Preneet Cheema Brar1, Brenda Kohn. 1. Division of Pediatric Endocrinology and Diabetes, Hassenfeld Children's Hospital, New York University School of Medicine, New York, NY USA.
Abstract
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.
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.
Authors: Ida Pastore; Andrea Mario Bolla; Laura Montefusco; Maria Elena Lunati; Antonio Rossi; Emma Assi; Gian Vincenzo Zuccotti; Paolo Fiorina Journal: Int J Mol Sci Date: 2020-07-12 Impact factor: 5.923
Authors: Sandra Mrozinska; Przemysław Kapusta; Tomasz Gosiewski; Agnieszka Sroka-Oleksiak; Agnieszka H Ludwig-Słomczyńska; Bartłomiej Matejko; Beata Kiec-Wilk; Malgorzata Bulanda; Maciej T Malecki; Pawel P Wolkow; Tomasz Klupa Journal: Microorganisms Date: 2021-01-12