| Attenuation of diet-induced weight gain and adiposity through increased energy expenditure in mice lacking angiotensin II type 1a receptor. | |
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MedLine Citation:
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PMID: 15878965 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Given that angiotensin II (AII) type 1 and 2 receptors (Agtr1 and Agtr2) are expressed in adipose tissue, AII may act directly on adipose tissue. However, regardless of whether AII directly modulates adipose tissue growth and metabolism in vivo and, if so, whether it is mediated via Agtr1 are still matters of debate. To understand the functional role of Agtr1 in adipose tissue growth and metabolism in vivo, we examined the metabolic phenotypes of mice lacking Agtr1a (Agtr1a-/- mice) during a high-fat diet. The Agtr1a-/- mice exhibited the attenuation of diet-induced body weight gain and adiposity, and insulin resistance relative to wild-type littermates (Agtr1a+/+ mice). They also showed increased energy expenditure accompanied by sympathetic activation, as revealed by increased rectal temperature and oxygen consumption, increased expression of uncoupling protein-1 mRNA in brown adipose tissue, and increased urinary catecholamine excretion. The heterozygous Agtr1a-deficient mice (Agtr1a+/- mice) also exhibited metabolic phenotypes similar to those of Agtr1a-/- mice. Using mouse embryonic fibroblasts derived from Agtr1a+/+ and Agtr1a-/- mice, we found no significant difference between genotypes in the ability to differentiate into lipid-laden mature adipocytes. In primary cultures of mouse mature adipocytes, AII increased the expression of mRNAs for some adipocytokines, which was abolished by pharmacological blockade of Agtr1. This study demonstrates that Agtr1a-/- mice exhibit attenuation of diet-induced weight gain and adiposity through increased energy expenditure. The data also suggest that AII does not affect directly adipocyte differentiation, but can modulate adipocytokine production via Agtr1. |
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Authors:
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Ryuji Kouyama; Takayoshi Suganami; Junko Nishida; Miyako Tanaka; Takuya Toyoda; Minako Kiso; Tsuyoshi Chiwata; Yoshihiro Miyamoto; Yasunao Yoshimasa; Akiyoshi Fukamizu; Masatsugu Horiuchi; Yukio Hirata; Yoshihiro Ogawa |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2005-05-05 |
Journal Detail:
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Title: Endocrinology Volume: 146 ISSN: 0013-7227 ISO Abbreviation: Endocrinology Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-07-12 Completed Date: 2005-09-26 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 3481-9 Citation Subset: AIM; IM |
Affiliation:
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Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kanda-surugadai, Chiyoda-ku, Tokyo 101-0062, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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physiology Animals Base Sequence DNA Primers Diet* Energy Intake Energy Metabolism Mice Mice, Inbred C57BL Obesity / prevention & control* Oxygen Consumption / physiology* Polymerase Chain Reaction / methods RNA, Messenger / genetics Receptor, Angiotensin, Type 1 / deficiency*, genetics, physiology* Receptor, Angiotensin, Type 2 / physiology Weight Gain |
| Chemical | |
Reg. No./Substance:
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0/DNA Primers; 0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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