School of Pharmacy and Medical Science and Sansom Institute for Health Research,University of South Australia,GPO Box 2471,Adelaide SA 5000,Australia.
Nutr Res Rev. 2018 Jun;31(1):35-51. doi: 10.1017/S095442241700018X. Epub 2017 Oct 17.
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.
动物研究表明,肠道微生物群的组成可能与胰岛素抵抗向 2 型糖尿病的发展有关。益生菌和/或益生元可能是一种很有前途的方法,可以通过有利地改变肠道微生物群落的组成、降低肠道内毒素浓度和减少能量收获来提高胰岛素敏感性。本综述的目的是调查益生菌、益生元和合生剂(益生菌和益生元的组合)在人类临床试验中对胰岛素抵抗的影响,并讨论益生菌和益生元改善葡萄糖代谢的潜在机制。益生菌的抗糖尿病作用包括通过 NF-κB 途径减少促炎细胞因子、降低肠道通透性和降低氧化应激。短链脂肪酸(SCFA)通过多种潜在的作用机制在葡萄糖稳态中发挥关键作用。SCFA 激活 L 细胞上的 G 蛋白偶联受体,促进胰高血糖素样肽-1 和肽 YY 的释放,导致胰岛素分泌增加和胰高血糖素分泌减少,从而抑制食欲。SCFA 可降低肠道通透性和循环内毒素,降低炎症和氧化应激。SCFA 还可以在脂肪细胞中具有抗脂肪分解作用,并通过上调肌肉和肝组织中的 5'-AMP 激活蛋白激酶信号通路,改善胰岛素敏感性和 GLUT4。抗性淀粉和合生剂似乎具有有利的抗糖尿病作用。然而,人类干预的研究很少。需要进一步进行精心设计的人类临床试验,以制定用益生菌和益生元预防 2 型糖尿病的建议。