Use of the microbiome in the management of children with type 2 diabetes mellitusBrar, Preneet Cheema; Kohn, BrendaCurrent Opinion in Pediatrics: August 2019 - Volume 31 - Issue 4 - p 524–530 doi: 10.1097/MOP.0000000000000781 ENDOCRINOLOGY AND METABOLISM: Edited by Sally Radovick Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The purpose of this review is to present recent data that defines our current understanding of the role of the gut microbiome in the development of T2DM. Recent findings Recent studies focus on the physiology and molecular pathways of the gut microbiome–host interaction. Short-chain fatty acids (SCFAs) derived from the fermentation of plant-based nonsoluble fiber bind to G-protein-coupled receptors (GPR) GPR 41 and GPR 43 to induce enteroendocrine molecules that control appetite, and to upregulate intestinal gluconeogenesis gene expression that controls glucose regulation. “Metabolic endotexemia” reflects a state of low-grade systemic inflammation that results from lipopolysaccharide (LPS) release from the gut into the systemic circulation in response to a high-fat diet. Inflammatory pathways induced by LPS, activation of toll-like receptor-4 (TLR-4), and other inflammatory signaling pathways are mediators of systemic inflammation, insulin resistance and type II diabetes mellitus. Summary Recent scientific data support that derangements in the composition of the microbiota, termed “microbiome dysbiosis” is a factor in the development of “metabolic endotoxemia” and T2DM. Therapeutic options that target the gut microbiome in the treatment of T2DM are explored. Division of Pediatric Endocrinology and Diabetes, Hassenfeld Children's Hospital, New York University School of Medicine, New York, NY USA Correspondence to Dr Preneet Cheema Brar, MD, MSCI, NYU Langone Health, 135 East 31st, Level 2, New York, NY 10016, USA. Tel: +1 212 263 5940; fax: +1 212 263 5808; e-mail: Preneet.Brar@nyulangone.org Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.