Cover Image

Hepatic transforming growth factor-β 1 stimulated clone-22 D1 controls systemic cholesterol metabolism

Disturbances in lipid homeostasis are hallmarks of severe metabolic disorders and their long-term complications, including obesity, diabetes, and atherosclerosis. Whereas elevation of triglyceride (TG)-rich very-low-density lipoproteins (VLDL) has been identified as a risk factor for cardiovascular...

Full description

Saved in:
Bibliographic Details
Main Authors: Jäger, Julia Maria (Author) , Greiner, Vera (Author) , Strzoda, Daniela (Author) , Seibert, Oksana (Author) , Niopek, Katharina (Author) , Sijmonsma, Tjeerd P. (Author) , Schäfer, Michaela (Author) , Jones, Allan (Author) , Guia, Roldan M. de (Author) , Martignoni, Marc (Author) , Dallinga-Thie, Geesje M. (Author) , Berriel Diaz, Mauricio (Author) , Hofmann, Thomas G. (Author) , Herzig, Stephan (Author)
Format: Article (Journal)
Language:English
Published: 8 January 2014
In: Molecular metabolism
Year: 2014, Volume: 3, Issue: 2, Pages: 155-166
ISSN:2212-8778
DOI:10.1016/j.molmet.2013.12.007
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.molmet.2013.12.007
Get full text
Author Notes:Julia Jäger, Vera Greiner, Daniela Strzoda, Oksana Seibert, Katharina Niopek, Tjeerd P. Sijmonsma, Michaela Schäfer, Allan Jones, Roldan De Guia, Marc Martignoni, Geesje M. Dallinga-Thie, Mauricio B. Diaz, Thomas G. Hofmann, Stephan Herzig
Description
Summary:Disturbances in lipid homeostasis are hallmarks of severe metabolic disorders and their long-term complications, including obesity, diabetes, and atherosclerosis. Whereas elevation of triglyceride (TG)-rich very-low-density lipoproteins (VLDL) has been identified as a risk factor for cardiovascular complications, high-density lipoprotein (HDL)-associated cholesterol confers atheroprotection under obese and/or diabetic conditions. Here we show that hepatocyte-specific deficiency of transcription factor transforming growth factor β 1-stimulated clone (TSC) 22 D1 led to a substantial reduction in HDL levels in both wild-type and obese mice, mediated through the transcriptional down-regulation of the HDL formation pathway in liver. Indeed, overexpression of TSC22D1 promoted high levels of HDL cholesterol in healthy animals, and hepatic expression of TSC22D1 was found to be aberrantly regulated in disease models of opposing energy availability. The hepatic TSC22D1 transcription factor complex may thus represent an attractive target in HDL raising strategies in obesity/diabetes-related dyslipidemia and atheroprotection.
Item Description:Gesehen am 10.11.2020
Physical Description:Online Resource
ISSN:2212-8778
DOI:10.1016/j.molmet.2013.12.007

Similar Items