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    How diabetes is linked to gut bacteria

    Manipulating the microbiome can play a role in preventing disease

    The majority of cells within our bodies are not human—nor is the majority of our DNA. We are hosts to 1014 bacterial cells (50 percent to 90 percent of all cells) that make up as much as 95 percent of our total DNA.1 Most of these organisms live within the gastrointestinal (GI) tract but also within the genitourinary tract, on our skin, and on the ocular surface—forming what is collectively known as the “microbiome.”

    Given this abundance of nonhuman species living on and within our bodies, it is not surprising that there is a link between specific bacteria to systemic and ocular disease—including diabetes and diabetes-related eye disease.

    What studies tell us

    A reduction in gut bacterial diversity precedes the onset of clinical diabetes.2 Reduction of intestinal species that produce short-chain fatty acids (SCFAs), especially butyrate but also propionate and acetate, appears to be particularly important. These SCFAs improve insulin sensitivity by stimulating peroxisome-proliferator agonist gamma receptors3 (PPARg), analogous to the PPARg diabetes medication, pioglitazone (Actos, Takeda).

    Previously from Dr. Chous: Using OCT with your diabetes patients

    Butyrate enhances production of the intestinal hormone, glucagon-like peptide-14 (GLP-1), which increases insulin production, decreases glucagon secretion, and inhibits appetite. The mechanism is analogous to GLP-1 analog drugs like exenatide (Byetta, Amylin) and liraglutide (Victoza, Novo Nordisk).

    Butyrate also enhances intestinal barrier function, preventing translocation of bacteria and lipopolysaccharides derived from the cell walls of Gram-negative organisms (endotoxemia) that leads to so-called “leaky gut syndrome.” Leaky gut syndrome has been linked to autoimmunity in type 1 diabetes and inflammatory cytokine production in type 2 diabetes (T2DM).5,6

    Related: How diabetes affects contact lens wear

    Introduction of butyrate-producing bacteria via probiotic supplementation has been shown to improve insulin sensitivity and reduce inflammation in humans with type 2 diabetes.7

    Perhaps more convincingly, transplanting fecal material from healthy adults with markedly higher numbers of butyrate-producing bacteria to obese patients with T2DM and lower numbers of such bacteria resulted in nearly 80 percent better insulin sensitivity in one small study.8

    Recent meta-analysis of 11 studies with more than 600 subjects shows that multi-species probiotic supplementation modestly but significantly improves insulin resistance, excess insulin production, fasting blood sugars, and mean blood glucose (HbA1c) in humans with T2DM.9

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    Optometry Times A/V