Resveratrol inhibits nonalcoholic fatty liver disease in rats

Bujanda, Luís; Hijona, Elizabeth; Larzábal, Mikel; Beraza, Marta; Aldazábal, P; García-Urkia, N; Sarasqueta, Cristina; Cosme, Ángel; Irastorza, Belen; Gonzalez, Alberto Bradshaw; Arenas, Juan

doi:10.1186/1471-230x-8-40

Cited by 188 publications

(146 citation statements)

References 37 publications

Supporting

Mentioning

128

Contrasting

Order By: Relevance

“…31,32 In fact, antioxidant supplements have been proposed to treat patients with NAFLD. 33,34 We also found increased hepatocellular apoptosis in obese rats exposed to CS. This mechanism of cell death has been recently implicated in the pathogenesis of NASH in humans.…”

Section: Discussionmentioning

confidence: 49%

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

et al. 2010

View full text Add to dashboard Cite

The prevalence of cigarette smoking (CS) is increased among obese subjects, who are susceptible to develop nonalcoholic fatty liver disease (NAFLD). We investigated the hepatic effects of CS in control and obese rats. Control and obese Zucker rats were divided into smokers and nonsmokers (n ‫؍‬ 12 per group). Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. The effects of CS were assessed by biochemical analysis, hepatic histological examination, immunohistochemistry, and gene expression analysis. Phosphorylation of AKT and extracellular signal-regulated kinase (ERK) and quantification of carbonylated proteins were assessed by western blotting. As expected, obese rats showed hypercholesterolemia, insulin resistance, and histological features of NAFLD. Smoking did not modify the lipidic or glucidic serum profiles. Smoking increased alanine aminotransferase serum levels and the degree of liver injury in obese rats, whereas it only induced minor changes in control rats. Importantly, CS increased the histological severity of NAFLD in obese rats. We also explored the potential mechanisms involved in the deleterious effects of CS. Smoking increased the degree of oxidative stress and hepatocellular apoptosis in obese rats, but not in controls. Similarly, smoking increased the hepatic expression of tissue inhibitor of metalloproteinase-1 and procollagen-alpha2(I) in obese rats, but not in controls. C igarette smoking (CS) is considered a worldwide major cause of preventable morbidity and mortality. 1 The main clinical consequences of prolonged exposure to CS are chronic respiratory diseases, increased incidence of a variety of cancers, and increased risk of atherothrombotic clinical events such as myocardial infarction. 2 Hepatologists have traditionally paid scant attention to the deleterious effects of CS. This reflects the fact that smoking per se does not appear to cause liver injury and therefore is not considered a causative agent for chronic liver diseases. 3 However, there is in-

show abstract

Section: Discussionmentioning

confidence: 49%

Cigarette Smoking Exacerbates Nonalcoholic Fatty Liver Disease in Obese Rats

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Among other effects, this compound decreases hepatic steatosis severity in rats (Bujanda et al, 2008) and exerts an inhibitory effect on insulin secretion (Szkudelski, 2007). Although antiobesity actions of resveratrol have been extensively described in isolated adipocytes and in mice, including increased lipolysis and reduced lipogenesis in mature adipocytes, decreased adipogenesis and viability in maturing preadipocytes or protection from HFD-induced weight gain in mice (Baile et al, 2011), for the moment there are no big intervention trials showing similar effects in humans.…”

Section: Polyphenols and Other Plant Compoundsmentioning

confidence: 99%

Dietary factors, epigenetic modifications and obesity outcomes: Progresses and perspectives

Milagro

Mansego

Miguel

et al. 2013

Molecular Aspects of Medicine

259

161

View full text Add to dashboard Cite

Nutritional factors play a life-long role in human health. Indeed, there is growing evidence that one of the mechanisms by which nutrients and bioactive compounds affect metabolic traits is epigenetics. Complex interactions among food components and histone modifications, DNA methylation, non-coding RNA expression and chromatin remodeling factors lead to a dynamic regulation of gene expression that controls the cellular phenotype. Although perinatal period is the time of highest phenotypic plasticity, contributing largely to developmental programming, also during adulthood there is evidence about a nutritional influence on epigenetic regulation. Similarly to type 2 diabetes, hypertension, atherosclerosis and other metabolic disorders, obesity predisposition and weight loss outcomes have been repeatedly associated to changes in epigenetic patterns. Different non-nutritional risk factors that usually accompany obesity seem also to be involved in these epigenetic modifications, especially hyperglycemia, inflammation, hypoxia and oxidative stress. There are currently three major objectives in epigenetic research in relation to obesity: to search for epigenetic biomarkers to predict future health problems or detect the individuals at most risk, to understand the obesity-related environmental factors that could modulate gene expression by affecting epigenetic mechanisms, and to study novel therapeutic strategies based on nutritional or pharmacological agents that can modify epigenetic marks. At this level, the major tasks are: development of robust epigenetic biomarkers of weight regulation, description of those epigenetic marks more susceptible to be modified by dietary exposures, identification of the active ingredients (and the doses) that alter the epigenome, assessment of the real importance of other obesity-related factors on epigenetic regulation, determination of the period of life in which best results are obtained, and understanding of the importance of the inheritance of these epigenetic marks.

show abstract

“…However, it is worthwhile to note that ALT is more commonly used for screening of liver problems, as the AST level may also be increased as a result of deficiencies or diseases in other bodyorgans. 31 Administering of Lead acetate to rats showed a significant increase of AST in the rat's serum compared with the control group. The high values of these enzymes came in agreement with the finding of Haque who reported that following lead acetate administration significant elevation of AST was observed.…”

Section: Discussionmentioning

confidence: 99%