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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampFolli, Franco Battista Ennio-
dc.typeArtigopt_BR
dc.titleSclerostin and insulin resistance in prediabetes: evidence of a cross talk between bone and glucose metabolismpt_BR
dc.contributor.authorDaniele, Giuseppe-
dc.contributor.authorWinnier, Deidre-
dc.contributor.authorMari, Andrea-
dc.contributor.authorBruder, Jan-
dc.contributor.authorFourcaudot, Marcel-
dc.contributor.authorPengou, Zuo-
dc.contributor.authorTripathy, Devjit-
dc.contributor.authorJenkinson, Christopher-
dc.contributor.authorFolli, Franco-
dc.subjectResistência à insulinapt_BR
dc.subjectPré-diabetespt_BR
dc.subject.otherlanguageInsulin resistancept_BR
dc.subject.otherlanguagePrediabetespt_BR
dc.description.abstractA gene mutation of the Wnt/β-catenin signaling cascade is present in rare patients with the insulin resistance syndrome. Sclerostin is a circulating peptide inhibiting Wnt/β-catenin signaling. Our aims were to evaluate serum sclerostin in subjects with prediabetes and to analyze its relationship with insulin resistance and β-cell function. We performed a cross-sectional study including 43 healthy normal glucose-tolerant (NGT) individuals and 79 individuals with impaired glucose regulation (IGR), which included subjects with impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and combined IFG-IGT, undergoing oral glucose tolerance test (OGTT) and dual-energy X-ray absorptiometry. A subgroup of 18 with NGT and 30 with IGR also underwent a euglycemic–hyperinsulinemic clamp with tracer. Sclerostin levels were higher in IGR compared with NGT (50.8 ± 2.4 vs. 38.7 ± 2.3 pmol/L; P = 0.01), positively correlated with HOMA-insulin resistance (IR) (r = 0.62; P < 0.001), and negatively correlated with insulin-mediated total body glucose disposal (r = −0.40; P < 0.001). Fasting endogenous glucose production (EGP) and hepatic and adipose tissue insulin resistance indexes were positively correlated with sclerostin levels (r = 0.48, r = 0.62, and r = 0.61, respectively; P < 0.001). Fasting and OGTT insulin clearance were inversely correlated with sclerostin serum levels (r = −0.52 and r = −0.44, respectively; both P < 0.001). Sclerostin levels were not correlated with β-cell function parameters. In multiple linear regression analysis, the addition of sclerostin levels to the traditional risk factors for insulin resistance improved the r2 associated with HOMA-IR (r2 change: 0.055; F change: 28.893; P = 0.001) and insulin-mediated total body glucose disposal (r2 change: 0.059; F change: 4.938; P = 0.033). Sclerostin levels are increased in individuals with prediabetes and correlated with insulin resistance in skeletal muscle, liver, and adipose tissue. The correlation between sclerostin and insulin clearance at fasting state and during OGTT is novel; thus, studies are needed to explore the potential causal relationship.pt_BR
dc.relation.ispartofDiabetes carept_BR
dc.publisher.cityArlington, VApt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherAmerican Diabetes Associationpt_BR
dc.date.issued2015-
dc.date.monthofcirculationAug.pt_BR
dc.language.isoengpt_BR
dc.description.volume38pt_BR
dc.description.issuenumber8pt_BR
dc.description.firstpage1509pt_BR
dc.description.lastpage1517pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0149-5992pt_BR
dc.identifier.eissn1935-5548pt_BR
dc.identifier.doi10.2337/dc14-2989pt_BR
dc.identifier.urlhttps://care.diabetesjournals.org/content/38/8/1509.longpt_BR
dc.date.available2021-01-08T16:24:14Z-
dc.date.accessioned2021-01-08T16:24:14Z-
dc.description.provenanceSubmitted by Bruna Maria Campos da Cunha (bcampos@unicamp.br) on 2021-01-08T16:24:14Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-02-19T18:02:31Z : No. of bitstreams: 1 000358673200028.pdf: 1226803 bytes, checksum: 78c6c4947363c1424278c4498d40b07d (MD5)en
dc.description.provenanceMade available in DSpace on 2021-01-08T16:24:14Z (GMT). No. of bitstreams: 0 Previous issue date: 2015en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/353803-
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000358673200028pt_BR
dc.creator.orcid0000-0001-9824-5222pt_BR
dc.type.formArtigopt_BR
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