Document Detail


Adipocyte-specific deficiency of angiotensinogen decreases plasma angiotensinogen concentration and systolic blood pressure in mice.
MedLine Citation:
PMID:  22071160     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies demonstrated that overexpression of angiotensinogen (AGT) in adipose tissue increased blood pressure. However, the contribution of endogenous AGT in adipocytes to the systemic renin-angiotensin system (RAS) and blood pressure control is undefined. To define a role of adipocyte-derived AGT, mice with loxP sites flanking exon 2 of the AGT gene (Agt(fl/fl)) were bred to transgenic mice expressing Cre recombinase under the control of an adipocyte fatty acid-binding protein 4 promoter (aP2) promoter to generate mice with adipocyte AGT deficiency (Agt(aP2)). AGT mRNA abundance in adipose tissue and AGT secretion from adipocytes were reduced markedly in adipose tissues of Agt(aP2) mice. To determine the contribution of adipocyte-derived AGT to the systemic RAS and blood pressure control, mice were fed normal laboratory diet for 2 or 12 mo. In males and females of each genotype, body weight and fat mass increased with age. However, there was no effect of adipocyte AGT deficiency on body weight, fat mass, or adipocyte size. At 2 and 12 mo of age, mice with deficiency of AGT in adipocytes had reduced plasma concentrations of AGT (by 24-28%) compared with controls. Moreover, mice lacking AGT in adipocytes exhibited reduced systolic blood pressures compared with controls (Agt(fl/fl), 117 ± 2; Agt(aP2), 110 ± 2 mmHg; P < 0.05). These results demonstrate that adipocyte-derived AGT contributes to the systemic RAS and blood pressure control.
Authors:
Frederique Yiannikouris; Michael Karounos; Richard Charnigo; Victoria L English; Debra L Rateri; Alan Daugherty; Lisa A Cassis
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-11-09
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  302     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-04     Completed Date:  2012-02-17     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R244-51     Citation Subset:  IM    
Affiliation:
Graduate Center for Nutritional Sciences, Univ. of Kentucky, Lexington, KY 40536-0200, USA.
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / metabolism*
Adiposity / physiology
Angiotensinogen / blood,  genetics,  metabolism*
Animals
Blood Glucose / physiology
Blood Pressure / physiology*
Body Weight / physiology
Female
Male
Mice
Mice, Transgenic
Renin-Angiotensin System / physiology*
Grant Support
ID/Acronym/Agency:
P20 RR021954-04/RR/NCRR NIH HHS; P20 RR021954-05/RR/NCRR NIH HHS; P20-RR-021954/RR/NCRR NIH HHS; R01 HL073085-08/HL/NHLBI NIH HHS; R01 HL073085-09/HL/NHLBI NIH HHS; R01-HL-073085/HL/NHLBI NIH HHS; T32-HL-091812/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 11002-13-4/Angiotensinogen
Comments/Corrections
Comment In:
Am J Physiol Regul Integr Comp Physiol. 2012 Jan 15;302(2):R242-3   [PMID:  22071163 ]

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


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