| Phenotype analysis of aquaporin-8 null mice. | |
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MedLine Citation:
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PMID: 15647389 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Aquaporin-8 (AQP8) is a water-transporting protein expressed in organs of the mammalian gastrointestinal tract (salivary gland, liver, pancreas, small intestine, and colon) and in the testes, heart, kidney, and airways. We studied the phenotype of AQP8-null mice, and mice lacking AQP8, together with AQP1 or AQP5. AQP8-knockout mice lacked detectable AQP8 transcript and protein, and had reduced water permeability in plasma membranes from testes. Breeding of AQP8 heterozygous mice yielded AQP8-null mice, whose number, survival, and growth were not different from those of wild-type mice. Organ weight and serum/urine chemistries were similar in wild-type and AQP8-null mice, except for increased testicular weight in the null mice (4.8 +/- 0.7 vs. 7.3 +/- 0.3 mg/g body wt). Urinary concentrating ability in AQP8-null mice was unimpaired as assessed by urine osmolality (3,590 +/- 360 mosmol/kgH(2)O) and weight loss (22 +/- 2%) after 36-h water deprivation; urinary concentrating ability was similarly impaired in AQP1-null mice vs. AQP8/AQP1 double-knockout mice. Agonist-driven fluid secretion in salivary gland was not different in AQP8 vs. wild-type mice ( approximately 1 microl.min(-1).g body wt(-1)) or in AQP5-null mice vs. AQP8/AQP5 double-knockout mice. Closed intestinal loop measurements in vivo indicated unimpaired osmotically driven water transport, active fluid absorption, and cholera toxin-driven fluid secretion in AQP8-null mice. After 21 days on a 50% fat diet, wild-type and AQP8-null mice had similar weight gain ( approximately 15 g), with no evidence of steatorrhea or abnormalities in blood chemistries, except for mild hypertriglyceridemia in the null mice. The mild phenotype of AQP8-null mice was surprising in view of the multiple phenotype abnormalities found in mouse models of AQP1-5 deficiency. |
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Authors:
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Baoxue Yang; Yuanlin Song; Dan Zhao; A S Verkman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2005-01-12 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 288 ISSN: 0363-6143 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2005 May |
Date Detail:
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Created Date: 2005-04-20 Completed Date: 2005-06-09 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C1161-70 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Institute, Univ. of California, San Francisco, CA 94143-0521, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aquaporins / genetics, metabolism* Cell Membrane Permeability / drug effects, physiology Cholera Toxin / toxicity Diet, Fat-Restricted Hypertriglyceridemia / physiopathology Ion Channels / genetics, metabolism* Kidney Concentrating Ability / drug effects, physiology Male Mice Mice, Knockout Osmolar Concentration Phenotype* Salivary Glands / abnormalities, drug effects, metabolism*, physiology Testis / abnormalities, drug effects, metabolism*, physiology Water-Electrolyte Balance / drug effects, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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DK-35124/DK/NIDDK NIH HHS; DK-66194/DK/NIDDK NIH HHS; EB-00415/EB/NIBIB NIH HHS; EY-13574/EY/NEI NIH HHS; HL-59198/HL/NHLBI NIH HHS; HL-73856/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Aquaporins; 0/Ion Channels; 0/aquaporin 8; 9012-63-9/Cholera Toxin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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