic exercise. A total of 112 Wistar rats were divided into four groups: aerobic exercise (A), aerobic exercise plus creatine supplementation (ACr), anaerobic exercise (An), and anaerobic exercise plus creatine-supplemented (AnCr). Creatine supplementation consisted of the addition of 2% creatine monohydrate to the diet. After 28 days, the rats performed an acute moderate aerobic exercise bout (1 h swimming with 4% of total body weight load) or an acute intense anaerobic exercise bout (6 × 30-s vertical jumps into the water with a 30-s rest between jumps, with 50% of total body weight load). The animals were killed before (pre) and at 0, 2, and 6 h (n = 8) after acute exercise. Plasma Hcy concentration increased significantly (P < 0.05) up to 2 h after anaerobic exercise (An group: pre 8.7 ± 1.2, 0 h 13.2 ± 2.3, 2 h 13.5 ± 4.2, and 6 h 12.1 ± 2.2, µmol/l). The same did not occur in acute aerobic exercised animals. Nevertheless, creatine supplementation significant decreased (P < 0.05) homocysteine concentration independent of exercise intensity (AnCr group: pre 17%, 0 h 80%, 2 h 107%, and 6 h 48%; ACr group: pre 17%, 0 h 19%, 2 h 28%, and 6 h 27%). Increased S-adenosylhomocysteine was also found in the An group. In conclusion, acute intense anaerobic exercise increased plasma Hcy concentration. On the other hand, creatine supplementation decreased plasma Hcy independent of exercise intensity.

Hyperhomocysteinemia and polymorphisms of the methylenetetrahydrofolate gene in hemodialysis and peritoneal dialysis patients.

Hyperhomocysteinemia has been documented in chronic renal failure (CRF). Premature as well as progressive occlusive vascular disease is common. Mutations or polymorphisms in the gene of the enzyme methylenetetrahydrofolate reductase (MTHFR), as C677T, A1298C and G1793A, are associated with hyperhomocysteinemia and possibly with elevated risk for vascular diseases. This study was conducted on 89 individuals with renal failure on dialysis to determine the allelic and genotypic frequencies of the mutations in the MTHFR gene and hyperhomocysteinemia. Blood samples were colleted for determination of homocysteine and DNA. The C677T, A1298C and G1793A mutations were detected. This study confirmed the high prevalence of hyperhomocysteinemia in patients on dialysis, which was diagnosed in 76 patients (85.39%) and high incidence of the C677T and A1298C mutation, 42 (47.19%) and 29 (32.58%) patients, respectively. Five patients (5.62%) presented the G1793A mutation and hyperhomocysteinemia. The authors concluded that there was no influence of the polymorphisms on homocysteine levels in these patients.