How food intake modifies the gut

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Mouse intestine section. Above, normal perintestinal (black) and villi (pink convolution). Binge-inducing dilated intestine after overeating-induced obesity with large lower villi and long villi. Credits: UNIGE / Mirko Trajkovski

Obesity is one of the most important health challenges, as more than 10% of the world’s population is obese and 40% are overweight. However, existing treatment options are still scarce and inefficient. A few years ago, scientists at the University of Geneva (UNIGE) in Switzerland discovered that certain external stimuli, such as exposure to the cold, alter the absorption surface and function of the intestine. Today, by using various mouse models in combination with human intestinal biopsy, they decipher the molecular mechanisms governing the plasticity of this amazing organ, and increased food intake enhances the absorption surface and function of the intestine. I will clarify that. Mechanistically, this is due to enhanced expression of PPARα, a regulatory protein required for increased binge-inducing ability of the intestine to absorb calories. In addition, if large amounts of food increase the absorption surface of the intestine, food restriction can reverse the process and bring it closer to normal. This phenomenon can be reproduced using pharmacological and genetic approaches, thereby suggesting potential means for limiting obesity.These results will be published in the journal Nature Communications..

Worldwide, hundreds of millions of adults and children are clinically obese. A condition that is closely associated with major causes of death such as heart disease and stroke. Obesity is primarily due to an imbalance between energy expenditure and caloric intake. This happens in the intestines where previously decomposed food is absorbed and enters the bloodstream, where it is distributed throughout the body. To absorb enough calories Intestinal wall Is layered with millions of convolutions called microvilli and villi that can cover the surface of the soccer field.

Impressive and quick effect

“A few years ago, we discovered that the intestines could become longer or shorter depending on environmental triggers and physiological needs,” said Mirko Trikovsky of the Faculty of Cell Physiology and Metabolism and the Diabetes Center of the University School of Medicine. The professor looks back. The author of this study. “Therefore, we wanted to understand what promotes this amazing intestinal plasticity.” Using various mouse models combined with human intestinal biopsy (3D artificial structure), the research team consumed. We observed that the amount of food consumed was the main regulator of intestinal length. “There was a relatively fast and physiologically impressive response to increasing the amount of food consumed. Intestinal length increased by more than 30%, with major growth of villi and microvilli. Coupled with this, it contributed to improving the caloric intake capacity of the intestines. ”Mirko Trikovsky is added. Importantly, these changes were reversible. By reducing the amount of food, the length and morphology of the intestines became closer to normal.

Plasticity under the control of PPARα protein

Dilation of the intestines requires a lot of energy. UNIGE scientists have discovered that increasing the absorption surface of the intestine mobilizes various metabolic pathways in the intestine, the steps by which cells convert food into energy. They discovered several potential pathways that could contribute to intestinal dilation, but one found that the PPARα pathway was essential. In fact, PPARα is a protein that appears to be very important not only for increasing the length of villi, but also for increasing the ability to take calories from food by increasing the level of another protein, PLIN2. Promotes the formation of lipid droplets. Intestinal cells, thereby promoting fat absorption. By inactivating PPARα in the intestine of mice, researchers were able to confirm this mechanism. “Intestinal PPARα deletion or its pharmacological inhibition has shown a significant effect in reducing intestinal absorption function. Intestinal-specific PPARα inhibition has fat accumulation and obesity, and high calorie feeding. It was enough to undo the impaired glucose tolerance caused by. “, Mirko Trikovsky explains.

Impressive bowel plasticity, which allows the bowel and villi to shrink or expand, is a reversible alternative to gastric bypass surgery or other interventions aimed at reducing weight gain and obesity-related complications. It is an asset that is further explored as. “PPARα is an important protein for many metabolic functions and is expressed in various tissues throughout the body. Therefore, prior to applying these findings to patients, they are selectively in the intestine without reaching other organs. We need to develop a way to inhibit it. “, Concludes the author.


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For more information:
Ozren Stojanovićetal, overeating, regulates the absorption and surface of the intestinal epithelium via PPARα in the intestine. Nature Communications (2021). DOI: 10.1038 / s41467-021-27133-7

Quote: How Food Intake Changes the Intestine (December 2, 2021) Obtained from December 2, 2021 https://medicalxpress.com/news/2021-12-food-intake-gut.html

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