Source:http://linkedlifedata.com/resource/pubmed/id/15024641
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2004-4-16
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pubmed:abstractText |
Infertility and hypercytolipidemic utero-ovarian involution are recognized consequences of the diabetes-obesity syndrome (DOS) in C57BL mice with either obese (ob/ob) or diabetes (db/db) single gene mutations. We have evaluated the interdependent deleterious influences of both mutation types and differences in the genomic background on utero-ovarian dysfunction in C57BL mice. Control ( +/?) C57BL mice were matched with littermate ob/ob and db/db mutants expressed on either the /KsJ or /6 background. Both ob/ob and db/db mutations increased body weights of /KsJ and /6 background strains relative to +/? groups. In contrast, uterine and ovarian weights were depressed by ob/ob and db/db mutations relative to +/?, regardless of the background strain, but especially when expressed on the /KsJ background. Functionally, both ob/ob and db/db mutations induced hyperglycemic-hyperinsulinemic states coupled with depressed serum estradiol-17-beta and progesterone concentrations when expressed on a /KsJ background. Microscopic analysis of utero-ovarian tissue samples revealed marked hypercytolipidemia in the follicular granulosa and endometrial epithelial tissue layers of both ob/ob and db/db mutant groups relative to normal +/? cytoarchitecture. The db/db mutation consistently promoted more severe hypercytolipidemic profiles than the ob/ob mutation, regardless of background strain. Thus, the severity of utero-ovarian hypercytolipidemia following the expression of ob/ob and db/db mutations in C57BL mice is influenced, or moderated, by the genomic background on which the mutation is expressed.
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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 |
May
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pubmed:issn |
0302-766X
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2004 Springer-Verlag
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pubmed:issnType |
Print
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pubmed:volume |
316
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
233-41
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15024641-Animals,
pubmed-meshheading:15024641-Blood Glucose,
pubmed-meshheading:15024641-Body Weight,
pubmed-meshheading:15024641-Diabetes Mellitus, Experimental,
pubmed-meshheading:15024641-Epithelium,
pubmed-meshheading:15024641-Estradiol,
pubmed-meshheading:15024641-Female,
pubmed-meshheading:15024641-Hyperlipidemias,
pubmed-meshheading:15024641-Insulin,
pubmed-meshheading:15024641-Mice,
pubmed-meshheading:15024641-Mice, Obese,
pubmed-meshheading:15024641-Microscopy, Electron, Transmission,
pubmed-meshheading:15024641-Mutation,
pubmed-meshheading:15024641-Obesity,
pubmed-meshheading:15024641-Ovary,
pubmed-meshheading:15024641-Uterus
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pubmed:year |
2004
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pubmed:articleTitle |
Genomic modulation of diabetes (db/db) and obese (ob/ob) mutation-induced hypercytolipidemia: cytochemical basis of female reproductive tract involution.
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pubmed:affiliation |
Division of Cell Biology and Biophysics, Schools of Medicine and Biological Sciences, University of Missouri-Kansas City, 5007 Rockhill Road, Kansas City, MO 64110, USA. garrisd@umkc.edu
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pubmed:publicationType |
Journal Article
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