Diabetes Starts in the Intestines, According to Study

by Mark Benson on February 16, 2012

Diabetes comes from intestines

According to scientists at the Washington University School of Medicine in St. Louis, the origins of diabetes may be controlled from the intestines and this is where blood sugar can eventually be controlled in the long run.

The study results were found in laboratory mice and may debunk long-held theories and conclusions about the cause of this metabolic condition. Since insulin is produced in the pancreas and sugar is stored in the liver, scientists have focused on these important digestive system organs to find the cause of diabetes.

These findings would be published in the February 16 of the Cell Host and Microbe Journal.

The new research studied laboratory mice that are unable to synthesize fatty acid synthase (FAS) in the intestinal tract. FAS are enzymes that are important in the production of lipids, a compound regulated by insulin. Individuals suffering from diabetes also have issues with their FAS levels. During the experiments, mice that do not produce the enzyme eventually develop inflammation in the stomach area, a known marker for diabetes.

According to principal study author Clay F. Semenkovich MD, “Diabetes may indeed start in your gut. When people become resistant to insulin, as happens when they gain weight, FAS doesn’t work properly, which causes inflammation that in turn, lead to diabetes.” Semenkovich is the current Herbert S. Gasser Professor of Medicine, professor of cell biology and physiology and Director of the Endocrinology, Metabolism and Lipid Research Division.

Another study author, Xiaochao Wei PhD and Semenkovich worked with specialists in gastroenterology and genome sciences to determine the issues related to the inability of producing the FAS enzyme in the mice intestines. He said, “The first striking thing we saw was that the mice began losing weight. They had diarrhea and other gastrointestinal symptoms and when we looked closely at the tissue in the gut, we found a lot of inflammation.”

The researchers initially theorized that the mice became sick due to the changes in the microbial mix that live in the gut where these help in digestion and synthesis of food and vitamins. Under further scrutiny with the Center for Genome Sciences and Systems Biology at the School of Medicine, the gut microbes in the mice were checked. They found that the mice had substantial changes in their gut microbiome but the problems were not because of the composition.

The study found that the reason the mice got sick because of the defect in the fatty acid synthase. Without the fatty acid synthase, the stomach lining of the mucus got thinner and this caused problems, as it is this lining that separated the microbes from the direct exposure to the cells. The thinner protective lining allowed bacteria to penetrate healthy cells in the gut resulting in the illness in the mice.

Wei added, “Fatty acid synthase is required to keep that mucosal layer intact. Without it, bad bacteria invade cells in the colon and the small intestine, creating inflammation and that in turn, contributes to insulin resistance and diabetes.”

Insulin resistance and inflammation helps each other, as inflammatory substances can cause insulin resistance and inhibit insulin production. These two conditions affect the regulation of blood sugar, as does insulin resistance, which promotes inflammation. The layer of mucosal cells was hindered with the lack of or low levels of FAS.

The opinions expressed in this article do not necessarily reflect the views of the DiabetesForum.com Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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