In the 1970s, stool tests were still looking for certain bacteria (colicems). Later, it became apparent that coli germs alone play only a minor role in the intestinal flora. So the stool examination disappeared again. It is only through research into the microbiome in recent years that it has taken on a new lease of life – with very interesting results, especially in diabetes.
Nestor of German diabetology
Who does not know him? Prof. Hellmut Mehnert, MD, has been active in the field of diabetology for over 50 years. Even today, the former chief physician of the 3rd Medical Clinic of the Munich-Schwabing Hospital gives lectures and does educational work. Prof. Mehnert wants to communicate diabetes research in such a way that it can also be implemented by general practitioners in private practice. In this spirit, “Mehnert’s Diabetes Tips” are also written, which will appear as a series in Allgemeinarzt and hopefully help you to take better care of your diabetes patients.
Studies in animals and humans suggest a possible link of intestinal microbiota with regard to insulin resistance and diabetes. Bacteria often play some role in the development, prevention and treatment of type 1 and type 2 diabetes.
Humans are hosts to billions of intestinal microbes, of which various genera populate our organism in large numbers. Their totality is called the microbiome. This includes not only the intestinal bacteria, but also all the microorganisms of our skin flora. Among the billions of microorganisms, bacteria mainly dominate. However, fungi, viruses and protozoa are also found. All of them together exceed the number of all other human cells by a factor of ten.
Genetics is more accurate
New genetic analyses allow detailed determination of the microbiome. This has led to a huge, worldwide increase in research. It turns out that bacteria from the gut can activate host cells. Scientists therefore studied the gut microbiome and glucose metabolism of type 2 diabetics. In this study, 18 men received a stool transplant (colonoscopic administration of a stool suspension) that was either a self-donation or came from outside donors of normal weight.
It was found that within six weeks after the procedure, the insulin resistance of the diabetic patients treated with foreign donation was significantly higher than with self-donation. This was true not only for peripheral insulin sensitivity, but also for hepatic insulin resistance. The researchers noted that this resulted in more butyrate-forming bacteria. Animal studies have shown that mice lacking a short-chain fatty acid receptor in the intestine became obese on a normal diet, while an overexpressed presence of the receptor resulted in normal weight even on a high-fat diet.
Energy balance was mostly positively affected in animal studies. For short-chain fatty acids, it could be shown by MRI that, when present in the intestine, they can cause a number of metabolic changes via binding to receptors, which also lead to changes in glucose balance.
Results for type 1
Similar studies to those described for type 2 diabetes are now also available for type 1 diabetes. In animal experiments, it was shown that germ-carrying mice could be protected against the occurrence of insulitis of the islets of Langerhans, which is typical for type 1 diabetes. This effect could not be shown in germ-free mice. On the contrary, they developed type 1 diabetes more frequently than the control group.
In further investigations, healthy test participants in a control group showed significantly higher numbers of butyrate- and lactate-forming bacterial strains compared to the group suffering from type 1 diabetes. These results suggest that a contribution of microorganisms to the occurrence of type 1 diabetes is at least possible.
There are a number of influencing factors beyond the so-called core microbiome and the three dominant enterotypes that can alter the composition of the microbiome under certain circumstances. The occurrence of other bacteria and infections, the use of antibiotics and, last but not least, the diet play a role here.
Specific beneficial effects have been associated with the addition of prebiotics or probiotics. Apparently, they can protect against insulin resistance and promote the desired effect of short-chain fatty acids. In contrast, a low-fiber and meat-based diet is associated with negative effects such as increased endotoxemia. However, antibiotic use also appears to be able to adversely alter the composition of the microbiome over a long period of time.
For the microbiome, we now have insights into its complicated relationships and metabolic pathways. However, further research is definitely needed to further understand the basic mechanisms. It is also important to note that the current results are mainly based on animal models and on simple study observations in humans with small numbers of cases.
Of course, fecal delivery – endoscopically via the colon – which yielded important results, is not feasible in practice. Much more thought should be given to capsules that dissolve in the colon and contain appropriately “beneficial” stool. The demand for a strict indication for the use of broad-spectrum antibiotics is derived from this. This has already been raised in view of the worldwide threat of an increase in bacterial resistance.
Bacterial infections, which can promote the composition of the microbiome, would of course have to be treated accordingly. The question is whether the devil must not be cast out with the Beelzebub here by giving antibiotics after all. The so-called core microbiome is apparently retained by humans throughout their lives.

Conclusion
The bottom line is that the decades of research into the pros and cons of the importance of the microbiome, especially the gut flora, have entered a new stage. What initially amounted to an overestimation of the coli germs has, after a low point in the history of the intestinal flora, now given way to new findings that assign a new significance to the microbiome with its billions of germs in the intestine, but also on the skin. It will be interesting to see what the results of further research will be and whether they can deliver what they promise on the basis of the initial investigations with regard to influencing the development of type 1 and type 2 diabetes.
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