%0 Journal Article
%T Postprandial gut microbiota-driven choline metabolism links dietary cues to adipose tissue dysfunction
%A Belinda Willard
%A J. Mark Brown
%A Rebecca C. Schugar
%A Zeneng Wang
%J Archive of "Adipocyte".
%D 2018
%R 10.1080/21623945.2017.1398295
%X The human body is an integrated circuit between microbial symbionts and our Homo sapien genome, which communicate bi-directionally to maintain homeostasis within the human meta-organism. There is now strong evidence that microbes resident in the human intestine can directly contribute to the pathogenesis of obesity and associated cardiometabolic disorders. In fact, gut microbes represent a filter of our greatest environmental exposure ¨C the foods we consume. It is now clear that we each experience a given meal differently, based on our unique gut microbial communities. Biologically active gut microbe-derived metabolites, such as short chain fatty acids, secondary bile acids, and trimethylamine-N-oxide (TMAO), are now uniquely recognized as contributors to obesity and related cardiometabolic disorders. However, mechanistic insights into how microbe-derived metabolites promote obesity are largely unknown. Recent work has demonstrated that the meta-organismal production of the bacterial co-metabolite TMAO is linked to suppression of beiging of white adipose tissue in mice and humans. Furthermore, the TMAO pathway is becoming an increasingly attractive therapeutic target in obesity-associated diseases such as type 2 diabetes, kidney failure, and cardiovascular disease. In this commentary we discuss recent findings linking the TMAO pathway to obesity-associated disorders, and provide additional insights into potential mechanisms driving this microbe-host interaction
%K microbiota
%K microbiome
%K nutrition
%K obesity
%K diabetes
%K adipose
%K trimethylamine N-oxide
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5915041/