Project description:Mice rendered obese with high fat diet were treated by IP injection with N-trans caffeoyltyramine (NCT) (200 mg/kg bid) for 14 days, followed by harvesting of the liver for analysis, including RNA isolation.
Project description:Mice rendered obese with high fat diet were treated by IP injection with N-trans caffeoyltyramine (NCT) (200 mg/kg bid) for 14 days, followed by harvesting of the intestine for analysis, including RNA isolation.
Project description:T6PNE human pancreatic cells were treated by DMSO or N-trans caffeoyltyramine (NCT) for 2 days with palmitate, followed by harvesting for RNA isolation.
Project description:Since leptin signaling in the hypothalamus is critical to regulate food intake and body weight, we investigated how celastrol alters the hypothalamic transcriptome of DIO mice. By doing this analysis, genes with potential relevance for celastrol-mediated leptin sensitization could be identified.
Project description:HNF4A is a transcription factor that controls metabolic features of several endodermal epithelia. Using an intestinal conditional mouse model, here we demonstrate that HNF4A is not required for intestinal lipid metabolism per se, but unexpectedly influences whole body energy expenditure under diet-induced obesity (DIO). Deletion of intestinal HNF4A causes mice to become DIO-resistant with preference for fat as an energy substrate and energetic changes in association with white adipose tissue (WAT) beiging. Intestinal HNF4A is crucial for fat-induced release of glucose-dependent insulinotropic polypeptide (GIP), while reintroduction of a stabilized GIP analog rescues the DIO-resistance phenotype of the mutant mice. Our study provides evidence that intestinal HNF4A plays a non-redundant role in whole body lipid homeostasis and points to a novel non-cell-autonomous regulatory circuit for body fat management.