Chikage Mataki

TL;DR: It is shown that the administration of BAs to mice increases energy expenditure in brown adipose tissue, preventing obesity and resistance to insulin, and indicates that BAs might be able to function beyond the control of BA homeostasis as general metabolic integrators.

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: It is concluded that AMPK acts as the primordial trigger for fasting- and exercise-induced adaptations in skeletal muscle and that activation of SIRT1 and its downstream signaling pathways are improperly triggered in AMPK-deficient states.

TL;DR: The metabolic phenotype of mice treated with SRT1720, a specific and potent synthetic activator of SIRT1 that is devoid of direct action on AMPK that robustly enhances endurance running performance and strongly protects from diet-induced obesity and insulin resistance by enhancing oxidative metabolism in skeletal muscle, liver, and brown adipose tissue is reported.

TL;DR: This paper evaluated the metabolic impact of farnesoid X receptor activation by administering a synthetic FXR agonist (GW4064) to mice in which obesity was induced by a high fat diet.