The gut microbiome is the term used to describe the bacterial ecosystem that lives within the human gut. We can carry up to 2 kg of bacteria within the bowel, and the total number of genes in the various species living within the gastrointestinal tract likely exceeds the number of human genes by at least two orders of magnitude. There is considerable variation between individuals in the composition of these bacteria. We could arguably consider each individual as a composite ecosystem of both human and bacteria. When viewed in these terms, it is perhaps not surprising that there is evidence of a relationship between the make-up of our bacterial flora and health or disease (Brenchley and Douek, 2012). The main focus, until recently, has been the relationship between the gut microbiota and obesity. Rodent studies suggest there are specific microbiota that may be more efficient at harvesting energy from the diet and so predispose to obesity. These can be transmitted between animals and are associated with weight gain. There is less evidence, however, that changing the intestinal flora is associated with weight loss.
Alkanani and colleagues present a study (summarised alongside) suggesting a link between alterations in intestinal bacterial composition and the risk of developing type 1 diabetes. The background to this paper is a number of studies showing a relationship between gut microbes and host immunity. These were mostly rodent studies. The Alkanani study differs as it had an observational design and was conducted in humans.
The authors use the term dysbiosis to describe changes in the intestinal microbe population that may contribute to disease – in this case type 1 diabetes. Stool samples were analysed from four cohorts: one group with new-onset type 1 diabetes, one group of autoantibody-positive individuals without diabetes, a group of first-degree relatives of individuals with type 1 diabetes (without autoantibodies) and a healthy control group.
The bacteria growing within the gut are diverse and the number of subjects studied was relatively small (20–35 in each group). As a consequence, the analysis is complicated and rather unclear. The authors describe differences in the bacterial makeup between seropositive and seronegative individuals and between healthy controls and the other groups. However, it is worth noting that these differences were only observed in a small number of what were multiple analyses. The idea is interesting but the authors have not yet proved their point.
To read the article summaries, please download the PDF
Attempts to achieve remission, or at least a substantial improvement in glycaemic control, should be the initial focus at type 2 diabetes diagnosis.
9 May 2024