Source:http://linkedlifedata.com/resource/pubmed/id/15240652
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
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umls-concept:C0441889,
umls-concept:C0681850,
umls-concept:C1550501,
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umls-concept:C1710263,
umls-concept:C2349001,
umls-concept:C2697811,
umls-concept:C2911684
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| pubmed:issue |
7
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| pubmed:dateCreated |
2004-7-8
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| pubmed:abstractText |
Our aim was to investigate the possible role of the type 2 diabetes susceptibility gene CAPN10 in obesity. A case control study consisting of 235 obese Swedish subjects [body mass index, 40 (35-45) kg/m(2)] and 235 controls matched for age and gender [body mass index, 22 (21-24) kg/m(2)], and a transmission disequilibrium test consisting of 116 parents-offspring trios, where the offspring was abdominally obese [waist, 100 (95-110) cm], were performed. CAPN10 mRNA expression was studied in adipose tissue biopsies from 33 of the obese subjects participating in the case control study. The CAPN10 single-nucleotide polymorphism (SNP)-43 was genotyped using PCR followed by NdeI digestion or by allelic discrimination. CAPN10 mRNA levels were quantified using real-time RT-PCR with Cyclophilin A as an internal standard. No significant associations between CAPN10 SNP-43 and obesity were seen, neither in the case control study nor in the transmission disequilibrium test, but obese subjects homozygous for the SNP-43 G allele had significantly elevated triglyceride levels compared with subjects carrying the A allele [1.7 (1.1-2.4) vs. 1.4 (1.0-2.0); P = 0.03]. The CAPN10 mRNA expression in sc fat was significantly reduced in subjects with the SNP-43 G/G genotype compared with carriers of SNP-43 G/A (G/G, 0.33 +/- 0.02, vs. G/A, 0.51 +/- 0.09; P = 0.048), and a similar trend was observed in visceral fat (G/G, 0.52 +/- 0.06, vs. G/A, 0.65 +/- 0.10; P = 0.22). Our data suggest that reduced CAPN10 expression may be a risk factor for features associated with the metabolic syndrome in obese subjects, although variation in the gene does not seem to contribute to the risk for developing obesity per se.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0021-972X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
89
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3601-5
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:15240652-Adipose Tissue,
pubmed-meshheading:15240652-Adult,
pubmed-meshheading:15240652-Alleles,
pubmed-meshheading:15240652-Calpain,
pubmed-meshheading:15240652-Case-Control Studies,
pubmed-meshheading:15240652-Female,
pubmed-meshheading:15240652-Genetic Variation,
pubmed-meshheading:15240652-Genotype,
pubmed-meshheading:15240652-Homozygote,
pubmed-meshheading:15240652-Humans,
pubmed-meshheading:15240652-Male,
pubmed-meshheading:15240652-Middle Aged,
pubmed-meshheading:15240652-Obesity,
pubmed-meshheading:15240652-Polymorphism, Single Nucleotide,
pubmed-meshheading:15240652-RNA, Messenger,
pubmed-meshheading:15240652-Subcutaneous Tissue,
pubmed-meshheading:15240652-Sweden,
pubmed-meshheading:15240652-Triglycerides,
pubmed-meshheading:15240652-Viscera
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| pubmed:year |
2004
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| pubmed:articleTitle |
Variation in the calpain-10 gene is associated with elevated triglyceride levels and reduced adipose tissue messenger ribonucleic acid expression in obese Swedish subjects.
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| pubmed:affiliation |
Department of Endocrinology, Lund University, Wallenberg Laboratory, Malmö University Hospital, S-205 02 Malmö, Sweden. emma.carlsson@endo.mas.lu.se
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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