Effects and Mechanisms of Probiotics, Prebiotics, Synbiotics, and Postbiotics on Metabolic Diseases Targeting Gut Microbiota: A Narrative Review

Abstract

Metabolic diseases are serious threats to public health and related to gut microbiota. Probiotics, prebiotics, synbiotics, and postbiotics (PPSP) are powerful regulators of gut microbiota, thus possessing prospects for preventing metabolic diseases. Therefore, the effects and mechanisms of PPSP on metabolic diseases targeting gut microbiota are worth discussing and clarifying. Generally, PPSP benefit metabolic diseases management, especially obesity and type 2 diabetes mellitus. The underlying gut microbial-related mechanisms are mainly the modulation of gut microbiota composition, regulation of gut microbial metabolites, and improvement of intestinal barrier function. Moreover, clinical trials showed the benefits of PPSP on patients with metabolic diseases, while the clinical strategies for gestational diabetes mellitus, optimal formula of synbiotics and health benefits of postbiotics need further study. This review fully summarizes the relationship between probiotics, prebiotics, synbiotics, postbiotics, and metabolic diseases, presents promising results and the one in dispute, and especially attention is paid to illustrates potential mechanisms and clinical effects, which could contribute to the next research and development of PPSP.

Keywords: gestational diabetes mellitus; gut microbiota; metabolic diseases; obesity; postbiotics; prebiotics; probiotics; synbiotics; type 2 diabetes mellitus.

Figure 1

Mechanisms of PPSP on metabolic diseases targeting gut microbiota. PPSP directly alleviate metabolic diseases by regulating the abundances of beneficial and harmful bacteria. Besides, PPSP indirectly ameliorate metabolic diseases by promoting the production of acetate, propionate, butyrate, isovalerate, lactic acid, and palmitoylethanolamide, while suppressing the production of LPS, TMAO and reducing the bile acid pools. Moreover, the improvement of intestinal barrier function played an important role in attenuating metabolic diseases, with upregulating claudin 1, GLP1, IL-10, occludin 1, and ZO-1 expressions. These mechanisms collectively improve the whole metabolic system by targeting several pivotal molecular, such as upregulating IRS1-Akt-GLUT2, SIRT1-AMPK-PPARα-CPR1α, TLR2-PPARγ-AMPK, and NOD-IRF4 signaling pathways. Abbreviation: ACC, acetyl-CoA carboxylase; Akt, protein kinase B; AMPK, adenosine monophosphate kinase; CPR1α, carnitine palmitoyltransferase 1α; GLUT2, glucose transporter 2; IRF4, interferon regulatory factor 4; IRS1, insulin receptor substrate 1; LPS, lipopolysaccharide; NOD2, oligomerization domain-containing protein 2; PPARα/γ, peroxisome proliferators activated receptor α/γ; SIRT1, sirtuin 1; TLR2, Toll-like receptor 2; TMAO, trimethylamine-n-oxide; ZO-1, zonula occludens-1.