Eating grapes may reduce the risk of fatty liver disease
In a recent study published in the journal foodconsumption of grapes may extend life expectancy by five years and reduce the risk of non-alcoholic fatty liver disease in mice fed a high-fat diet.
Study: Consumption of grapes modulates gene expression, reduces non-alcoholic fatty liver disease and prolongs longevity in C57BL/6J female mice fed a Western-style high-fat diet. Image Credit: EduardSV / Shutterstock
Nutrition plays a vital role in maintaining good health, preventing the onset of disease and improving longevity. The basic concept of a healthy diet includes increased consumption of vegetables, fruits and whole grains and reduced consumption of trans fats, saturated fats and refined carbohydrates. According to the United States Department of Agriculture’s Economic Research Service, a daily diet should include at least two cups of fruit and 2.5 cups of vegetables.
Vegetables and fruits are essential for maintaining homeostasis in the body and improving disease conditions. In recent years, evidence has accumulated that vegetables and fruits can modulate gene expression and regulate metabolic pathways.
Grapes are considered wonderful fruits. The bioactive components of grapes are known to modulate the pathophysiology of various diseases, including diabetes, obesity, cancer and inflammatory diseases. Additionally, components of grapes are also known to control the aging process and improve longevity.
In the current study, scientists evaluated the effectiveness of grapes in mitigating adverse health effects induced by a high-fat Western diet.
A diet high in saturated fats, refined carbohydrates and salt increases the risk of obesity, cardiovascular disease and metabolic diseases, such as diabetes and non-alcoholic fatty liver disease. The diet is also known to reduce the lifespan of mice by 34%.
The scientists specifically aimed to understand the impact of grape consumption on liver gene expression, lipid metabolism, longevity, and non-alcoholic fatty liver disease. Mice fed a high-fat diet supplemented with 5% grape powder or a semi-synthetic diet were used as experimental models.
Supplementation of mice with 5% grape powder was estimated to be equivalent to the daily consumption of approximately 300 g of fresh grapes by a person weighing 70 kg.
Grape supplementation in the standard semi-synthetic diet
Part of the study investigated the difference in gene expression between mice fed a standard diet with and without grape supplementation.
RNA sequencing analysis revealed distinct differences between the two groups. Specifically, grape supplementation caused an induction in the structural integrity of the ribosome, mitochondrial protein complex, and protein translation pathways. Ribosomal gene enrichment is associated with cell growth, proliferation, differentiation and development.
Additionally, enrichment of drug metabolism, detoxification, antioxidant and oxidative stress-related pathways was observed in mice fed a standard grape-enriched diet. Glutathione-S-transferase P1 (GSTP1) is an antioxidant enzyme and is commonly involved in these pathways. RNA-seq results revealed that grape supplementation increased the expression of GSTP1, in addition to inducing the expression of other antioxidant enzymes, including glutathione peroxidase, glutathione synthetase, and superoxide dismutase.
These results indicate that dietary grape supplementation helps maintain cellular redox homeostasis, neutralize reactive free radicals, and prevent oxidative stress.
Grape supplementation in a high-fat diet
Consuming a high-fat diet increases the risk of various health complications, including non-alcoholic fatty liver disease. The worldwide prevalence of this disease is estimated at around 25%.
Comparison between mice fed a high-fat diet with and without grape supplementation revealed that grape consumption reduced lipid accumulation in the liver, a major hallmark of non-alcoholic fatty liver disease.
RNA-seq findings indicated differential expression of more than 5600 genes between the two groups. Several of these genes are implicated in the reduction of hepatic steatosis, including mitochondrial and peroxisomal degradation, esterification, phospholipid metabolism, sequestration, and hydrolysis.
Further analysis revealed that grape supplementation is associated with the regulation of catabolic processes induced by a high-fat diet and the enrichment of mitochondrial energy metabolism. Specifically, grape supplementation increased the expression of genes related to fatty acid transport and degradation, esterification, and free fatty acid sequestration.
Grape supplementation has also been observed to negatively regulate the expression of genes associated with lipid enrichment, cholesterol synthesis, and redistribution of lipids from muscle and fat to the liver.
Since a high-fat diet is known to reduce lifespan in mice, the study also investigated the effect of grape supplementation on longevity. The results revealed that lifetime food consumption of grapes is associated with a significant improvement in survival.
As observed in the study, alterations in the expression of fatty liver-related genes by grapes may have helped reduce the adverse effects of a high-fat diet, which in turn helped improve the lifespan of grapes. mouse.
A modest enrichment of adiponectin receptor gene expression was observed in mice supplemented with grape. Overexpression of adiponectin receptors is known to improve glucose metabolism and hepatic insulin sensitivity, justifying the positive impact of grape consumption on longevity.
Significance of the study
Researchers found that grape consumption was helpful in reducing the risk of high-fat diet-induced non-alcoholic fatty liver disease in mice, as well as improving their longevity. Additionally, by altering gene expression patterns, grapes mitigate the adverse effects of a high-fat diet.
- Dave A. 2022. Consumption of grapes modulates gene expression, reduces nonalcoholic fatty liver disease, and prolongs longevity in female C57BL/6J mice fed a high-fat Western diet. Food. https://www.mdpi.com/2304-8158/11/13/1984/htm