Gut Microbiota and Diabetes

Type 2 diabetes is a disorder of the body’s energy supply system which absorbs dietary glucose (its primary energy source) from the gut and either transports it to organs requiring energy or stores the energy as fat until needed. Genetic, dietetic, and metabolic factors have long been known to contribute to the development of the disorder. More recently, the gut microbiota has also been identified as a factor.

The hallmarks of Type 2 diabetes are: 1. an excess of dietary glucose; 2. reduced insulin production; and 3. decreased sensitivity to insulin (called insulin resistance). The gut microbiota affects all these elements.

The Gut Microbiota Increases Available Glucose from the Gut

The gut microbiota makes additional glucose and other sugars available to its host by degrading complex carbohydrates present in the gut which the host’s digestive system could not. Mice raised germ-free (a condition that can only be maintained in a laboratory), and, thus lacking gut microbiota, typically have less body fat than those raised conventionally. But when these germ-free mice are seeded with gut microbiota from conventionally raised mice, they soon develop as much fat as the conventional mice. The source of this fat is the additional sugars and metabolites made available by the microbiota. In addition, the microbiota upregulates the host’s metabolic storage pathway, storing the energy from these nutrients in fat storage cells, though how it does this is not known.

Sensitivity to insulin decreases with chronic high blood glucose well before one becomes diabetic. There are also noticeable changes in gut microbiota composition, one being a decrease in butyrate producing bacteria.

Gut Microbiota Dysfunction Exacerbates Inflammation That Affects Insulin Production

The chronically high blood glucose levels characteristic of obesity and prediabetes initiate inflammation in the pancreatic islets where insulin is produced. If the inflammation becomes chronic, islet cells will die, thus reducing insulin output. Deleterious changes in the gut microbiota contribute to this chronic state of inflammation. The same chronically high blood glucose levels that initiate inflammation in the pancreatic islets also affect the composition of the gut microbiota. Under such conditions, the population of microorganisms that produce short chain fatty acids (SCFAs) decreases significantly. One of the roles of SCFA’s is to maintain the integrity of the gut wall lining, the semipermeable membrane that selectively controls what enters the host’s blood stream. As SCFA levels decrease, the gut wall becomes more permeable, allowing lipopolysaccharides (LPS’s) to pass into the blood. LPS’s are toxic molecules that shed from the cell walls of certain bacteria (whose numbers also increase with chronically high blood glucose). LPS’s are potent initiators of inflammation, so as they continuously feed into the blood, the inflammation becomes chronic.

Changes in Gut Microbiota Composition Protect Against Insulin Resistance

Sensitivity to insulin decreases with chronic high blood glucose well before one becomes diabetic. There are also noticeable changes in gut microbiota composition, one being a decrease in butyrate producing bacteria. When gut microbiota is transplanted from lean healthy human males into males who are prediabetic the transplant recipients become more sensitive to insulin and the composition of their gut microbiota changes, becoming similar to that of the donor. Studies in mice have linked such increased insulin sensitivity to an increase in butyrate producing bacteria in the gut. Unfortunately, the improved insulin sensitivity and the changes in microbiota composition only last for several months, indicating that host and diet exert an ongoing influence on microbiota composition.


The composition of the gut microbiota influences the essential elements of Type 2 diabetes by determining what undigested materials will be degraded, what products will be produced, and in what quantities. While much research has been done in the last 20 years, much more needs to be done to understand the mechanisms and other details that will allow us safely to provide effective solutions for prevention and treatment of Type 2 diabetes.

[1] Donath, M. Y., Dalmas, É., Sauter, N. S., & Böni-Schnetzler, M. (2013). Inflammation in obesity and diabetes: islet dysfunction and therapeutic opportunity. Cell metabolism, 17(6), 860–872.

[2] Janssen, A. W., & Kersten, S. (2017). Potential mediators linking gut bacteria to metabolic health: a critical view. The Journal of physiology, 595(2), 477–487.

[3] Mandaliya, D. K. & Seshadri, S. (2019). Short Chain Fatty Acids, pancreatic dysfunction and type 2 diabetes. Pancreatology, 19(2), 280–284.

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