Animal studies indicate that the composition of gut microbiota may be involved in the progression of insulin resistance to type 2 diabetes. Probiotics and/or prebiotics could be a promising approach to improve insulin sensitivity by favourably modifying the composition of the gut microbial community, reducing intestinal endotoxin concentrations and decreasing energy harvest. The aim of the present review was to investigate the effects of probiotics, prebiotics and synbiotics (a combination of probiotics and prebiotics) on insulin resistance in human clinical trials and to discuss the potential mechanisms whereby probiotics and prebiotics improve glucose metabolism. The anti-diabetic effects of probiotics include reducing pro-inflammatory cytokines via a NF-κB pathway, reduced intestinal permeability, and lowered oxidative stress. SCFA play a key role in glucose homeostasis through multiple potential mechanisms of action. Activation of G-protein-coupled receptors on L-cells by SCFA promotes the release of glucagon-like peptide-1 and peptide YY resulting in increased insulin and decreased glucagon secretion, and suppressed appetite. SCFA can decrease intestinal permeability and decrease circulating endotoxins, lowering inflammation and oxidative stress. SCFA may also have anti-lipolytic activities in adipocytes and improve insulin sensitivity via GLUT4 through the up-regulation of 5'-AMP-activated protein kinase signalling in muscle and liver tissues. Resistant starch and synbiotics appear to have favourable anti-diabetic effects. However, there are few human interventions. Further well-designed human clinical studies are required to develop recommendations for the prevention of type 2 diabetes with pro- and prebiotics.
Keywords: AMPK 5’-AMP-activated protein kinase; ANGPTL4 angiopoietin-like protein 4; CFU colony-forming unit; FFAR free fatty acid receptor; FIAF fasting-induced adipose factor; FOS fructo-oligosaccharide; GLP-1 glucagon like peptide-1; GPR G-protein-coupled receptor; GPx glutathione peroxidase; HOMA-IR homoeostasis model assessment for insulin resistance; HbA1c glycated Hb; IGN intestinal gluconeogenesis; LPS lipopolysaccharide; MCP-1 macrophage chemoattractant protein-1; PBMC peripheral blood mononuclear cell; PYY peptide YY; SOD superoxide dismutase; T2DM type 2 diabetes mellitus; Clinical trials; Insulin sensitivity; Prebiotics; Probiotics; SCFA.