Probiotic yogurt is suggested as a nutritional approach in type 2 diabetes (T2D) and obesity. We performed a systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating the effects of probiotic yogurt on glycemic outcomes in T2D or obesity. The databases used to search for RCTs included Medline and Scopus. The RCTs were eligible if outcomes included selected glycemic markers. In nine eligible trials, 237 and 235 subjects were in treatment (probiotic yogurt) and control (mostly conventional yogurt) groups, respectively. There was no significant difference for pooled unstandardized mean difference (USMD) hemoglobin A1c (HbA1c) by probiotic yogurt compared with the control in T2D (USMD: −0.366; 95% CI: −0.755, 0.024, p = 0.066) and obesity (USMD: 0.116, 95% CI: −0.007, 0.238, p = 0.065). Similarly, there were no effects of probiotic yogurt on fasting blood glucose, fasting insulin, or insulin resistance (estimated by homeostatic model assessment of insulin resistance (HOMA-IR)) in either T2D or obesity. In conclusion, the present meta-analysis has not demonstrated the benefits of consuming probiotic compared with conventional yogurt for improving glucose control in patients with diabetes or obesity. Larger trials are needed to verify the benefits of probiotic and/or conventional yogurt or other probiotic fermented milk (e.g., kefir) on glycemic markers in patients with diabetes and obesity.

The gut microbiota is known to be related to type 2 diabetes (T2D), psychiatric conditions, and opioid use. In this study, we tested the hypothesis that variability in gut microbiota in T2D is associated with psycho-metabolic health. A cross-sectional study was conducted among African American men (AAM) (n = 99) that were outpatients at a Chicago VA Medical Center. The main outcome measures included fecal microbiota ecology (by 16S rRNA gene sequencing), psychiatric disorders including opioid use, and circulating leptin and oxytocin as representative hormone biomarkers for obesity and psychological pro-social behavior. The study subjects had prevalent overweight/obesity (78%), T2D (50%) and co-morbid psychiatric (65%) and opioid use (45%) disorders. In the analysis of microbiota, the data showed interactions of opioids, T2D and metformin with Bifidobacterium and Prevotella genera. The differential analysis of Bifidobacterium stratified by opioids, T2D and metformin, showed significant interactions among these factors indicating that the effect of one factor was changed by the other (FDR-adjusted p [q] < 0.01). In addition, the pair-wise comparison showed that participants with T2D not taking metformin had a significant 6.74 log2 fold increase in Bifidobacterium in opioid users as compared to non-users (q = 2.2 x 10⁻⁸). Since metformin was not included in this pair-wise comparison, the significant ‘q’ suggested association of opioid use with Bifidobacterium abundance. The differences in Bifidobacterium abundance could possibly be explained by opioids acting as organic cation transporter 1 (OCT1) inhibitors. Analysis stratified by lower and higher leptin and oxytocin (divided by the 50^th percentile) in the subgroup without T2D showed lower Dialister in High-Leptin vs. Low-Leptin (p = 0.03). Contrary, the opposite was shown for oxytocin, higher Dialister in High-Oxytocin vs. Low-Oxytocin (p = 0.04). The study demonstrated for the first time that Bifidobacterium and Prevotella abundance was affected by interactions of T2D, metformin and opioid use. Also, in subjects without T2D Dialister abundance varied according to circulating leptin and oxytocin.