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. 2022 Jul 18:9:825897.
doi: 10.3389/fnut.2022.825897. eCollection 2022.

Comparative analysis of the efficacies of probiotic supplementation and glucose-lowering drugs for the treatment of type 2 diabetes: A systematic review and meta-analysis

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Comparative analysis of the efficacies of probiotic supplementation and glucose-lowering drugs for the treatment of type 2 diabetes: A systematic review and meta-analysis

Tingting Liang et al. Front Nutr. .

Abstract

The aim of this systematic review and meta-analysis was to evaluate the effects of probiotics and glucose-lowering drugs (thiazolidinedione [TZD], glucagon-like pep-tide-1 receptor agonists [GLP-1 RA], dipeptidyl peptidase IV inhibitors, and sodium glucose co-transporter 2 inhibitors [SGLT-2i]) in patients with type 2 diabetes from randomized con-trolled trials (RCTs). The PubMed, Web of science, Embase, and Cochrane Library databases were searched on the treatment effects of probiotics and glucose-lowering drugs on glycemia, lipids, and blood pressure metabolism published between Jan 2015 and April 2021. We performed meta-analyses using the random-effects model. We included 25 RCTs (2,843 participants). Overall, GLP-1RA, SGLT-2i, and TZD significantly reduce fasting blood sugar (FBS) and glycated hemoglobin (HbA1c), whereas GLP-1 RA increased the risk of hypoglycaemia. Multispecies probiotics decrease FBS, total cholesterol (TC), and systolic and diastolic blood pressure (SBP, DBP). Moreover, subgroup analyses indicated that participants aged >55 years, BMI ≥30 kg/m2, longer duration of intervention, and subjects from Eastern countries, showed significantly higher reduction in FBS and HbA1c, TC, TG and SBP. This meta-analysis revealed that including multiple probiotic rather than glucose-lowering drugs might be more beneficial regarding T2D prevention who suffering from simultaneously hyperglycemia, hypercholesterolemia, and hypertension.

Keywords: glucose-lowering drugs; glycemic; lipids; meta-analysis; probiotics; type 2 diabetes.

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Figures

Figure 1
Figure 1
Flow chart depicting the literature search and selection strategy (based on PRISMA guideline).
Figure 2
Figure 2
Risk of bias analysis (A) the analysis of the individual studies included in the systermatic review and meta-analysis. (B) The summary of the risk of bias analysis.
Figure 3
Figure 3
Forest plots for the effect of probiotics supplementation and glucose-lowering drugs on FBS (mg/dL) (A), HbA1c (%) (B), Insulin (mU/mL) (C), and HOMA-IR (D), compared to placebo in pooled analysis. For each study, the solid black diamonds represent the point estimate of the intervention effect. The horizontal line joins the lower and upper limits of the 95% CI of this effect. The open diamonds represent the subgroup and overall SMD determined with a random-effects model.
Figure 4
Figure 4
Forest plots for the effect of probiotics supplementation and glucose-lowering drugs on TC (mg/dL) (A), TG (mg/dL) (B), HDL-C (mg/dL) (C), and LDL-C(mg/dL) (D) compared to placebo in pooled analysis. For each study, the solid black diamonds represent the point estimate of the intervention effect. The horizontal line joins the lower and upper limits of the 95% CI of this effect. The open diamonds represent the subgroup and overall SMD determined with a random-effects model.
Figure 5
Figure 5
Forest plot for the effect of probiotics supplementation and glucose-lowering drugs on SBP (mmHg) (A) and DBP (mmHg) (B) compared to placebo. For each study, the solid black diamonds represent the point estimate of the intervention effect. The horizontal line joins the lower and upper limits of the 95% CI of this effect. The open diamonds represent the subgroup and overall SMD determined with a random-effects model.
Figure 6
Figure 6
The targeted regulation mechanisms of probiotics and glucose-lowering drugs on antidiabetic. (1) TZDs can inhibit lipolysis in adipose tissue, and decrease hyperglycemia. (2) TZDs and GLP1-RAs can promote blood glucose uptake by the skeletal muscle contributes to reduce blood glucose. (3) GLP1-RA can promote the secretion of insulin from pancreas, meanwhile, GLP1-RA and DPP-4i can inhibit glucagon secretion by pancreas, and contribute to reduce the blood glucose. (4) TZDs, and GLP1-RA can inhibit endogenous hepatic glucose production, and reduce hyperglycemia. (5) GLP-1RA can inhibit DPP-4 enzymatic activity in circulation participates in decrease blood hyperglycemia. (6) SGLT2i (Sodium-Glucose cotransporter 2 inhibitors) blocks glucose reabsorption in kidneys, and reduce the blood glucose. (7) GLP1-RA can inhibit appetite by the brain, contribute to decrease blood glucose (8–13).

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