Improved Metabolic Control by Depletion of Liver X Receptors in Mice.
From: Department of Biosciences and Nutrition, Karolinska University Hospital, Novum, Karolinska Institutet, S-141 57 Huddinge, Sweden. gschuster@ucdavis.edu
Biochemical and biophysical research communications
- Publish Date: Sep 2006
- ISSN: 0006-291X
- Volume: 348
- Issue: 1
- Pages: 176-82
- Medium: Print
- Language: English
- Citation (JAMA): Schuster Gertrud U, Johansson Lisen, Kietz Silke, et al. Improved Metabolic Control by Depletion of Liver X Receptors in Mice.. Biochem. Biophys. Res. Commun. Sep 2006;348:176-82
Abstract
Liver X Receptors (LXRs) coordinate the regulation of lipid and carbohydrate metabolism and insulin signaling. LXR-ligands lower plasma glucose in hyperglycemic rodents and have consequently been proposed as anti-diabetic agents. We investigated the metabolic effects induced by high carbohydrate diet in LXRalpha(-/-)beta(-/-) mice. Irrespective of diets, LXRalpha(-/-)beta(-/-) mice had reduced fatty acid, insulin, and C-peptide plasma levels than wild-type controls, suggesting a lower insulin production. High carbohydrate diet decreased the plasma glucose levels and the homeostasis model assessment (HOMA)-index in LXRalpha(-/-)beta(-/-) mice and increased hepatic triglyceride content and mRNA levels of lipogenic genes in wild-type and LXRalpha(-/-)beta(-/-) mice, proportionally. In wild-type mice high carbohydrate diet was associated with induced expression of LXR (1.5-fold), despite unchanged SREBP-1c expression. LXRalpha(-/-)beta(-/-) mice responded to this diet by induction of SREBP-1c. Our study suggests that in LXRalpha(-/-)beta(-/-) mice, glucose utilization seems to be privileged possibly due to reduced circulating free fatty acid levels.
Mesh Headings (Keywords): Animals, Blood Glucose, Carbohydrate Metabolism, DNA-Binding Proteins, Diet, Gene Deletion, Insulin, Lipid Metabolism, Mice, Receptors, Cytoplasmic and Nuclear
Check for Full Text / PubMed Unique Identifier (PMID): 16876124
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.