Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-29
pubmed:abstractText
The purpose of this study was to test whether the melanocortin-4 receptor (MC4R) is critical in the development of hypertension associated with obesity and its metabolic disorders. MC4R-deficient homozygous (-/-) and heterozygous (+/-) and wild-type (WT) C57BL/6J mice 17 to 19 weeks old (n=5 to 7 per group) were implanted with telemetry devices for monitoring 24-hour mean arterial pressure (MAP) and heart rate (HR). After 3-day stable control measurements on normal-salt diet (NSD; 0.4% NaCl), mice received a high-salt diet (HSD; 4% NaCl) for 7 days, followed by 3-day recovery on NSD. MC4R (-/-) mice were severely obese compared with MC4R (+/-) and WT mice (body weight 48+/-1.5 versus 31+/-0.6 and 30+/-0.5 g respectively). On NSD, MAP was similar in all groups of mice (MC4R (-/-) 110+/-3 mm Hg; MC4R (+/-) 109+/-2 mm Hg; WT 114+/-2 mm Hg), and HR in MC4R (-/-) was lower than in WT (604+/-5 versus 645+/-9 bpm; P<0.05) but not different from MC4R (+/-) (625+/-13 bpm) mice. HSD did not significantly alter MAP or HR in any of the groups. Epididymal and retroperitoneal fat weights and plasma leptin levels were several-fold greater in MC4R (-/-) compared with MC4R (+/-) and WT mice. Plasma insulin and glucose levels were also significantly greater in MC4R (-/-) than in MC4R (+/-) and WT mice. These data suggest that despite obesity, visceral adiposity, hyperleptinemia, and hyperinsulinemia, MC4R (-/-) mice are neither hypertensive nor salt sensitive, indicating that a functional MC4R may be necessary for the development of hypertension associated with obesity and its metabolic abnormalities.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
326-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16027245-Adipose Tissue, pubmed-meshheading:16027245-Animals, pubmed-meshheading:16027245-Blood Pressure, pubmed-meshheading:16027245-Body Size, pubmed-meshheading:16027245-Dose-Response Relationship, Drug, pubmed-meshheading:16027245-Drinking, pubmed-meshheading:16027245-Eating, pubmed-meshheading:16027245-Heart Rate, pubmed-meshheading:16027245-Hormones, pubmed-meshheading:16027245-Hyperinsulinism, pubmed-meshheading:16027245-Hypertension, pubmed-meshheading:16027245-Leptin, pubmed-meshheading:16027245-Mice, pubmed-meshheading:16027245-Mice, Inbred C57BL, pubmed-meshheading:16027245-Mice, Knockout, pubmed-meshheading:16027245-Obesity, pubmed-meshheading:16027245-Receptor, Melanocortin, Type 4, pubmed-meshheading:16027245-Sodium Chloride, pubmed-meshheading:16027245-Sodium Chloride, Dietary, pubmed-meshheading:16027245-Viscera, pubmed-meshheading:16027245-Weight Gain
pubmed:year
2005
pubmed:articleTitle
Melanocortin-4 receptor-deficient mice are not hypertensive or salt-sensitive despite obesity, hyperinsulinemia, and hyperleptinemia.
pubmed:affiliation
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505, USA. ltallam@physiology.umsmed.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural