As obesity soars globally, diabetes is close behind.
Type 1 is not connected to obesity. It results from autoimmune destruction of pancreatic beta cells which produce insulin. But microbiota may play a role in its development.
Another form is glucose intolerance caused by the stresses of pregnancy—gestational diabetes. Most women will return to normal blood sugars after delivery but remain at increased risk for Type 2 diabetes.
Type 2 results from impaired insulin production and from insulin resistance in muscles, liver and fat cells. Obesity comes into play here; it is a major risk factor.
Restoration of normal blood sugars is the goal in all three types. Medication, diet, and exercise are key therapies.
Probiotics are now being investigated as adjuncts to optimum blood sugar control. Here’s why:
In obesity, a major risk factor for diabetes, there is an imbalance between two dominant groups of bacteria, the Bacteroidetes and the Firmicutes; the amounts differ between lean and obese mice. Obese mice had a higher proportion of Firmicutes to Bacteroidetes than the lean mice.
Often in Type 2 diabetes, insulin is sufficient but the cells are resistant to its passage. Intestinal bacteria are known to play a critical role in insulin resistance. In a number of studies in both rodents and humans, microbial food supplements have been effective in treating insulin resistance.
Insulin resistance is linked to systemic inflammation.
In the liver, the inflammatory process is partially moderated by T cells of the natural killer and T varieties (NKT). It is hypothesized that high fat diet depletes NKT cells in the liver, precipitating harmful inflammatory signaling and metabolic changes such as insulin resistance.
Probiotics may have a role in restoring NKT cells in the liver thereby lessening insulin resistance.
In addition, a June 2014 review of 121 studies in Nutrition Journal by Aline Corado Gomes and colleagues suggests that with an optimum microbiota, there is an “ increase the expression of adhesion proteins within the intestinal epithelium, reducing intestinal permeability. Such effects increase insulin sensitivity and reduce autoimmune response.” This mechanism may also facilitate the absorption of antigens which can injure pancreatic β cells in Type 1 diabetes. However, this is not fully understood.
Diabetes is not going away.
It burdens families and governments with suffering and exorbitant costs in treatment. Further research into a link between our microbiota and this epidemic of diabetes will be most welcome.