Changes in Oral and Intestinal Bacterial Flora Associated with Pain Thresholds

Small fiber neuropathy (SFN) manifests from the early stages of diabetic polyneuropathy. Changes in the oral and intestinal bacterial flora are known to be associated with the onset and progression of diabetes and its complications. However, correlation between SFN and each bacterial flora has not yet been investigated. In the 2018 Iwaki health promotion project, which is a local health promotion study in Aomori prefecture, 1037 participants (431 males and 6females including 814 non-glucose metabolism disorders, 143 fasting hyperglycemia (IFG) , and 80 type 2 diabetic cases (DM) , were evaluated. SFN was evaluated by the pain threshold evoked by intraepidermal electrical stimulation (PINT) . A PINT value of 0.or less was designated as Pint-L, and otherwise was designated as Pint-H. DNA was isolated from saliva and feces and relative bacterial abundance was determined with a next-generation sequencer. Bacteria that account for 1% or more of all bacteria were examined. PINT was significantly increased in IFG (0.12 ± 0.11mA) and DM (0.15 ± 0.13mA) compared to healthy subjects (0.± 0.08mA) (p<0.vs. IFG, p <0.vs. DM) . No significant difference was found depending on the PINT value in the bacteria flora of oral cavity. There were significant differences of gut bacterial flor in α and β-diversity (p<0.05) and principal component analysis (p <0.01) depending on the PINT value. The genus Bacteroides was significantly higher in PINT-H than in PINT-L (p<0.01) . After IFG and DM cases were excluded, a significant difference was maintained. The amount of bacteroides was significantly correlated with age, abdominal circumference, fasting blood glucose, HbA1c (p<0.001) , BMI and PINT value (p <0.05) . In the multiple regression analysis adjusted for these factors, PINT was significantly correlated with the amount of Bacteroides (β = -0.089, p = 0.026) . Our results suggest that the gut Bacteroides may correlate with SFN. The involvement of deterioration of glucose metabolism may not be high in this correlation. Disclosure K.Kudoh: None. Y.Takeuchi: None. S.Osonoi: None. T.Sasaki: None. S.Ogasawara: None. S.Yagihashi: None. H.Mizukami: None.