Display omitted
•The vegetable oils intake induces changes in metabolic and inflammatory parameters.•Coconut oil induces glycometabolic and hepatic alterations in healthy rats.•Linseed oil reduces ...serum TAG and IL-6.•Sunflower oil increases superoxide dismutase and catalase activity and reduces total glutathione, IL-6 e TNF.•Sunflower oil increases hepatic lipogenesis and reduces serum lipids.
Our goal was to carry out a comparative study to evaluate the metabolic and inflammatory effects and the redox status of commercial vegetable oils supplementation linseed (LO), coconut (VCO), and sunflower (SO) in metabolically healthy rats. The results found in this study showed that the LO group decreased the HOMA-IR and hepatic cholesterol, and increased the serum levels of IL-6. Supplementation with VCO increased glucose and HOMA-IR, cholesterol concentration and serum triacylglycerol (TAG). In this group, there was also an increase in TBARS. In the SO group there was a decrease in serum concentrations of cholesterol and TAG and an increase in hepatic concentration of these lipids. In addition, in the SO group there was a decrease in hepatic and serum concentrations of IL-6 and hepatic levels of TNF, as well as a decrease in the GSH/GSSG ratio, suggesting changes in glutathione metabolism and inflammatory mediators.
•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.
Açai improves non-alcoholic fatty liver disease (NAFLD) induced by fructose Carvalho, Mayara Medeiros de Freitas; Reis, Larissa Lélis Teixeira; Lopes, Juliana Márcia Macedo ...
Nutrición hospitalaria : organo oficial de la Sociedad Española de Nutrición Parenteral y Enteral,
2018-Feb-16, Letnik:
35, Številka:
2
Journal Article
Odprti dostop
the excessive consumption of fructose can cause liver damage, characteristic of non-alcoholic fatty liver disease (NAFLD) associated with changes in lipid metabolism and antioxidant defenses. Açai, ...the fruit of Euterpe oleraceaMart., has demonstrated numerous biological activities, including anti-inflammatory, antioxidant, and lipid metabolism modulating action.
we evaluated the benefits of açai supplementation on liver damage caused by replacing starch with fructose in rats.
thirty male Fischerrats were divided into two groups, the control group (C, 10 animals), which consumed a standard diet (AIN-93M), and the fructose (F, 20 animals) group, which consumed a diet containing 60% of fructose. After eight weeks, 10 animals from the fructose group received 2% of lyophilized açai, and were called the açai fructose group (FA). The animals were fed ad libitumwith these diets for another ten weeks. Serum, hepatic and fecal lipid profile, antioxidant enzymes and carbonylated protein were assessed and histopathological characterization of the liver was performed.
açai promoted the reduction of ALT activity in relation to the fructose group (F), reduced alkaline phosphatase to a level similar to that of the control group (C) in relation to the fructose group (F), and reduced catalase activity. The fruit also increased the ratio of total/oxidized glutathione (GSH/GSSG) and reduced the degree of macrovesicular steatosis and the number of inflammatory cells.
the replacement of starch by fructose during this period was effective in promoting NAFLD. Açai showed attenuating effects on some markers of hepatic steatosis and inflammation.
Immunometabolic changes in the liver and white adipose tissue caused by high-fat (HF) diet intake may worse metabolic adaptation and protection against pathogens in sepsis. We investigate the effect ...of chronic HF diet (15 weeks) on mortality and immunometabolic responses in female mice after sepsis induced by cecum ligation and perforation (CLP). At week 14, animals were divided into four groups: sham C diet, sepsis C diet (C-Sp), sham HF diet (HF-Sh) and sepsis HF diet (HF-Sp). The surviving animals were euthanized on the 7th day. The HF diet decreased survival rate (58.3% vs. 76.2% C-Sp group), increased serum cytokine storm (IL-6 1.41 ×; vs. HF-Sh, IL-1β 1.37 ×; vs. C-Sp, TNF 1.34 ×; vs. C-Sp and 1.72 ×; vs. HF-Sh, IL-17 1.44 ×; vs. HF-Sh, IL-10 1.55 ×; vs. C-Sp and 1.41 ×; HF-Sh), white adipose tissue inflammation (IL-6 8.7 ×; vs. C-Sp and 2.4 ×; vs. HF-Sh, TNF 5 ×; vs. C-Sp and 1.7 ×; vs. HF-Sh, IL-17 1.7 ×; vs. C-Sp, IL-10 7.4 ×; vs. C-Sp and 1.3 ×; vs. HF-Sh), and modulated lipid metabolism in septic mice. In the HF-Sp group liver's, we observed hepatomegaly, hydropic degeneration, necrosis, an increase in oxidative stress (reduction of CAT activity −81.7%; vs. HF-Sh; increase MDA levels 82.8%; vs. HF-Sh, and hepatic IL-6 1.9 ×; vs. HF-Sh, and TNF 1.3 × %; vs. HF-Sh) production. Furthermore, we found a decrease in the total number of inflammatory, mononuclear cells, and in the regenerative processes, and binucleated hepatocytes in a HF-Sp group livers. Our results suggested that the organism under metabolic stress of a HF diet during sepsis may worsen the inflammatory landscape and hepatocellular injury and may harm the liver regenerative process.
Display omitted
Non-alcoholic fatty liver disease (NAFLD), the most predominant liver disease worldwide, is a progressive condition that encompasses a spectrum of disorders ranging from steatosis to steatohepatitis, ...and, ultimately, cirrhosis and hepatocellular carcinoma. Although the underlying mechanism is complex and multifactorial, several intracellular events leading to its progression have been identified, including oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, and altered endoplasmic reticulum (ER) homeostasis. Phenolic compounds, such as those present in açai (Euterpe oleracea Mart.), are considered promising therapeutic agents due to their possible beneficial effects on the prevention and treatment of NAFLD. We tested in vitro effects of aqueous açai extract (AAE) in HepG2 cells and its influence on oxidative stress, endoplasmic reticulum stress, and inflammation in a murine model of high fat diet-induced NAFLD. In vitro AAE exhibited high antioxidant capacity, high potential to inhibit reactive oxygen species production, and no cytotoxicity. In vivo, AAE administration (3 g/kg) for six weeks attenuated liver damage (alanine aminotransferase levels), inflammatory process (number of inflammatory cells and serum TNFα), and oxidative stress, through the reduction of lipid peroxidation and carbonylation of proteins determined by OxyBlot and modulation of the antioxidant enzymes: glutathione reductase, SOD and catalase. No change was observed in collagen content indicating an absence of fibrosis, stress-related genes in RE, and protein expression of caspase-3, a marker of apoptosis. With these results, we provide evidence that açai exhibits hepatoprotective effects and may prevent the progression of liver damage related to NAFLD by targeting pathways involved in its progression.
In yeast, as in other eukaryotes, calcium plays an essential role in signaling transduction to regulate different processes. Many pieces of evidence suggest that glucose-induced activation of plasma ...membrane H.sup.+-ATPase, essential for yeast physiology, is related to calcium signaling. Until now, no protein that could be regulated by calcium in this context has been identified. Lpx1p, a serine-protease that is also involved in the glucose-induced activation of the plasma membrane H.sup.+-ATPase, could be a candidate to respond to intracellular calcium signaling involved in this process. In this work, by using different approaches, we obtained many pieces of evidence suggesting that the requirement of calcium signaling for activation of the plasma membrane H.sup.+ -ATPase is due to its requirement for activation of Lpx1p. According to the current model, activation of Lpx1p would cause hydrolysis of an acetylated tubulin that maintains the plasma membrane H.sup.+-ATPase in an inactive state. Therefore, after its activation, Lpx1p would hydrolyze the acetylated tubulin making the plasma membrane H.sup.+-ATPase accessible for phosphorylation by at least one protein kinase.
In yeast, as in other eukaryotes, calcium plays an essential role in signaling transduction to regulate different processes. Many pieces of evidence suggest that glucose-induced activation of plasma ...membrane H+-ATPase, essential for yeast physiology, is related to calcium signaling. Until now, no protein that could be regulated by calcium in this context has been identified. Lpx1p, a serine-protease that is also involved in the glucose-induced activation of the plasma membrane H+-ATPase, could be a candidate to respond to intracellular calcium signaling involved in this process. In this work, by using different approaches, we obtained many pieces of evidence suggesting that the requirement of calcium signaling for activation of the plasma membrane H+-ATPase is due to its requirement for activation of Lpx1p. According to the current model, activation of Lpx1p would cause hydrolysis of an acetylated tubulin that maintains the plasma membrane H+-ATPase in an inactive state. Therefore, after its activation, Lpx1p would hydrolyze the acetylated tubulin making the plasma membrane H+-ATPase accessible for phosphorylation by at least one protein kinase.
Buriti pulp flour (BPF) contains significant levels of antioxidants. This study evaluated the effect of BPF on biomarkers of oxidative damage in the liver, heart, and pancreas of diabetic rats. The ...chemical composition, antioxidant capacity, and polyphenol content of BPF were determined. Thirty-six female Fisher rats were divided into four groups: control (C); control + BPF (CB); diabetic (D); diabetic + BPF (DB). Diabetes was induced by treatment with streptozotocin. Thirty days after the induction of diabetes, glucose, total cholesterol and triacylglycerides serum levels, aminotransferase and paraoxonase activities were evaluated. Oxidative damage to lipids and proteins was assessed through thiobarbituric acid reactive substances (TBARS) and protein carbonyl analyses, respectively. Histopathological analyses were also performed. BPF contained high concentrations of phenolic compounds, lipids, and fibers, and exhibited a high capacity to neutralize the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical. Diabetes was evidenced by equivalent high levels of glucose in plasma from rats in the D and DB groups. Diabetic rats in both groups also presented the same increased activity of aminotransferases. Protein carbonyl levels were increased in liver, heart, and pancreas in the D compared with C group. Although treatment with BPF did not result in any histopathological alterations, it reduced significantly the levels of TBARS in the heart and protein carbonyls in the liver and heart. No effect on blood glucose and tissue histology was observed following treatment with BPF. However, BPF diminished oxidative damage in liver and heart, indicating a possible antioxidant potential in vivo, in addition to in vitro.
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.
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.
PDF
