Robert G. Nichols

TL;DR: It is concluded that metformin acts in part through a B. fragilis–GUDCA–intestinal FXR axis to improve metabolic dysfunction, including hyperglycemia, and improves the metabolic health of humans and mice.

TL;DR: It is demonstrated that inhibition of an intestinal FXR/ceramide axis mediates gut microbiota-associated NAFLD development, linking the microbiome, nuclear receptor signaling, andNAFLD.

TL;DR: It is shown that an every-other-day fasting (EODF) regimen selectively stimulates beige fat development within white adipose tissue and dramatically ameliorates obesity, insulin resistance, and hepatic steatosis.

TL;DR: A mechanism in which activation of intestinal FXR shaped the gut microbiota to activate TGR5/GLP‐1 signaling to improve hepatic glucose and insulin sensitivity and increase adipose tissue browning is uncovered; the gut microbiome plays a critical role in bile acid metabolism and signaling to regulate metabolic homeostasis in health and disease.

TL;DR: Findings provide new insights into the biochemical consequences of TCDF exposure involving the alteration of the gut microbiota, modulation of nuclear receptor signaling, and disruption of host metabolism.