title: Targeting gut microbiota as a possible therapy for diabetes.
abstract: The incidence of diabetes has increased rapidly across the entire world in the last 2 decades. Accumulating evidence suggests that gut microbiota contribute to the pathogenesis of diabetes. Several studies have demonstrated that patients with diabetes are characterized by a moderate degree of gut microbial dysbiosis. However, there are still substantial controversies regarding altered composition of the gut microbiota and the underlying mechanisms by which gut microbiota interact with the body's metabolism. The purpose of this review is to define the association between gut microbiota and diabetes. In doing so an electronic search of studies published in English from January 2004 to the November 2014 in the National Library of Medicine, including the original studies that addressed the effects of gut microbiota on diabetes, energy metabolism, inflammation, the immune system, gut permeability and insulin resistance, was performed. Herein, we discuss the possible mechanisms by which the gut microbiota are involved in the development of diabetes, including energy metabolism, inflammation, the innate immune system, and the bowel function of the intestinal barrier. The compositional changes in the gut microbiota in type 2 and type 1 diabetes are also discussed. Moreover, we introduce the new findings of fecal transplantation, and use of probiotics and prebiotics as new treatment strategies for diabetes. Future research should be focused on defining the primary species of the gut microbiota and their exact roles in diabetes, potentially increasing the possibility of fecal transplants as a therapeutic strategy for diabetes.
authors.affiliation: School of Food Science and Engineering, Harbin Institute of Technology, Harbin 150090, China.
authors.forename: Canxia
authors.initials: C
authors.lastname: He
authors.affiliation: School of Food Science and Engineering, Harbin Institute of Technology, Harbin 150090, China. Electronic address: yujuan72@163.com.
authors.forename: Yujuan
authors.initials: Y
authors.lastname: Shan
authors.affiliation: School of Food Science and Engineering, Harbin Institute of Technology, Harbin 150090, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Song
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D064806:Dysbiosis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology / Q000628:therapy*; D019446:Endotoxemia / Q000209:etiology / Q000517:prevention & control; D004734:Energy Metabolism; D019317:Evidence-Based Medicine; D000069467:Fecal Microbiota Transplantation; D005759:Gastroenteritis / Q000209:etiology / Q000517:prevention & control; D000069196:Gastrointestinal Microbiome / Q000276:immunology; D041981:Gastrointestinal Tract / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology; D006801:Humans; D007113:Immunity, Innate; D007333:Insulin Resistance; D008954:Models, Biological; D010539:Permeability; D056692:Prebiotics / Q000008:administration & dosage; D019936:Probiotics / Q000627:therapeutic use
chemical_list: D056692:Prebiotics
keywords: Diabetes; Fecal transplant; Gut microbiota; Inflammation; Metabolism