Charles Thomas

TL;DR: It is shown here that TGR5 signaling induces intestinal glucagon-like peptide-1 (GLP-1) release, leading to improved liver and pancreatic function and enhanced glucose tolerance in obese mice, and suggested that pharmacological targeting of T GR5 may constitute a promising incretin-based strategy for the treatment of diabesity and associated metabolic disorders.

TL;DR: How the signalling functions of bile acids can be exploited in the development of drugs for obesity, type 2 diabetes, hypertriglyceridaemia and atherosclerosis, as well as other associated chronic diseases such as non-alcoholic steatohepatitis are reviewed.

TL;DR: The deletion of the poly(ADP-ribose) polymerase-1 (PARP-1) gene, encoding a major NAD(+)-consuming enzyme, increases NAD(+) content and SIRT1 activity in brown adipose tissue and muscle and the pharmacologic inhibition of PARP in vitro and in vivo is shown.

TL;DR: This work systemically integrated in vivo phenotyping with gene expression, biochemical analysis, and metabolomics, thereby identifying a distinguishing metabolic footprint of aging, and found glucose and fatty acid metabolism, and redox homeostasis are affected.

TL;DR: It is demonstrated that activation of TGR5 in macrophages by 6α-ethyl-23(S)-methylcholic acid (6-EMCA, INT-777), a semisynthetic BA, inhibits proinflammatory cytokine production, an effect mediated by T GR5-induced cAMP signaling and subsequent NF-κB inhibition.