Açai (Euterpe oleracea Mart.), a fruit from the Amazon region, has emerged as a promising source of polyphenols. Açai consumption has been increasing owing to ascribed health benefits and antioxidant ...properties; however, its effects on hepatic injury are limited. In this study, we evaluated the antioxidant effect of filtered açai pulp on the expression of paraoxonase (PON) isoforms and PON1 activity in rats with nonalcoholic fatty liver disease (NAFLD). The rats were fed a standard AIN-93M (control) diet or a high-fat (HF) diet containing 25% soy oil and 1% cholesterol with or without açai pulp (2 g/day) for 6 weeks. Our results show that açai pulp prevented low-density lipoprotein (LDL) oxidation, increased serum and hepatic PON1 activity, and upregulated the expression of PON1 and ApoA-I in the liver. In HF diet-fed rats, treatment with açai pulp attenuated liver damage, reducing fat infiltration and triglyceride (TG) content. In rats receiving açai, increased serum PON1 activity was correlated with a reduction in hepatic steatosis and hepatic injury. These findings suggest the use of açai as a potential therapy for liver injuries, supporting the idea that dietary antioxidants are a promising approach to enhance the defensive systems against oxidative stress.
•Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease.•Açai (Euterpe oleracea) fruit contains high levels of polyphenols, e.g. anthocyanins.•Mice with high-fat diet-induced ...NAFLD received oral aqueous açai extract (AAE).•AAE increased adiponectin levels, insulin sensitivity and PPAR-α-mediated fatty acid oxidation, decreasing liver lipids.
Polyphenols, especially anthocyanins, have been considered promising for the prevention of nonalcoholic fatty liver disease (NAFLD). This study investigated whether açai (Euterpe oleracea Mart.), a source of anthocyanins and recognized as one of the new “superfruits”, could alleviate high-fat diet (HFD)-induced NAFLD in mice. In HFD mice, aqueous açai extract (AAE) administration (3 g/kg) for six weeks improved insulin resistance index and increased adiponectin mRNA expression in adipose tissue and serum levels. Furthermore, AAE decreased the total liver triacylglycerol content and attenuated HFD-induced hepatic steatosis. This reduced hepatic lipid content was associated with AAE-mediated up-regulation of genes involved in adiponectin signaling, including adiponectin receptor 2, PPAR-α, and its target gene, carnitine palmitoyltransferase. Thus, dietary açai can protect liver from steatosis through its enhancement of adiponectin levels, improvement of insulin sensitivity, and increase in PPAR-α-mediated fatty acid oxidation.
AIMSTo investigate the effects of endurance training on stress-induced cardiometabolic perturbations given the elevated release of stress hormones and subsequent glucose homeostasis perturbations. ...MATERIALS AND METHODSRats were randomized into non-trained rats, rats submitted to endurance training, non-trained rats submitted to stress, and trained rats submitted to stress. Endurance training was applied for 8 weeks, while chronic stress was applied at the 4th, 5th, and 6th weeks of the training period. Two weeks after the last stressor stimuli, rats were euthanized, and blood and heart were collected for biochemical tests. KEY FINDINGSExacerbated corticosterone levels were observed in both stressed groups, and chronic stress per se impaired glucose tolerance and insulin sensitivity. Training reduced circulating adrenaline, even though noradrenaline levels were elevated in the blood and heart of trained rats. While stress-induced high circulating serotonin levels were further increased by endurance training, cardiac serotonin levels were attenuated in trained rats. Endurance training mitigated the stress-induced higher circulating lipids. Cardiac TBARs and GPx activity increased in trained rats while CAT and GPx were reduced in response to chronic stress. Endurance training not only attenuated the stress-induced higher circulating ACE/ACE2 ratio but also reduced ACE/ACE2 balance in the heart. Glucose intolerance, insulin resistance, and altered stress hormones release were linked to impairment of cardiometabolic responses, elevated oxidative stress, and dysregulation of ACE/ACE2 ratio. SIGNIFICANCEEndurance training mitigated the stress-related pathophysiological responses, which could be related to improvements in the antioxidant capacity and the balance of ACE/ACE2 activity.
Abstract only
The chronic hyperglycemia of diabetes mellitus (DM) is associated with long‐term damage and dysfunction of different organs, including the liver. Hyperglycemia induces hepatic ...mitochondrial dysfunction causing changes that include decreased oxidative phosphorylation, increased oxidative stress, ultra‐structural abnormalities, which in turn worse metabolic health. The disturbance in metabolic homeostasis also modulates gut microbiota by a variety of mechanisms while the maintenance of intestinal microbiota has a significant influence on metabolic state. The aim of this study was to evaluate the hypothesis that streptozotocin‐diabetic mice treated with
Saccharomyces boulardii
THT 500101 strain (
S. boulardii
, THT: Probiotics and Starters Cultures, Belgium) present improvement of blood glucose, reduction of oxidative stress and maintenance of hepatocytes structure, concomitant with a beneficial impact in the gut microbiota profile. C57BL/6 male mice were randomly assigned into four groups: Control (C), Control + Probiotic (CP), Diabetes (D), and Diabetes + Probiotic (DP) (n = 9/group). Diabetic mice treated with
S. boulardii
presented a reduction of blood glucose (~30%) when compared to D group (DP = 251.9 ± 36.40 mg/dl vs. D = 362.9 ± 21.26 mg/dl, p<0.05). D group presented a higher level of carbonylated proteins compared with C and CP groups (C = 3.26 ± 0.42, CP = 3.00 ± 0.37
vs
. D = 3.62 ± 0.33 nmol/mg), and probiotics reduced hepatic protein damage in DP (DP = 3.29 ± 0.58 nmol/mg). Diabetes reduced the activity of antioxidant enzymes superoxide dismutase (SOD) (D = 8.00 ± 0.12 vs. C = 8.49 ± 0.10, CP = 8.44 ± 0.05 USOD/mg, p<0.05) and glutathione peroxidase (GPx) (D = 73.50 ± 9.50 vs. C = 83.00 ± 4.00, CP = 81.00 ± 7.25 nmol/min/mg, p<0.05) and
S. boulardii
increased the activity of both enzymes in DP group as compared with D (SOD: DP =8.20 ± 0.14 USOD/mg and GPx: DP = 5.08 ± 2.29 nmol/mg, p<0.05). Signs of severe hydropic degeneration were noticed in hepatocytes from D group and to a lesser extent in hepatocytes from DP group.
S. boulardii
treatment was associated with increased proportion in
Bacteroidetes, Firmicutes and Deferribacteres
, and a decreased proportion of
Proteobacteria and Verrucomicrobia
phylum in DP group, as compared with D. Thus, the data presented here show up a novel potential therapeutic role of
S. boulardii
for glycemic control and attenuation of diabetes‐induced liver injury.
Support or Funding Information
FAPESP 2016/24059‐2
This study aimed to determine whether a hypercholesterolemic diet induces hepatic steatosis, alterations in mRNA expression of NADPH oxidase subunits, and antioxidant defenses.
Fischer rats were ...divided into two groups of eight animals according to the treatment, control (C) and hypercholesterolemic diet (H). Those in group C were fed a standard diet (AIN-93M), and those of the group H were fed a hypercholesterolemic diet (25% soybean oil and 1% cholesterol).
The hypercholesterolemic diet did not affect body weight, but resulted in the accumulation of lipids in the liver, increased serum activities of aminotransferases and cholesterol levels. Biomarker of lipid peroxidation (TBARS) and mRNA expression of NADPH oxidase subunits p22(phox) and p47(phox) were increased in the liver of animals in group H. Besides, the activity and expression of antioxidant enzymes were altered.
The results show increased mRNA expression of NADPH oxidase subunits and changes in antioxidant enzyme activities in diet-induced hepatic steatosis.
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A doença hepática gordurosa não alcoólica (DHGNA) é uma doença caracterizada pelo acúmulo de gordura no fígado de pacientes sem história de abuso de álcool. É a doença hepática mais comum no mundo ocidental, e sua prevalência está aumentando. A DHGNA é classificada em dois tipos: esteatose, na qual ocorre somente a deposição de gordura nos hepatócitos e esteato-hepatite não alcoólica (EHNA), na qual ocorre, além da esteatose, necroinflamação. A hipótese mais comumente aceita para explicar a progressão da esteatose à EHNA é a hipótese “Two-hit”, o primeiro “hit” refere-se aos fatores que podem promover esteatose hepática e o segundo “hit” refere-se aos fatores que podem agravar a esteatose hepática levando à esteato-hepatite. O estresse oxidativo, definido como um desequilíbrio entre a produção de espécies reativas e a capacidade dos sistemas de defesa antioxidante em neutralizá-las e prevenir seus efeitos deletérios, é um fator responsável pelo segundo “hit”. Elucidar os mecanismos de lesão induzida por estresse oxidativo no fígado é essencial para a compreensão da patogênese da doença. Assim, nossos objetivos foram determinar se a dieta hipercolesterolemiante provoca alterações histológicas no fígado de ratas e verificar se a mesma dieta induz alterações no status antioxidante por meio da expressão de mRNA da NADPH oxidase e das enzimas antioxidantes; da atividade das enzimas catalase, SOD Cu-Zn, glutationa total; e do marcador de peroxidação lipídica (TBARS). Ratas Fischer foram divididas em dois grupos de oito animais de acordo com o tratamento recebido, Controle (C) e Hipercolesterolêmico (H), sendo aquelas do grupo C alimentadas com dieta padrão (AIN-93M) e aquelas do grupo H alimentadas com dieta hipercolesterolemiante (25% de óleo de soja e 1% de colesterol). Ao final de oito semanas, os animais foram anestesiados e eutanasiados. Os dados paramétricos foram avaliados por teste T de Student e os não paramétricos por Mann-Whitney. A dieta hipercolesterolemiante não alterou o peso corporal, mas resultou em acúmulo de lipídios no fígado, aumentando os níveis séricos das aminotransferases e de colesterol. A expressão de mRNA de subunidades da NADPH oxidase estava aumentada no fígado de animais do grupo H e alterações na atividade e expressão de enzimas antioxidantes e de TBARS foram observadas. Esses resultados sugerem que a dieta hipercolesterolemiante induziu esteatose hepática em ratas, constituindo-se, portanto, em um bom modelo para o estudo de esteatose. __________________________________________________________________________________________
ABSTRACT: The Nonalcoholic fatty liver disease (NAFLD) is a disease characterized by the accumulation of fat in the liver of patients with no history of alcohol abuse. It is the most common liver disease in the Western world, and its prevalence is increasing. NAFLD is classified into two types: steatosis, which occurs only fat deposition in hepatocytes and non-alcoholic steatohepatitis (NASH), which occurs, in addition to steatosis, necroinflamation. The most commonly accepted hypothesis to explain the progression of steatosis to NASH is the hypothesis "Two-hit", the first "hit" refers to factors that may promote hepatic steatosis and the second "hit" refers to factors that can intensify hepatic steatosis leading to steatohepatitis. Oxidative stress, defined as an imbalance between the production of reactive species and the capacity of antioxidant defense systems to neutralize them and prevent their harmful effects, is a factor responsible for the second "hit". Elucidating the mechanisms of injury-induced oxidative stress in the liver is essential for understanding the pathogenesis of the disease. Thus, our aims were to determine whether the hypercholesterolemic diet causes histological changes in the liver of rats and verify if the same diet induces changes in antioxidant status through the mRNA expression of NADPH oxidase and antioxidant enzymes, the activity of catalase, SOD-Cu/Zn, total glutathione, and the marker of lipid peroxidation (TBARS). Fischer rats were divided into two groups of eight animals according to treatment received, control (C) and hypercholesterolemic (H), those in group C were fed with standard diet (AIN-93M) and those of the H group were fed with hypercholesterolemic diet (25% soybean oil and 1% cholesterol). At the end of eight weeks, the animals were anesthetized and euthanized. Parametric data were analyzed by Student's t test and the nonparametric by Mann-Whitney test. The hypercholesterolemic diet did not affect body weight, but resulted in accumulation of lipids in the liver, increased serum levels of aminotranferases and cholesterol. The mRNA expression of subunits of the NADPH oxidase was increased in the liver of animals from group H and alterations in activity and expression of antioxidant enzymes and TBARS were observed. These results suggest that the hypercholesterolemic diet induced hepatic steatosis in rats constituting, therefore, a good model for the study of steatosis.
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