Lucose by epigenetic mechanisms Pemetrexed Antimetabolites inhibitor of bile hen Acid synthesis in response to foods obtained. However, in diabetic mice M, The increased CYP7A1 Hen hyperglycemia Chemistry basal expression by epigenetic mechanisms, but I refuel Does not increase CYP7A1 expression. Discussion In this study, we showed for the first time in both wild-type and humanized mouse CYP7A1 Tg, glucose and insulin rapidly induces CYP7A1 gene expression and bile Acid synthesis, leading to a size E of bile Acid pool expanded and increased bile acids circulating Hten. Postprandial stimulation of bile Acid synthesis may be a mechanism for controlled L is the postprandial glucose and lipid homeostasis Hom By bile Acid signaling are considered. The identification of glucose as a physiological regulator of CYP7A1 connects the activation of the synthesis of bile Acids to hrstoffen the availability of N. Tats Chlich the protein synthesis in the liver, cholesterol, fatty Acids and glycogen controlled primarily by glucose and insulin-signaling pathway through mechanisms such as stimulating the release of insulin and produces an intermediate product of glycolysis, and Change the epigenetic histone code. These processes will need during the postprandial periods for controlled L-glucose, lipid and energy metabolism and storage are stimulated.
In this study we have shown that glucose can directly activate CYP7A1 by histone hyperacetylation of the CYP7A1 gene promoter. A r The key Gallen Acid activated FXR signaling in mediating the regulation of bile Acid hepatic synthesis of bile acids By numerous studies using pharmacological doses of bile acids, FXR agonists have been shown, or FGF19 or genetic knockout of FXR gene in M mice. Direct evidence that FXR-dependent play Independent signaling an r In the regulation of CYP7A1 gene transcription in normal physiological conditions is still pending. Ourresults this study show little fluctuation in Bile Acid pool and FGF15 in the intestine I Has the transition to refuel. The modest transient increase in bile Be no acids in the gut after food intake sufficient to sen intestinal FXR signal auszul, Which demonstrated the lack of induction of FGF15 protein and ileal bile Acid-binding. , Recent studies Bortezomib Velcade have shown that the transfusion stimulate activated human hepatic FGF19 MAPK / ERK glycogen synthesis and to suppress glucose production in the liver of M Mice demonstrated, suggesting that may FGF15 act as a regulator of insulin independent Ngig of postprandial glucose Hom homeostasis. This study shows that dietary restriction induces CYP7A1 and bile Acid synthesis, but not FGF15 mRNA, suggesting that the stimulatory effect of glucose and insulin is applied, can overcome the inhibitory effect of FXR / SHP and FXR / FGF15 signaling acids obtained by the state to hen postprandial circulating bile. It seems that the movement of bile acids ActivateTGR5to, the secretion of GLP-1 in the intestine and energy expenditure in brown fat f Wheels, the insulin sensitivity obtained Hen and weight gain. An important finding of this study is that the axis of the glucose / insulin hepatic synthesis of bile Acids regulates refeeding fasted mice on M. In both mouse models of type I and type II diabetes, the bile Acid Poolgr S ht be obtained, But I Do to food regulation of CYP7A1 gene was lost. In ob / ob mice M, Both the manner in which the insulin / glucose-stimulated FOXO1 and epigenetic mechanisms contribute to the Erh Increase Basa