Document Detail


Regulation of energy substrate utilization and hepatic insulin sensitivity by phosphatidylcholine transfer protein/StarD2.
MedLine Citation:
PMID:  18347010     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Phosphatidylcholine transfer protein (PC-TP, also known as StarD2) is a highly specific intracellular lipid binding protein with accentuated expression in oxidative tissues. Here we show that decreased plasma concentrations of glucose and free fatty acids in fasting PC-TP-deficient (Pctp(-/-)) mice are attributable to increased hepatic insulin sensitivity. In hyperinsulinemic-euglycemic clamp studies, Pctp(-/-) mice exhibited profound reductions in hepatic glucose production, gluconeogenesis, glycogenolysis, and glucose cycling. These changes were explained in part by the lack of PC-TP expression in liver per se and in part by marked alterations in body fat composition. Reduced respiratory quotients in Pctp(-/-) mice were indicative of preferential fatty acid utilization for energy production in oxidative tissues. In the setting of decreased hepatic fatty acid synthesis, increased clearance rates of dietary triglycerides and increased hepatic triglyceride production rates reflected higher turnover in Pctp(-/-) mice. Collectively, these data support a key biological role for PC-TP in the regulation of energy substrate utilization.
Authors:
Erez F Scapa; Alessandro Pocai; Michele K Wu; Roger Gutierrez-Juarez; Lauren Glenz; Keishi Kanno; Hua Li; Sudha Biddinger; Linda A Jelicks; Luciano Rossetti; David E Cohen
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural     Date:  2008-03-17
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  22     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-07-02     Completed Date:  2008-08-12     Revised Date:  2014-03-06    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2579-90     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Carrier Proteins / metabolism
Cell Culture Techniques
Crosses, Genetic
Energy Metabolism
Fatty Acids, Nonesterified / blood
Gene Expression Regulation
Glucose Clamp Technique
Glucose Tolerance Test
Hepatocytes / cytology,  physiology
Insulin / physiology*
Lipids / physiology
Liver / physiology*
Mice
Mice, Knockout
Phospholipid Transfer Proteins / deficiency*,  genetics,  metabolism*
RNA, Messenger / genetics
Triglycerides / metabolism*
Grant Support
ID/Acronym/Agency:
DK-48873/DK/NIDDK NIH HHS; DK-56626/DK/NIDDK NIH HHS; R01 DK056626/DK/NIDDK NIH HHS; R37 DK048873/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Carrier Proteins; 0/Fatty Acids, Nonesterified; 0/Insulin; 0/Lipids; 0/Phospholipid Transfer Proteins; 0/RNA, Messenger; 0/Triglycerides

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The novel small molecule drug Rabeximod is effective in reducing disease severity of mouse models of...
Next Document:  Suppression of hepatic glucose production by human neutrophil alpha-defensins through a signaling pa...