Linked Life Data

18029473

Source:http://linkedlifedata.com/resource/pubmed/id/18029473

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-11-21
pubmed:abstractText
11Beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) plays a key role in the regulation of intracellular glucocorticoid concentrations. Increased message and/or activity of adipose 11beta-HSD-1 are characteristics of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is colocalized with 11beta-HSD-1 and may be a critical factor in determining the oxo-reductase activity of 11beta-HSD-1. This study examined the effects of sucrose solution access on body weight, body composition, and message of 11beta-HSD-1 and H6PDH in mesenteric adipose and liver. Rats were assigned to 3 groups: 1) control (ad libitum intake of nonpurified diet and water only); 2) ad libitum intake of 16% sucrose solution (S16); or 3) ad libitum intake of 32% sucrose solution (S32) in addition to ad libitum intake of diet and water. The S32 group consumed more energy daily than the S16 and control groups, yet body weight did not differ among groups. Percentages of body fat did not differ between the S16 and S32 groups but were higher than in controls. Hepatic 11beta-HSD-1 message was suppressed by 46% in the S16 group and by 47% in the S32 group, whereas the H6PDH message nearly doubled in the S16 group compared to the control group. In mesenteric fat, 11beta-HSD-1 message increased 23-fold in the S16 group and 32-fold in the S32 group and the H6PDH message increased 3.5-fold in the S16 group compared to the control group. These data demonstrate that sucrose can promote increased 11beta-HSD-1 and H6PDH message in mesenteric fat while concomitantly decreasing 11beta-HSD-1 message and increasing H6PDH message in liver. These observations support the hypothesis that sucrose access causes obesity via its ability to increase adipose 11beta-HSD-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1541-6100
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
137
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2616-21
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18029473-11-beta-Hydroxysteroid Dehydrogenase Type 1, pubmed-meshheading:18029473-Adipose Tissue, pubmed-meshheading:18029473-Animals, pubmed-meshheading:18029473-Blood Glucose, pubmed-meshheading:18029473-Body Composition, pubmed-meshheading:18029473-Body Weight, pubmed-meshheading:18029473-Carbohydrate Dehydrogenases, pubmed-meshheading:18029473-Energy Metabolism, pubmed-meshheading:18029473-Feeding Behavior, pubmed-meshheading:18029473-Food Deprivation, pubmed-meshheading:18029473-Insulin, pubmed-meshheading:18029473-Leptin, pubmed-meshheading:18029473-Liver, pubmed-meshheading:18029473-Male, pubmed-meshheading:18029473-Rats, pubmed-meshheading:18029473-Rats, Sprague-Dawley, pubmed-meshheading:18029473-Signal Transduction, pubmed-meshheading:18029473-Sucrose, pubmed-meshheading:18029473-Time Factors
pubmed:year
2007
pubmed:articleTitle
Sucrose access differentially modifies 11beta-hydroxysteroid dehydrogenase-1 and hexose-6-phosphate dehydrogenase message in liver and adipose tissue in rats.
pubmed:affiliation
Department of Nutrition and Food Science, University of Maryland, College Park, MD 20742, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't