| pubmed-article:11018080 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0026845 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0035696 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0021655 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:11018080 | lifeskim:mentions | umls-concept:C0678951 | lld:lifeskim |
| pubmed-article:11018080 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:11018080 | pubmed:dateCreated | 2000-10-30 | lld:pubmed |
| pubmed-article:11018080 | pubmed:abstractText | Previous linkage studies in Mexican-Americans localized a major susceptibility locus for type 2 diabetes, NIDDM1, to chromosome 2q. This evidence for linkage to type 2 diabetes was recently found to be associated with a common G-->A polymorphism (UCSNP-43) within the CAPN10 gene. The at-risk genotype was homozygous for the UCSNP-43 G allele. In the present study among Pima Indians, the UCSNP-43 G/G genotype was not associated with an increased prevalence of type 2 diabetes. However, Pima Indians with normal glucose tolerance, who have a G/G genotype at UCSNP-43, were found to have decreased rates of postabsorptive and insulin-stimulated glucose turnover that appear to result from decreased rates of glucose oxidation. In addition, G/G homozygotes were found to have reduced CAPN10 mRNA expression in their skeletal muscle. A decreased rate of insulin-mediated glucose turnover, or insulin resistance, is one mechanism by which the polymorphism in CAPN10 may increase susceptibility to type 2 diabetes mellitus in older persons. | lld:pubmed |
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| pubmed-article:11018080 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11018080 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11018080 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11018080 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11018080 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11018080 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:HorikawaYY | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:COLEL JLJ | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:ROT KTK | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:HansonR LRL | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:BogardusCC | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:CoxN JNJ | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:KnowlerW CWC | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:MottDD | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:YangXX | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:PratleyR ERE | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:PermanaP APA | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:BaierL JLJ | lld:pubmed |
| pubmed-article:11018080 | pubmed:author | pubmed-author:ShenG QGQ | lld:pubmed |
| pubmed-article:11018080 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11018080 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:11018080 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11018080 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11018080 | pubmed:pagination | R69-73 | lld:pubmed |
| pubmed-article:11018080 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:11018080 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11018080 | pubmed:articleTitle | A calpain-10 gene polymorphism is associated with reduced muscle mRNA levels and insulin resistance. | lld:pubmed |
| pubmed-article:11018080 | pubmed:affiliation | Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Phoenix, Arizona 85016, USA. lbaier@phx.niddk.nih.gov | lld:pubmed |
| pubmed-article:11018080 | pubmed:publicationType | Journal Article | lld:pubmed |
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