Document Detail


Enhanced fatty acid flux triggered by adiponectin overexpression.
MedLine Citation:
PMID:  22045665     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Adiponectin overexpression in mice increases insulin sensitivity independent of adiposity. Here, we combined stable isotope infusion and in vivo measurements of lipid flux with transcriptomic analysis to characterize fatty acid metabolism in transgenic mice that overexpress adiponectin via the aP2-promoter (ADNTg). Compared with controls, fasted ADNTg mice demonstrated a 31% reduction in plasma free fatty acid concentrations (P = 0.008), a doubling of ketones (P = 0.028), and a 68% increase in free fatty acid turnover in plasma (15.1 ± 1.5 vs. 25.3 ± 6.8 mg/kg · min, P = 0.011). ADNTg mice had 2-fold more brown adipose tissue mass, and triglyceride synthesis and turnover were 5-fold greater in this organ (P = 0.046). Epididymal white adipose tissue was slightly reduced, possibly due to the approximately 1.5-fold increase in the expression of genes involved in oxidation (peroxisome proliferator-activated receptor α, peroxisome proliferator-activated receptor-γ coactivator 1α, and uncoupling protein 3). In ADNTg liver, lipogenic gene expression was reduced, but there was an unexpected increase in the expression of retinoid pathway genes (hepatic retinol binding protein 1 and retinoic acid receptor beta and adipose Cyp26A1) and liver retinyl ester content (64% higher, P < 0.02). Combined, these data support a physiological link between adiponectin signaling and increased efficiency of triglyceride synthesis and hydrolysis, a process that can be controlled by retinoids. Interactions between adiponectin and retinoids may underlie adiponectin's effects on intermediary metabolism.
Authors:
Shoba Shetty; Maria A Ramos-Roman; You-Ree Cho; Jonathan Brown; Jorge Plutzky; Eric S Muise; Jay D Horton; Philipp E Scherer; Elizabeth J Parks
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-11-01
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-23     Completed Date:  2012-03-05     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  113-22     Citation Subset:  AIM; IM    
Affiliation:
Touchstone Diabetes Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9052, USA.
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MeSH Terms
Descriptor/Qualifier:
Adiponectin / genetics,  metabolism
Animals
Fatty Acids / metabolism*
Gene Expression
Liver / metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
RNA, Messenger / genetics,  metabolism
Recombinant Proteins / genetics,  metabolism
Retinoids / metabolism
Signal Transduction
Triglycerides / metabolism
Vitamin A / analogs & derivatives,  metabolism
Grant Support
ID/Acronym/Agency:
5PL1DK081182/DK/NIDDK NIH HHS; 5RL1DK081187/DK/NIDDK NIH HHS; 5UL1DE019584/DE/NIDCR NIH HHS; P01DK088761/DK/NIDDK NIH HHS; R01-DK55758/DK/NIDDK NIH HHS; RC1 DK086629/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Adiponectin; 0/Adipoq protein, mouse; 0/Fatty Acids; 0/RNA, Messenger; 0/Recombinant Proteins; 0/Retinoids; 0/Triglycerides; 11103-57-4/Vitamin A
Comments/Corrections

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


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