Grant: Project Grant

Consuming excessive fructose, either directly or as part of sucrose (table sugar), can lead to a fatty liver and high blood sugar. One concern is that too much fructose might increase gut fat absorption, but we are not sure how it affects the absorption of glucose, the primary source of energy for our bodies. We know the gut microbiota (the community of bacteria living in our intestines) can modulate gut glucose absorption. We think the gut microbiota during high fructose influences the gut's capacity to absorb glucose, which can contribute to problems like fatty liver and diabetes. We know that some of the excess fructose ends up in the liver, but it also accumulates in the lower part of the small intestine and colon. Here, gut bacteria break down fructose into various products. We still do not understand how these microbial by-products of fructose can cause metabolic disease. Our research involves using mice to study the effects of a high-fructose diet. We have found that excessive fructose can enlarge the surface area of the gut, leading to increased glucose absorption, high blood sugar, and a fatty liver. We will now examine different sections of the intestine to see how the gut microbiota and the structures involved in sugar absorption change in these mice. To further explore the role of the microbiota, we will transfer the bacteria from high-fructose-fed mice to mice without any bacteria. This will help us determine if the microbiota alone can contribute to fatty liver and high blood sugar. Additionally, we'll use labeled fructose to track how the bacterial by-products of fructose are used by the body. Our research will shed light on how gut bacteria can link excessive fructose consumption to metabolic problems. Our work will lay the groundwork for new gut microbiota-based strategies to fight diabetes and fatty liver disease.