Glycation of gut proteins initiates microbial dysbiosis and can promote establishment of diabetes in experimental animals

Diabetes and obesity is associated with change in the gut microbiota, however, the reason for such transition is still unknown. The secondary complications in diabetes mainly stem from protein glycation, oxidative stress and inflammatory response. It is intended to study the correlation between gut proteins glycation and microbial dysbiosis and thereby progression to diabetes. The study was carried out through feeding high fructose to male Wistar rats and evaluating their gut microbiota. The rate of gut flora excretion via faecal matter was found to decrease on fructose feed for 7 days. Intestinal flora was drastically reduced and pathogenic succession observed. Intestinal fluorescence studies confirmed that there is heavy glycation of gut proteins. Microbes obtained from fructose fed animals could grow on glycated BSA. There was significant increase in level of TNF-alpha and IFN-gamma providing evidence of inflammation. Though microbial dysbiosis was observed in diabetes, the cause for this remained elusive. In the present study we prove that high fructose feed and glycation of the gut proteins probably prevent adherence/survival of the gut microflora in control animals and promotes transition to a changed microflora which is capable of adhering/utilizing glycated proteins as well as high fructose. The changed microbiota, enhanced protein glycation and inflammation help in establishing insulin resistance.

Automated summary

The study reveals that high fructose feed can lead to microbial dysbiosis, reducing gut flora and promoting pathogenic succession, thereby exacerbating glycation of gut proteins and triggering an inflammatory response. These changes increase the likelihood of insulin resistance.