dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:21:01Z
dc.date.available2014-05-27T11:21:01Z
dc.date.created2014-05-27T11:21:01Z
dc.date.issued2004-02-01
dc.identifierDiabetes Research and Clinical Practice, v. 63, n. 2, p. 87-92, 2004.
dc.identifier0168-8227
dc.identifierhttp://hdl.handle.net/11449/67631
dc.identifier10.1016/j.diabres.2003.09.008
dc.identifier2-s2.0-0346671134
dc.identifier6758680388835078
dc.identifier8727897080522289
dc.identifier0000-0002-9227-832X
dc.description.abstractWe evaluated insulin release and insulin sensitivity in women with basal and/or postprandial hyperglycemia but normal oral glucose tolerance test (OGTT) in previous pregnancy (GHG). These women were individually matched with females without previous hyperglycemia (NGT). Both groups consisted of normal glucose-tolerant women at the time of this study. They underwent OGTT (75g; n= 32 pairs) and hyperglycemic clamp experiments (10mmoll-1; n=27 pairs) with plasma glucose, insulin, and C-peptide measurements and calculation of insulinogenic index, first- and second-phase insulin release, and insulin sensitivity index (ISI). The GHG group showed higher glycosylated hemoglobin levels (6.2±0.6% versus 5.8±0.8%; P<0.05); lower insulinogenic index at 30min (134.03±62.69pmolmmol-1 versus 181.59±70.26pmolmmoll-1; P<0.05) and diminished C-peptide response in relation to glucose (4.05±0.36nmolmmol-1 versus 4.23±0.36nmolmmol-1; P<0.05) at OGTT. Both groups did not show difference in insulin secretion and ISI by hyperglycemic clamp technique. We concluded that in up to 12 years from index pregnancy, women with previous GHG, presenting normal glucose tolerance and well-matched with their controls, showed β-cell dysfunction without change in ISI. As women with previous GHG are at risk of type 2 diabetes, β-cell dysfunction may be its primary defect. © 2003 Elsevier B.V. All rights reserved.
dc.languageeng
dc.relationDiabetes Research and Clinical Practice
dc.relation2.548
dc.relation1,538
dc.rightsAcesso restrito
dc.sourceScopus
dc.subjectGestational hyperglycemia
dc.subjectInsulin release
dc.subjectInsulin sensitivity
dc.subjectType 2 diabetes
dc.subjectC peptide
dc.subjectglucose
dc.subjectglycosylated hemoglobin
dc.subjectadult
dc.subjectcalculation
dc.subjectclinical article
dc.subjectcontrolled study
dc.subjectfemale
dc.subjectglucose blood level
dc.subjecthigh risk population
dc.subjecthuman
dc.subjecthyperglycemia
dc.subjectinsulin blood level
dc.subjectinsulin release
dc.subjectinsulin sensitivity
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectoral glucose tolerance test
dc.subjectpancreas disease
dc.subjectpancreas islet beta cell
dc.subjectpostprandial state
dc.subjectpregnancy
dc.subjectpregnancy diabetes mellitus
dc.subjectprotein blood level
dc.subjectrisk assessment
dc.subjectBlood Glucose
dc.subjectC-Peptide
dc.subjectDiabetes Mellitus, Type 2
dc.subjectFemale
dc.subjectFood
dc.subjectGlucose Clamp Technique
dc.subjectGlucose Tolerance Test
dc.subjectHemoglobin A, Glycosylated
dc.subjectHumans
dc.subjectHyperglycemia
dc.subjectInsulin
dc.subjectInsulin Resistance
dc.subjectIslets of Langerhans
dc.subjectPregnancy
dc.subjectRisk Factors
dc.titlePancreatic β-cell defects in women at risk of type 2 diabetes
dc.typeArtículos de revistas


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