A high-fat/high-carbohydrate diet or Western diet has been reported to produce changes in the intestine, explained researchers from the Universitat Rovira i Virgili in Tarragona, Spain.
“Concretely, several recent studies have provided compelling new evidence to suggest that changes in the epithelial barrier function and intestinal inflammation are associated with and could even lead to altered regulation of body weight and glucose homeostasis,” they added.
“The main consequence of the gut barrier dysfunction has been proposed to be the entry of toxins from the intestinal lumen, which can trigger local inflammation or gain access to the circulation and induce systemic inflammation through cytokine release.”
Their new research indicated that a grape seed proanthocyanidin extract (GSPE) may protect the gut from such harmful effects.
Data published in Molecular Nutrition and Food Research reveals that supplementing the diet of lab rats with medium or high-dose proanthocyanidins had beneficial impacts on intestinal inflammation, oxidative stress, and barrier function. The medium dose was 25 mg/kg, which is a dose similar to the dietary proanthocyanidin intake in humans, explained the researchers. The high dose (50 mg/kg) would exceed the dietary proanthocyanidin intake in humans.
Thirty-six week-old rats were fed a Western diet for 15 weeks and then divided into one of four supplementation groups, receiving 0 mg/kg (control), 5 mg/kg (low dose), 25 mg/kg, or 50 mg/kg for an additional three weeks.
Results showed that intestinal inflammation, assessed by measuring myeloperoxidase (MPO) activity, significantly increased in the control animals, but these increases were reduced in the rats receiving the grape seed extract.
In addition, significant reductions in plasma levels of reactive oxygen species were observed in the medium and high dose groups, compared to the control group.
The researchers also examined the function of the intestinal barrier, and looked specifically at so-called tight junctions (TJ) between cells in the lining of the intestine – the epithelium. On one side is the intestinal cavity and on the other is a mass of cells and tissues. In a healthy system, materials in the cavity find their way into tissues by passing through the cells, which controls which substances pass through. In an unhealthy system, the tight junctions are not so tight and materials can bypass the cells and find their way into tissues via the tight junctions. This increase in intestinal permeability has been referred to as "leaky gut".
“Another point of interest in this study was to evaluate whether GSPE could modulate the alterations in the permeability of the intestinal barrier that are related to the state of intestinal inflammation,” wrote the researchers. “Our findings indicate that the TJ proteins were negatively associated with measures of adiposity and with the circulating levels of [triglycerides]. These are not causal associations, but they suggest that increased adiposity is accompanied by lower expression of TJ components, which is in agreement with the hypothesis that obesity and a [high-fat diet] are associated with increased intestinal permeability. Then, given the importance of having a healthy barrier function, dietary interventions that can modulate the intestinal permeability might afford an effective tool for the prevention and treatment of metabolic diseases associated with obesity.”
The researchers concluded: “Our findings indicate that orally administered GSPE modulates the intestinal inflammation, oxidative stress, and possibly the barrier function. Based on these findings, our data suggest that nutritional and/or therapeutic interventions focused on gut health and modulation of the intestinal permeability should be extensively explored in the context of obesity.”
Source: Molecular Nutrition and Food Research
Published online ahead of print, doi: 10.1002/mnfr.201601039
“Chronic supplementation with dietary proanthocyanidins protects from diet-induced intestinal alterations in obese rats”
Authors: K. Gil-Cardoso et al.