Agaricus brasiliensis (sun mushroom) affects the expression of genes related to cholesterol homeostasis.

PURPOSE: The sun mushroom (Agaricus brasiliensis) is considered a major source of bioactive compounds with potential health benefits. Mushrooms typically act as lipid-lowering agents; however, little is known about the mechanisms of action of A. brasiliensis in biological systems. This study aimed to determine the underlying mechanism involved in the cholesterol-lowering effect of A. brasiliensis through the assessment of fecal and serum lipid profiles in addition to gene expression analysis of specific transcription factors, enzymes, and transporters involved in cholesterol homeostasis. METHODS: Twenty-four albino Fischer rats approximately 90 days old, with an average weight of 205 g, were divided into four groups of 6 each and fed a standard AIN-93 M diet (C), hypercholesterolemic diet (H), hypercholesterolemic diet +1 % A. brasiliensis (HAb), or hypercholesterolemic diet +0.008 % simvastatin (HS) for 6 weeks. Simvastatin was used as a positive control, as it is a typical drug prescribed for lipid disorders. Subsequently, blood, liver, and feces samples were collected for lipid profile and quantitative real-time polymerase chain reaction gene expression analyses. RESULTS: Diet supplementation with A. brasiliensis significantly improved serum lipid profiles, comparable to the effect observed for simvastatin. In addition, A. brasiliensis dietary supplementation markedly promoted fecal cholesterol excretion. Increased expression of 7α-hydroxylase (CYP7A1), ATP-binding cassette subfamily G-transporters (ABCG5/G8), and low-density lipoprotein receptor (LDLR) was observed following A. brasiliensis administration. CONCLUSIONS: Our results suggest that consumption of A. brasiliensis improves the serum lipid profile in hypercholesterolemic rats by modulating the expression of key genes involved in hepatic cholesterol metabolism.

Whey protein precludes lipid and protein oxidation and improves body weight gain in resistance-exercised rats.

BACKGROUND: Resistance exercise such as weight-lifting (WL) increases oxidation products in plasma, but less is known regarding the effect of WL on oxidative damage to tissues. Dietary compounds are known to improve antioxidant defences. Whey protein (WP) is a source of protein in a variety of sport supplements and can enhance physical performance. AIM: To evaluate the effect of WL on biomarkers of lipid and protein oxidation, on liver antioxidants and on muscle growth in the absence or presence of WP in rats. METHODS: Thirty-two male Fisher rats were randomly assigned to sedentary or exercise-trained groups and were fed with control or WP diets. The WL programme consisted of inducing the animals to perform sets of jumps with weights attached to the chest. After 8 weeks, arteriovenous blood samples, abdominal fat, liver and gastrocnemius muscle were collected for analysis. RESULTS: WP precludes WL-mediated increases in muscle protein carbonyl content and maintains low levels of TBARS in exercised and sedentary animals. WL reduced liver CAT activity, whereas WP increased hepatic glutathione content. In addition, WL plus WP generated higher body and muscle weight than exercise without WP. CONCLUSIONS: These data suggest that WP improves antioxidant defences, which contribute to the reduction of lipid and protein oxidation as well as body and muscle weight gain in resistance-exercised rats.

Whey protein modifies gene expression related to protein metabolism affecting muscle weight in resistance-exercised rats.

OBJECTIVE: The aim of this study was to evaluate the effects of resistance exercise on the mRNA expression of muscle mammalian target of rapamycin (mTOR), muscle-specific RING finger-1 (MuRF-1), and muscle atrophy F-box (MAFbx) in the presence or absence of whey protein ingestion. We hypothesized that resistance exercise in combination with whey protein ingestion alters the gene expression of proteins related to muscle protein synthesis (mTOR) and/or degradation (MuRF-1 and MAFbx), thus affecting muscle weight gain in rats. METHODS: Thirty-two male Fischer rats were randomly assigned to the following four experimental groups (n = 8/group): Control sedentary, control exercised, whey protein sedentary, and whey protein exercised. Exercise consisted of inducing the animals to perform sets of jumps for 8 wk. Body weight gain, muscle weights, food intake, and feeding efficiency were evaluated. Gene expressions were analyzed by quantitative real-time reverse transcription polymerase chain reaction. Statistical evaluation was performed using a two-way analysis of variance with a Tukey post hoc test. RESULTS: Whey protein exercised rats exhibited higher body and muscle weight gain compared with control-exercised rats (P = 0.032). The expression of mTOR was reduced by exercise but increased when whey protein was consumed as a dietary protein (P = 0.005). MuRF-1 expression was reduced by exercise (P < 0.001), whereas MAFbx was reduced only by whey protein ingestion (P = 0.008) independent of exercise. CONCLUSIONS: A reduction in MAFbx gene transcription induced by whey protein and the interaction between exercise and whey protein ingestion on mTOR gene expression contributed significantly to differences in body and muscle weight gain.

Diet supplementation with beta-carotene improves the serum lipid profile in rats fed a cholesterol-enriched diet.

The present study investigated the underlying mechanism associated with the hypocholesterolemic activity of beta-carotene by examining its effects on the serum lipid profile, fecal cholesterol excretion, and gene expression of the major receptors, enzymes, and transporters involved in cholesterol metabolism. Female Fischer rats were divided into three groups and were fed either a control or a hypercholesterolemic diet supplemented or not supplemented with 0.2 % beta-carotene. After 6 weeks of feeding, blood, livers, and feces were collected for analysis, and quantitative real-time polymerase chain reaction (qRT-PCR) was performed. Dietary supplementation with 0.2 % beta-carotene decreased serum total cholesterol, non-HDL cholesterol, the atherogenic index, and hepatic total lipid and cholesterol contents. These changes were accompanied by an increase in the total lipid and cholesterol contents excreted in the feces. The qRT-PCR analyses demonstrated that the hypercholesterolemic diet promoted a decrease in the gene expression of sterol regulatory element-binding protein 2, 3-hydroxy-3-methylglutaryl CoA reductase, and low-density lipoprotein receptor and an increase in the gene expression of peroxisome proliferator-activated receptor α and cholesterol-7a-hydroxylase. The expression of these genes and gene expression of ATP-binding cassette subfamily G transporters 5and 8 were unaffected by beta-carotene supplementation. In conclusion, the decrease in serum cholesterol and the elevation of fecal cholesterol obtained following beta-carotene administration indicate that this substance may decrease cholesterol absorption in the intestine and increase cholesterol excretion into the feces without a direct effect on the expression of cholesterol metabolism genes.

High dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.

In this study we investigated the hypothesis that a high-salt diet to hyperinsulinemic rats might impair antioxidant defense owing to its involvement in the activation of sodium reabsorption to lead to higher oxidative stress. Rats were fed a standard (CON), a high-salt (HS), or a high-fructose (HF) diet for 10 weeks after which, 50% of the animals belonging to the HF group were switched to a regimen of high-fructose and high-salt diet (HFS) for 10 more weeks, while the other groups were fed with their respective diets. Animals were then euthanized and their blood and liver were examined. Fasting plasma glucose was found to be significantly higher (approximately 50%) in fructose-fed rats than in the control and HS rats, whereas fat liver also differed in these animals, producing steatosis. Feeding fructose-fed rats with the high-salt diet triggered hyperinsulinemia and lowered insulin sensitivity, which led to increased levels of serum sodium compared to the HS group. This resulted in membrane perturbation, which in the presence of steatosis potentially enhanced hepatic lipid peroxidation, thereby decreasing the level of antioxidant defenses, as shown by GSH/GSSG ratio (HFS rats, 7.098±2.1 versus CON rats, 13.2±6.1) and superoxide dismutase (HFS rats, 2.1±0.05 versus CON rats, 2.3±0.1%), and catalase (HFS rats, 526.6±88.6 versus CON rats, 745.8±228.7 U/mg ptn) activities. Our results indicate that consumption of a salt-rich diet by insulin-resistant rats may lead to regulation of sodium reabsorption, worsening hepatic lipid peroxidation associated with impaired antioxidant defenses.

Salt overload in fructose-fed insulin-resistant rats decreases paraoxonase-1 activity.

Paraoxonase 1 (PON1) is a HDL-associated esterase/lactonase and its activity is inversely related to the risk of cardiovascular diseases. The aim of the present study was to evaluate the effect of a high-salt diet on serum PON1 activity in fructose-fed insulin-resistant rats. Adult male Fischer rats were initially divided into two groups. Control (CON), which received a normal salt diet and drinking water throughout the study; high fructose (HF), which received a normal salt diet and 20% fructose supplemented drinking water. After 10 weeks, half of the animals from HF group were randomly switched to a high-salt diet and 20% fructose supplemented drinking water (HFS) for more 10 weeks. Serum PON1 activity was determined by synthetic substrate phenyl acetate. HFS rats showed markedly decreased PON1 activity (HFS rats, 44.3 ± 14.4 g/dL versus CON rats, 64.4 ± 13.3 g/dL, P < 0.05) as compared to controls. In parallel, the level of oxidative stress, as indicated by thiobarbituric acid reactive substances (TBARS), was increased in HFS rats by 1.2-fold in the liver in relation to controls and was negatively correlated with PON activity. Differential leukocyte counts in blood showed a significant change in lymphocytes and monocytes profile. In conclusion, these results show that PON1 activity is decreased in fructose-fed insulin-resistant rats on a high-salt diet, which may be associated with increased oxidative stress, leading to inflammation.