|  Help  |  About  |  Contact Us

Publication : Adipose triglyceride lipase is a TG hydrolase of the small intestine and regulates intestinal PPARα signaling.

First Author  Obrowsky S Year  2013
Journal  J Lipid Res Volume  54
Issue  2 Pages  425-35
PubMed ID  23220585 Mgi Jnum  J:193091
Mgi Id  MGI:5467647 Doi  10.1194/jlr.M031716
Citation  Obrowsky S, et al. (2013) Adipose triglyceride lipase is a TG hydrolase of the small intestine and regulates intestinal PPARalpha signaling. J Lipid Res 54(2):425-35
abstractText  Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme mediating triglyceride (TG) hydrolysis. The lack of ATGL results in TG accumulation in multiple tissues, underscoring the critical role of ATGL in maintaining lipid homeostasis. Recent evidence suggests that ATGL affects TG metabolism via activation of peroxisome proliferator-activated receptor alpha (PPARalpha). To investigate specific effects of intestinal ATGL on lipid metabolism we generated mice lacking ATGL exclusively in the intestine (ATGLiKO). We found decreased TG hydrolase activity and increased intracellular TG content in ATGLiKO small intestines. Intragastric administration of [(3)H]trioleate resulted in the accumulation of radioactive TG in the intestine, whereas absorption into the systemic circulation was unchanged. Intraperitoneally injected [(3)H]oleate also accumulated within TG in ATGLiKO intestines, indicating that ATGL mobilizes fatty acids from the systemic circulation absorbed by the basolateral side from the blood. Down-regulation of PPARalpha target genes suggested modulation of cholesterol absorption by intestinal ATGL. Accordingly, ATGL deficiency in the intestine resulted in delayed cholesterol absorption. Importantly, this study provides evidence that ATGL has no impact on intestinal TG absorption but hydrolyzes TGs taken up from the intestinal lumen and systemic circulation. Our data support the role of ATGL in modulating PPARalpha-dependent processes also in the small intestine.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

7 Bio Entities

0 Expression