Source:http://linkedlifedata.com/resource/pubmed/id/16954332
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2007-1-4
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| pubmed:abstractText |
Gravidas with obesity and diabetes ("diabesity") may transmit this syndrome to their children through genetic and nongenetic mechanisms. Here, we used the Lepr(db/+) diabese mouse to examine the magnitude of these transmission modes, focusing on adipose tissue (AT). We compared the following six groups: wild-type (+/+) offspring from +/+ or db/+ dams (different early life environment) and db/+ offspring from db/+ dams, fed a standard or high-fat diet. Weight gain (0-8 wk) was higher in +/+ offspring from db/+ vs. +/+ mothers, and even higher in db/+ vs. +/+ offspring from db/+ mothers. In addition, we observed a stepwise increase in AT and adipocyte size in +/+ from +/+ mice, +/+ from db/+ mice, and db/+ mice at 8 wk. Differences in weight and adiposity between +/+ offspring from db/+ vs. +/+ dams were more pronounced in males than in females. Leptin and apelin mRNA levels in white and brown AT were higher in +/+ offspring from db/+ vs. +/+ dams; however, leptin, apelin, and tumor necrosis factor-alpha expression were boosted more robustly in db/+ offspring. The high-fat diet amplified AT differences between db/+ vs. +/+ offspring from db/+ dams, but not between +/+ offspring from db/+ vs. +/+ dams. Moreover, db/+ but not +/+ offspring from db/+ mothers were insulin-resistant and hyperinsulinemic after a glucose challenge. In conclusion, the genetic transmission of the diabesity phenotype clearly prevailed, but the early-life diabesity environment had discernible effects on postnatal weight gain as well as on adipocyte size and adipokine expression at a postpubertal age.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0193-1849
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
292
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
E262-71
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16954332-Adipose Tissue,
pubmed-meshheading:16954332-Animals,
pubmed-meshheading:16954332-Animals, Newborn,
pubmed-meshheading:16954332-Birth Weight,
pubmed-meshheading:16954332-Body Weight,
pubmed-meshheading:16954332-Crosses, Genetic,
pubmed-meshheading:16954332-Diabetes Complications,
pubmed-meshheading:16954332-Female,
pubmed-meshheading:16954332-Gene Expression,
pubmed-meshheading:16954332-Genotype,
pubmed-meshheading:16954332-Glucose Intolerance,
pubmed-meshheading:16954332-Insulin Resistance,
pubmed-meshheading:16954332-Male,
pubmed-meshheading:16954332-Mice,
pubmed-meshheading:16954332-Mice, Inbred C57BL,
pubmed-meshheading:16954332-Mice, Mutant Strains,
pubmed-meshheading:16954332-Mice, Transgenic,
pubmed-meshheading:16954332-Obesity,
pubmed-meshheading:16954332-Phenotype,
pubmed-meshheading:16954332-Receptors, Cell Surface,
pubmed-meshheading:16954332-Receptors, Leptin,
pubmed-meshheading:16954332-Weight Gain
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| pubmed:year |
2007
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| pubmed:articleTitle |
Adipose tissue in offspring of Lepr(db/+) mice: early-life environment vs. genotype.
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| pubmed:affiliation |
Experimental Obstetrics and Gynecology, Onderwijs en Navorsing, Campus Gasthuisberg box 611, Herestraat 49, 3000 Leuven, Belgium. suzan.lambin@med.kuleuven.be
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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