| First Author | Scott CH | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 11 | Pages | e0186543 |
| PubMed ID | 29190746 | Mgi Jnum | J:252629 |
| Mgi Id | MGI:6103373 | Doi | 10.1371/journal.pone.0186543 |
| Citation | Scott CH, et al. (2017) Hepatic Aryl hydrocarbon Receptor Nuclear Translocator (ARNT) regulates metabolism in mice. PLoS One 12(11):e0186543 |
| abstractText | BACKGROUND & AIMS: Aryl hydrocarbon Receptor Nuclear Translocator (ARNT) and its partners hypoxia-inducible factors (HIF)-1alpha and HIF-2alpha are candidate factors for the well-known link between the liver, metabolic dysfunction and elevation in circulating lipids and glucose. Methods: Hepatocyte-specific ARNT-null (LARNT), HIF-1alpha-null (LHIF1alpha) and HIF-2alpha-null (LHIF2alpha) mice were created. RESULTS: LARNT mice had increased fasting glucose, impaired glucose tolerance, increased glucose production, raised post-prandial serum triglycerides (TG) and markedly lower hepatic ATP versus littermate controls. There was increased expression of G6Pase, Chrebp, Fas and Scd-1 mRNAs in LARNT animals. Surprisingly, LHIF1alpha and LHIF2alpha mice exhibited no alterations in any metabolic parameter assessed. CONCLUSIONS: These results provide convincing evidence that reduced hepatic ARNT can contribute to inappropriate hepatic glucose production and post-prandial dyslipidaemia. Hepatic ARNT may be a novel therapeutic target for improving post-prandial hypertriglyceridemia and glucose homeostasis. |
