1, 2, 3 diabetes

The human gut harbours trillions of bacteria in a great diversity. The composition of the intestinal bacteria in obese people differs from that in lean people. As such that wouldn't have to mean a thing, but the bacteria of obese people appear to be more effective in extracting usable calories (in the form of short chain fatty acids) from food fibres. This can be the perfect excuse for your overweight: blame the bugs! But there’s more to it. Those obese bacteria also have a negative effect on the barrier function of the gut epithelium and this line of defence becomes more permeable. As a consequence, bacterial compounds such as lipopolysaccharide (LPS in short) can pass the gut wall, enter the body and cause chronic inflammation. This chronic inflammation, in mysterious ways, causes insulin resistance, metabolic syndrome, and ultimately type 2 diabetes. 

Now also for type 1 diabetes a relation with gut microbiota has been found. Huriya Beyan, in a paper in Current Diabetes Reports has coined the phrase Guts, Germs and Meals to this relation, with reference to the bestseller by Jarred Diamond. Do realize that type 1 diabetes is totally different from type 2. Type 1 is an autoimmune disease in which the immune system attacks and destroys the (insulin producing) beta cells in the isles of Langerhans in the pancreas. Children with type 1 diabetes have a different composition of the intestinal bacteria as compared with healthy children. As such that wouldn't have to mean a thing, but now there are fascinating new data from a mouse model of type 1 diabetes. These mice are called NOD mice, which stands for Non-Obese Diabetic. Female NOD mice will develop a more severe diabetes than male NOD mice, and at an earlier age. When gutmicrobiota from male mice are transferred to female mice, the female mice will develop a less severe diabetes, and at a later age. What do we learn from this? There are differences in gut microbiota between male and female mice (also between male and female humans). The term microgenderome is used to describe this phenomenon. Furthermore: this difference is relevant for type 1 diabetes and may offer a novel opportunity for treatment. 

What about type 3 diabetes? Epidemiologically there is an overlap of Alzheimer’s Disease and type 2 diabetes. The term type 3 diabetes which now is popping up in the medical literature is debatable because at the level of the brain there is no hyperglycemia, but there is insulin resistance. Apart from the metabolic resemblance, also the inflammation in Alzheimer may be similar to that in type 2 diabetes. A direct link between Alzheimer and gutmicrobiota has not been established but it is attractive to speculate. Even more attractive it is to start research into this field, because more knowledge about the intricate relations between nutrition, gutmicrobiota, immunity and brain function eventually could lead to novel ways for prevention and treatment.