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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. [ABSTRACT FROM AUTHOR]

The article focuses on the comparative studies in the application of skinfold thickness (SKF) and bioelectrical impedance for body composition estimation in athletes. It mentions that studies published in 1900 and 2007 were reviewed wherein seven critical reviews were assessed to rate the studies including number of subjects, performance level of the athletes studied and statistical methods applied. Moreover, it states that SKF is the better method to estimate body composition in athletes.

Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Background: In 2019, the European Working Group on Sarcopenia in Older People (EWGSOP2) proposed low muscle strength as the primary outcome for sarcopenia diagnosis instead of low muscle mass, as proposed in 2010 (EWGSOP1). Therefore, the aim of this study was to compare the prevalence of sarcopenia using both EWGSOP1 and EWGSOP2 operational definitions in people living with HIV (PLHIV) and to determine the agreement and correlation between different tests proposed by EWGSOP2., Setting: Cross-sectional study, where 302 PLHIV (151 men), 51.7 ± 9.0 years old were evaluated for the presence of sarcopenia using both EWGSOP1 and EWGSOP2 operational definitions., Methods: Appendicular skeletal muscle was estimated using bioimpedance analysis. Handgrip strength, chair stand, gait speed, and static balance were used as muscle function measures. Agreement was determined using Cohen kappa and Pearson correlation coefficient was calculated., Results: Sarcopenia prevalence was 4.3% using EWGSOP1 and 1.0% using EWGSOP2. Agreement for sarcopenia diagnosis between EWGSOP1 and EWGSOP2 was fair (k = 0.37, P < 0.01). From the 13 cases of sarcopenia diagnosed using EWGSOP1, only 3 cases (23.1%) were also diagnosed using EWGSOP2. A medium correlation (r = -0.32, P < 0.01) and poor agreement (k = 0.14, P < 0.01) between muscle strength tests (handgrip strength and chair stand) were observed. Concordance between handgrip and chair stand was observed in 11 participants only, whereas 65 participants were considered to have low muscle strength using chair stand but not using handgrip., Conclusions: Lower sarcopenia prevalence using EWGSOP2 and low agreement between EWGSOP1 and EWGSOP2 operational definitions in diagnosing sarcopenia were observed in PLHIV., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Purpose: We aimed to determine the effects of different intensities of acute exercise on Hcy plasma levels, and the exercise-induced changes in Hcy liver metabolism., Method: First, thirty-two Wistar rats were randomly submitted to an acute bout of swimming exercise carrying a load of 2% (n=8), 4% (n=8) and 6% (n=8) of their total body weight attached in their tail. Control rats remained rested (n=8). Blood samples were taken from tail vein for plasma S-containing amino acids determination before (Rest) and post, 1, 2, 3, 4, 6, and 10h after acute swimming exercise. Second, 56 exercised rats (4% loads) were euthanized before (Rest) and1, 2, 3, 4, 6, and 10h after acute swimming exercise. Blood and liver samples were collected for amino acids and keys genes involved in the Hcy metabolism assay., Results: Acute exercise increases (P<0.05) plasma Hcy concentration in an intensity-dependent manner (rest 7.7±0.8; 6% load 13.8±3.6; 4% load 12.2±2.9±and 2% load 10.1±2.6, μmol/L); this increase is transient and does not promote hyperhomocysteinemia (<15μmol/L).Exercise-induced increased plasma Hcywas accompanied by the decreased liver S-adenosylmethionine/S-adenosylhomocysteine ratio and elevated MAT1a mRNA content. Acute exercise also caused elevated mRNA of key enzymes of transsulfuration (CBS) and remethylation (BHMT and the MTRR)., Conclusion: Our data provided evidence that acute exercise increases plasma Hcy concentration due to the augmented requirement for methylated compounds that increases liver SAM consumption. Also, Hcy remethylation and transsulfuration are coordinately regulated to maintain methyl balance., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Human Immunodeficiency Virus positive subjects present impairment in muscle function, neural activation, balance, and gait. In other populations, all of these factors have been associated with muscle strength asymmetry., Objective: To investigate the existence of muscle strength asymmetry between dominant and non-dominant lower limbs and to determine the hamstrings-to-quadriceps strength ratio in Human Immunodeficiency Virus positive subjects., Methods: In this cross-sectional study, 48 subjects were included (22 men and 26 women; mean age 44.6 years), all of them under highly active antiretroviral therapy. They performed isokinetic strength efforts at speeds of 60°/s and 180°/s for knee extension and flexion in concentric-concentric mode., Results: Peak torque was higher (p<0.01) at 60°/s for quadriceps (193, SD=57 vs. 173, SD=55% body mass) and hamstrings (97, SD=36 vs. 90, SD=37% body mass) in dominant compared to non-dominant. Similarly, peak torque was higher at 180°/s (quadriceps 128, SD=44 vs. 112, SD=42; hamstrings 64, SD=24 vs. 57, SD=26% body mass) in dominant. Average power was also higher for all muscle groups and speeds, comparing dominant with non-dominant. The hamstrings-to-quadriceps ratio at 60°/s was 0.50 for dominant and 0.52 for non-dominant, and at 180°/s, it was 0.51 for both limbs, with no significant difference between them. The percentage of subjects with strength asymmetry ranged from 46 to 58%, depending upon muscle group and speed analyzed., Conclusion: Human Immunodeficiency Virus positive subjects present muscle strength asymmetry between lower limbs, assessed through isokinetic dynamometry., (Copyright © 2017 Associação Brasileira de Pesquisa e Pós-Graduação em Fisioterapia. Publicado por Elsevier Editora Ltda. All rights reserved.)

Purpose: Muscle atrophy and strength decline are two of the most prominent characteristics in cancer patients undergoing cancer therapy, leading to decreased functional ability and reduced quality of life. Therefore, the aim is to systematically review research evidence of the effects of resistance exercise (RE) on lower-limb muscular strength, lean body mass (LBM), and body fat (BF) in cancer patients undertaking neoadjuvant or adjuvant therapy., Methods: This research was conducted using the following online database: Clinical Trial Register, Cochrane Trial Register, PubMed, SPORT Discus, and SciELO, from September 2014 until May 2015. We used the following keywords in various combinations with a systematic search: "Cancer therapy," "Wasting muscle," "Muscle loss," "Muscle function," "Neoadjuvant therapy," "Adjuvant thera-py," "Resistance Training," "Weight training," and "Exercise." After selection of 272 full-text articles, 14 publications were included in this meta-analysis., Results: Resistance exercise (RE) during neoadjuvant or adjuvant therapy increased lower-limb muscular strength (mean: 26.22 kg, 95% CI [16.01, 36.43], heterogeneity: P = <0.01, I 2  = 76%, P = 0.00001) when compared to controls over time. Similarly, lean body mass (LBM) increased (mean 0.8 kg, 95% CI [0.7, 0.9], heterogeneity: P = 0.99, I 2  = 0%, P < 0.00001), and decreased body fat (BF) (mean: -1.3 kg, 95% CI [-1.5, 1.1], heterogeneity: P = 0.93, I 2  = 0%, P < 0.00001) compared to controls over time., Conclusion: RE is effective to increase lower-limb muscular strength, increase LBM, and decrease BF in cancer patients undergoing neoadjuvant and adjuvant therapy regardless of the kind of treatment., Implications for Cancer Survivors: RE increases muscle strength, maintains LBM, and reduces BF in cancer patients undergoing adjuvant and neoadjuvant therapies. Cancer patients and survivors should consider undertaking RE as an effective countermeasure for treatment-related adverse effects to the musculoskeletal system.

Objective: The aim of this study was to investigate changes in homocysteine (Hcy) metabolism and redox balance in response to exercise treatment in a tumor-bearing rat model., Methods: Male Wistar rats were exposed, or not, to a resistance exercise program 6 wk before inoculation with Walker-256 tumor cells or vehicle. After application, rats maintained their routine for 12 d and were then sacrificed for plasma and liver analyses., Results: Impaired Hcy metabolism was evident after 12 d of tumor cell inoculation as demonstrated by significantly increased (P < 0.05) plasma total homocysteine (tHcy) concentration (53%) and decreased plasma cysteine, methionine, and vitamin B12 concentrations. Decreased hepatic cystathionine β-synthase (CBS) and betaine-homocysteine S-methyltransferase mRNA levels were found in tumor-bearing rats but not in controls. Tumor inoculation also decreased levels of liver reduced glutathione (GSH) and increased hepatic oxidative stress compared with non-tumor controls. However, resistance exercise prevented the tumor-impaired transsulfuration pathway as demonstrated by the decreased plasma tHcy, hepatic CBS expression, and increased GSH in tumor-exercised versus tumor-sedentary rats. Remarkably, all measures of liver oxidative stress were suppressed by exercise training. Tumor weight was unchanged between groups., Conclusion: Resistance exercise prevented tHcy accumulation and liver oxidative damage caused by Walker-256 tumor cell inoculation; the modulatory effects of resistance exercise on Hcy metabolism appear to be at the level of transsulfuration pathway., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Aims: Well-characterized animal tumor models of cancer cachexia are warranted to elucidate underlying mechanisms and provide a better approach to the human scenario. We aimed to investigate whether solid Ehrlich carcinoma reproduces clinical, functional and biological conditions of tumor-induced cachexia in mice., Methods: Eight-week old female Swiss mice were subcutaneously inoculated with Ehrlich tumor cells (tumor-bearing, TB group) or vehicle (sham) into the right flank and monitored for 28days. Tumor histopathological features and tumor-host interaction, including tissue weight, muscle structure, strength and biochemical parameters were carried out., Key Findings: Tumor growth curve demonstrated a linear pattern with no difference in final carcass weight between groups. A well-defined capsule composed by connective tissue infiltrated by inflammatory and neoplastic cells surrounded the tumors. The TB group had reduced handgrip strength, aside from lower cross sectional area (CSA) and critically reduced parametrial fat pads. Plasma parameters of lactate dehydrogenase (LDH), creatine kinase (CK) and tumor necrosis factor-α (TNF-α) were higher in the TB group, suggesting predominance of catabolic and pro-inflammatory activities. Conversely, food intake and tissue weight did not differ between groups., Significance: Our data elucidated that the solid Ehrlich tumor model is feasible and effective in reproducing some of the relevant issues experienced by cancer patients with cachexia. The solid Ehrlich carcinoma emerges as an alternative tool against more aggressive cancer cachexia models during preclinical research., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Aims: The aim of this study was to evaluate possible beneficial effects of treatment with thiamine or benfotiamine in an animal model of acute ethanol intoxication., Main Methods: Thirty male Wistar rats were separated at random into three groups of 10 animals each: Ethanol (E), Ethanol treated with thiamine (T) and Ethanol treated with benfotiamine (BE). Rats were gavaged with single dose of ethanol (5g/kg, 40% v:v). After 30min of ethanol gavage the animals were treated with thiamine or benfotiamine. Six hours after first gavage, the animals were euthanized and blood and liver samples were collected for ethanol and oxidative stress biomarkers quantification., Key Findings: Serum ethanol levels were higher in animals treated with thiamine or benfotiamine while hepatic alcohol levels were higher in animals of the group treated with benfotiamine comparing to controls or thiamine treated groups. The lipid peroxidation biomarkers were diminished for the groups treated with thiamine or benfotiamine comparing to E animals. Concerning protein oxidative damage parameters, they were enhanced for animals treated with benfotiamine in relation to other groups., Significance: In conclusion, the treatment with thiamine or benfotiamine even 30min after the massive dose of ethanol has proven to be beneficial against liver damage. Improved results were obtained with benfotiamine in relation to oxidative damage from aqueous compartments., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating the oxidative insult caused by Trypanosoma cruzi during the development of the chronic phase of Chagas disease, Swiss mice were infected intraperitoneally with 5.0 × 104 trypomastigotes of T. cruzi QM1strain., Methods: Mice were given supplements of two different doses of vitamin C for 180 days. Levels of lipid oxidation (as indicated by thiobarbituric acid reactive substances-TBARS), total peroxide, vitamin C, and reduced glutathione were measured in the plasma, TBARS, total peroxide and vitamin C were measured in the myocardium and histopathologic analysis was undertaken in heart, colon and skeletal muscle., Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed increased production of ROS in plasma and myocardium and a greater degree of inflammation and necrosis in skeletal muscles than those that received a lower dose or no vitamin C whatsoever., Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results showed that animals subject to a 500 mg dose of vitamin C showed greater tissue damage in the chronic phase of Chagas disease, probably due to the paradoxical actions of the substance, which in this pathology, will have acted as a pro-oxidant or pro-inflammatory.

The tissue changes that occur in Chagas disease are related to the degree of oxidative stress and antioxidant capacity of affected tissue. Studies with vitamin C supplementation did not develop oxidative damage caused by Chagas disease in the host, but other studies cite the use of peroxiredoxins ascorbate - dependent on T. cruzi to offer protection against immune reaction. Based on these propositions, thirty "Swiss" mice were infected with T. cruzi QM1 strain and treated with two different vitamin C doses in order to study the parasitemia evolution, histopathological changes and lipid peroxidation biomarkers during the acute phase of Chagas disease. The results showed that the parasite clearance was greater in animals fed with vitamin C overdose. There were no significant differences regarding the biomarkers of lipid peroxidation and inflammatory process or the increase of myocardium in animals treated with the recommended dosage. The largest amount of parasite growth towards the end of the acute phase suggests the benefit of high doses of vitamin C for trypomastigotes. The supplementation doesn't influence the production of free radicals or the number of amastigote nests in the acute phase of Chagas disease.

Hyperhomocysteinaemia is an independent risk factor for CVD. Recent data show a relationship between homocysteine (Hcy) and free radical formation. Since creatine synthesis is responsible for most of the methyl group transfers that result in Hcy formation, creatine supplementation might inhibit Hcy production and reduce free radical formation. The present study investigated the effects of creatine supplementation on Hcy levels and lipid peroxidation biomarkers. Thirty rats were divided into three groups: control group; diet with creatine group (DCr; 2 % creatine in the diet for 28 d); creatine overload plus diet with creatine group (CrO + D; 5 g creatine/kg by oral administration for 5 d+2 % in the diet for 23 d). Plasma Hcy was significantly lower (P < 0.05) in DCr (7.5 (sd 1.2) micromol/l) and CrO + D (7.2 (sd 1.7) micromol/l) groups compared with the control group (12.4 (sd 2.2) micromol/l). Both plasma thiobarbituric acid-reactive species (TBARS) (control, 10 (sd 3.4); DCr, 4.9 (sd 0.7); CrO + D, 2.4 (sd 1) micromol/l) and plasma total glutathione (control, 4.3 (sd 1.9); DCr, 2.5 (sd 0.8); CrO + D, 1.8 (sd 0.5) micromol/l) were lower in the groups that received creatine (P < 0.05). In addition, Hcy showed significant negative correlation (P < 0.05) with plasma creatine (r - 0.61) and positive correlation with plasma TBARS (r 0.74). Plasma creatine was negatively correlated with plasma TBARS (r - 0.75) and total peroxide (r - 0.40). We conclude that creatine supplementation reduces plasma Hcy levels and lipid peroxidation biomarkers, suggesting a protective role against oxidative damage. Modulating Hcy formation may, however, influence glutathione synthesis and thereby affect the redox state of the cells.