Compositional and functional differences in gut bacteria exist between adults with normal glucose tolerance, IGT and type 2 diabetes and can change with dietary factors. We compared the gut microbiome between adults with impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and IFG+IGT and evaluated the impact of dietary glycemic index (GI) on the gut microbiome. The study enrolled 53 adults (mean±SEM: age 53.0±1.4 y, BMI 32.5±0.9 kg/m2) with IFG (n=20), IGT (n=10) or both IFG+IGT (n=23). Stool samples were collected in RNAlater after 2 weeks on a control, moderate GI diet (GI 55-58) and again after a 4 week dietary intervention of a low GI (GI<35, n=18) or high GI diet (GI>70, n=18 on placebo and n=17 on the antioxidant N-acetyl-cysteine 1200 mg po BID). Diets had the same macronutrient composition (55%carbohydrate/30% fat/15% protein) but more fiber in the LGI (65.1±2.2 g/d) vs. HGI diet (25.8±0.8 g/d). The stool microbiome was analyzed using 16S rRNA gene sequencing (V1-V3).

Results: α diversity was significantly higher in IGT vs. IFG+IGT (7.2±0.08 vs. 7.0±0.06, p<0.05). Linear regression analysis adjusted for age, sex, BMI, race and sequencing plate showed 3 genera differed across groups on the control diet: Fusicatenibacter (p=0.01) and Lachnospiraceae UCG-008 (p=0.02) were lower in IGT vs. IFG+IGT; Oxalobacter was reduced in IFG (p=0.04) and enriched in IGT (p=0.004) vs. IFG+IGT. After 4 weeks on LGI or HGI diets α diversity did not differ and NAC had no effect on the microbiome. Adjusted regression analysis showed only the genus Anaerostipes differed, being higher in the LGI group (p<0.0001).

Conclusions: Differences in microbiota were observed between IGT and IFG+IGT. These associations may contribute to poorer metabolic function in IFG+IGT, but would need further testing to determine cause and effect. The LGI diet was associated with higher Anaerostipes, a butyrate producing bacteria with beneficial anti-inflammatory effects. This may be related to the higher fiber content of the LGI diet.

Disclosure

K. Utzschneider: Other Relationship; Self; Medtronic. M.L. Neuhouser: None. K.M. Newton: None. K. Breymeyer: None. M.A. Hullar: None.

Funding

National Institutes of Health (R01DK092568, P30DK017047, UL1TR002319, P30CA015704, KL2TR002317, TL1TR002318)

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