Nuclear receptor corepressor (NCoR1) interacts with various nuclear receptors and regulates the anabolism and catabolism of lipids. An imbalance in lipid/energy homeostasis is also an important factor in obesity and metabolic syndrome development. In this study, we found that the deletion of NCoR1 in intestinal epithelial cells (IECs) mainly activated the nuclear receptor PPARα and attenuated metabolic syndrome by stimulating thermogenesis. The increase in brown adipose tissue thermogenesis was mediated by gut-derived tricarboxylic acid cycle intermediate succinate, whose production was significantly enhanced by PPARα activation in the fed state. Additionally, NCoR1 deletion derepressed intestinal LXR, increased cholesterol excretion, and impaired duodenal lipid absorption by decreasing bile acid hydrophobicity, thereby reversing the possible negative effects of intestinal PPARα activation. Therefore, the simultaneous regulatory effect of intestinal NCoR1 on both lipid intake and energy expenditure strongly suggests that it is a promising target for developing metabolic syndrome treatment.

Objective:To provide reference for clinical pharmacists' participation in treatment of drug-induced autoimmune hypo-glycemia. Methods:Clinical pharmacists participated in drug treatment of a case of insulin aspart-induced autoimmune hypoglycemia, analyzed treatment and provided suggestion and pharmaceutical care. Results:Clinical pharmacists' suggestion was accepted and the patient was cured and discharged from the hospital. Conclusion: Clinical pharmacists' participation could help doctors to make safe and effective medication, provide good pharmaceutical care and medication education for patients.