Document Detail


Angiotensin II reduces food intake by altering orexigenic neuropeptide expression in the mouse hypothalamus.
MedLine Citation:
PMID:  22234465     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Angiotensin II (Ang II), which is elevated in many chronic disease states such as end-stage renal disease and congestive heart failure, induces cachexia and skeletal muscle wasting by increasing muscle protein breakdown and reducing food intake. Neurohormonal mechanisms that mediate Ang II-induced appetite suppression are unknown. Consequently, we examined the effect of Ang II on expression of genes regulating appetite. Systemic Ang II (1 μg/kg · min) infusion in FVB mice rapidly reduced hypothalamic expression of neuropeptide Y (Npy) and orexin and decreased food intake at 6 h compared with sham-infused controls but did not change peripheral leptin, ghrelin, adiponectin, glucagon-like peptide, peptide YY, or cholecystokinin levels. These effects were completely blocked by the Ang II type I receptor antagonist candesartan or deletion of Ang II type 1a receptor. Ang II markedly reduced phosphorylation of AMP-activated protein kinase (AMPK), an enzyme that is known to regulate Npy expression. Intracerebroventricular Ang II infusion (50 ng/kg · min) caused a reduction of food intake, and Ang II dose dependently reduced Npy and orexin expression in the hypothalamus cultured ex vivo. The reduction of Npy and orexin in hypothalamic cultures was completely prevented by candesartan or the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside. Thus, Ang II type 1a receptor-dependent Ang II signaling reduces food intake by suppressing the hypothalamic expression of Npy and orexin, likely via AMPK dephosphorylation. These findings have major implications for understanding mechanisms of cachexia in chronic disease states such as congestive heart failure and end-stage renal disease, in which the renin-angiotensin system is activated.
Authors:
Tadashi Yoshida; Laura Semprun-Prieto; Richard D Wainford; Sergiy Sukhanov; Daniel R Kapusta; Patrice Delafontaine
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-01-10
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-02-22     Completed Date:  2012-04-16     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1411-20     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism*
Animals
Cachexia / metabolism
Cholecystokinin / metabolism
Eating / drug effects
Feeding Behavior*
Gene Expression Regulation*
Hypothalamus / metabolism*
Infusions, Intraventricular
Intracellular Signaling Peptides and Proteins / metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neuropeptide Y / metabolism
Neuropeptides / biosynthesis*,  chemistry,  metabolism
Phosphorylation
Time Factors
Grant Support
ID/Acronym/Agency:
P20RR018766/RR/NCRR NIH HHS; R01 HL070241/HL/NHLBI NIH HHS; R01 HL070241-10/HL/NHLBI NIH HHS; R01 HL080682/HL/NHLBI NIH HHS; R01 HL080682-05/HL/NHLBI NIH HHS; R01 HL107330/HL/NHLBI NIH HHS; R01HL070241/HL/NHLBI NIH HHS; R01HL080682/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Intracellular Signaling Peptides and Proteins; 0/Neuropeptide Y; 0/Neuropeptides; 0/orexins; 11128-99-7/Angiotensin II; 9011-97-6/Cholecystokinin
Comments/Corrections

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