Is Type 2 diabetes a disease of the gut?

Kathleen Blanchard's picture
Type 2 diabetes might start in the intestine, finds new research.

New research challenges the way Type 2 diabetes starts. According to new findings the disease might start in the gut. The pancreas produce insulin and sugar is stored in the liver, which has led to researchers to look at the two organs rather than the intestines for the cause of diabetes.

Fatty acid synthase, inflammation in the gut, diabetes link

In a study published in the journal Cell Host & Microbe, researchers found mice unable to produce fatty acid synthase (FAS) in the intestine develop chronic inflammation in the gut, which it also a strong predictor of diabetes. The enzyme is crucial for the production of lipids that are part of the cell membrane structure and essential for energy storage.

Clay F. Semenkovich, MD., a study investigator said in a media release, “When people become resistant to insulin, as happens when they gain weight, FAS doesn’t work properly, which causes inflammation that, in turn, can lead to diabetes.”

When people develop insulin resistance that precedes diabetes they begin to gain weight. The researchers noted when FAS in the gut wasn’t working the mice lost weight and had diarrhea and other gastrointestinal symptoms.

At first the scientists from University of Washington who conducted the study thought the mice were unhealthy from an imbalance of microbes in the intestine, but it turns out the mice were sick from inability to synthesize FAS.


First author Xiaochao Wei, PhD, and Semenkovich, the Herbert S. Gasser Professor of Medicine, professor of cell biology and physiology and director of the Division of Endocrinology, Metabolism and Lipid Research said in a press release, “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.”

Inflammation is linked to a variety of serious diseases, including diabetes. Insulin resistance causes inflammation; conversely inflammation can cause insulin resistance.

The scientists found faulty FAS also prevented the intestine’s ability to build an important and protective thin layer of mucosal cells.

Next the researchers plan to study people with Type 2 diabetes to see if the gut enzyme is altered in the same way found in the mouse study. If it turns out to be so, it may be possible to treat diabetes by targeting FAS in addition to a key component in the intestinal mucosa called Muc2.

Semenkovich says it makes sense that Type 2 diabetes might start in the gut. Many people with diabetes develop gastrointestinal difficulties, he notes, with diarrhea and abdominal pain being the most common complaint.

Cell Host and Microbe
"Fatty Acid Synthase Modulates Intestinal Barrier Function through Palmitoylation of Mucin 2"
Xiaochao Wei, et al.
February 16, 2012

Image credit: Wikimedia commons



Have had all sorts of problems with stomach etc feeling icky etc. for many years before being diagnosed with typt 2
I remember at like 12yrs old my stomach giving me a lot of problems, and it has giving me problems into my adulthood. Well before i was diagnosed in 2006.
I can remember since I was 5 always having terrible stomach problems and years and years of diarrhea.
Could it be possible for the bacteria called H -pylori caues diabetis?
I don't know, but H.Pylori affects the stomach. The researchers see a relationship between what happens lower down in the intestines, so I would think not. - but more research will be interesting or sure.
Look at all the patients who have had Lapband or similar. Thier blood sugars are under control before they leave the hospital. That is not weight loss, like we have always been told. Don't get me wrong, weight loss is a very good thing. But I am beginning to think there is more to it. My mother weighed 100 lbs, my father about 140, and my brother is very slim. Not me it , it is a constant struggle, and I will never ever be where I should..