Gut microbiome and its role in obesity and insulin resistance

Obesity is a complex metabolic disease caused, in part, by the interaction between an individual's genetics, metabolism, and environment. Emerging evidence supports the role of gut microbiota in mediating the interaction between the host and environment by extracting energy from food otherwise...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Annals of the New York Academy of Sciences 2020-02, Vol.1461 (1), p.37-52
Hauptverfasser: Lee, Clare J., Sears, Cynthia L., Maruthur, Nisa
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Obesity is a complex metabolic disease caused, in part, by the interaction between an individual's genetics, metabolism, and environment. Emerging evidence supports the role of gut microbiota in mediating the interaction between the host and environment by extracting energy from food otherwise indigestible by the host and producing metabolites and cytokines that affect host metabolism. Furthermore, gut microbial imbalance or dysbiosis has been shown in metabolic diseases including obesity, and recent studies are beginning to unravel the mechanisms involved. The gut microbiota affects host metabolism and obesity through several pathways involving gut barrier integrity, production of metabolites affecting satiety and insulin resistance, epigenetic factors, and metabolism of bile acids and subsequent changes in metabolic signaling. While the field of gut microbiome and its role in obesity is early in its stage of development, it holds a promising future in providing us with novel therapeutic targets that may restore the gut microbiome to a healthy state and help in the prevention and treatment of obesity. In this review, we provide the latest updates on the gut microbiome and proposed mechanisms through which it contributes to human obesity and insulin resistance.
ISSN:0077-8923
1749-6632
DOI:10.1111/nyas.14107