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-α and IFN-γ 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.