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http://purl.uniprot.org/citations/11009458http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11009458http://www.w3.org/2000/01/rdf-schema#comment"Obesity plays a pivotal role in the pathophysiology of metabolic and cardiovascular diseases. Resistance to insulin is commonly seen in metabolic disorders such as obesity and diabetes. Insulin-like growth factor-I (IGF-I) mimics insulin in many tissues and has been shown to enhance cardiac contractile function and growth. Because IGF-I resistance often accompanies resistance to insulin, we sought to determine whether IGF-I-induced myocardial contractile was elevated and whether heart and kidney size were enlarged in obese compared with lean rats. The myocyte contraction profile in the obese rats showed a decreased peak shortening associated with prolonged relengthening and normal shortening duration, a pattern similar to that observed in diabetes. IGF-I (1-500 ng/ml) caused a dose-dependent increase in peak shortening in lean but not obese animals, but it did not alter the duration of shortening and relengthening. Consistent with contractile data, IGF-I induced a dose-dependent increase in Ca(2+) transients only in myocytes of lean rats. IGF-I receptor mRNA levels were significantly reduced in obese rat hearts. These results suggest that the IGF-I-induced cardiac contractile responses are attenuated in the Zucker model of obesity. The mechanisms underlying this alteration may be related to the decreased receptor number and/or changes in intracellular Ca(2+) handling in these animals."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.org/dc/terms/identifier"doi:10.1152/ajpheart.2000.279.4.h1708"xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/author"Ren J."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/author"Brown R.A."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/author"Sowers J.R."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/author"Walsh M.F."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/name"Am J Physiol Heart Circ Physiol"xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/pages"H1708-14"xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/title"Reduced contractile response to insulin and IGF-I in ventricular myocytes from genetically obese Zucker rats."xsd:string
http://purl.uniprot.org/citations/11009458http://purl.uniprot.org/core/volume"279"xsd:string
http://purl.uniprot.org/citations/11009458http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11009458
http://purl.uniprot.org/citations/11009458http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11009458
http://purl.uniprot.org/uniprot/#_A0A140TAB8-mappedCitation-11009458http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11009458
http://purl.uniprot.org/uniprot/#_P24062-mappedCitation-11009458http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11009458
http://purl.uniprot.org/uniprot/A0A140TAB8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11009458
http://purl.uniprot.org/uniprot/P24062http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11009458