Lack of insulin inhibition on insulin secretion in non-diabetic morbidly obese patients

dc.creatorMuscelli, E
dc.creatorPereira, JA
dc.creatorLazarin, MACT
dc.creatorda Silva, CA
dc.creatorPareja, JC
dc.creatorSaad, MJA
dc.date2001
dc.dateJUN
dc.date2014-07-30T14:36:02Z
dc.date2015-11-26T17:15:13Z
dc.date2014-07-30T14:36:02Z
dc.date2015-11-26T17:15:13Z
dc.date.accessioned2018-03-29T00:03:29Z
dc.date.available2018-03-29T00:03:29Z
dc.identifierInternational Journal Of Obesity. Nature Publishing Group, v. 25, n. 6, n. 798, n. 804, 2001.
dc.identifier0307-0565
dc.identifierWOS:000168919300007
dc.identifier10.1038/sj.ijo.0801607
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/61066
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/61066
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281995
dc.descriptionOBJECTIVE: Insulin inhibition of insulin secretion has been described in normal lean subjects. In this study, we examined whether this phenomenon also occurs in the morbidly obese who often have severe peripheral insulin resistance. SUBJECTS: Twelve obese patients, normotolerant to glucose (8F/4M, body mass index (BMI) = 54.8 +/-2.5 kg/m(2), 39y) and 16 lean control subjects (10F/6M, BMI = 22.0 +/-0.5 kg/m(2), 31y). DESIGN AND MEASUREMENTS: An experimental study using various parameters, including an euglycemic hyperinsulinemic clamp (280pmol/min/m(2) of body surface), an oral glucose tolerance test (OGTT), electrical bioimpedance and indirect calorimetry. RESULTS: The obese subjects were insulin resistant (M = 19.8 +/-1.6 vs 48.7 +/-2.6 mu mol/min kg FFM, P < 0.0001) and hyperinsulinemic in the fasted state and after glucose ingestion. Fasting plasma C-peptide levels (obese 1425 +/- 131 pmol/l vs lean 550 +/- 63 pmol/l; P < 0.0001) decreased less during the clamp in the obese groups (-16.9 +/-6.9% vs -43.0 +/-5.6% relative to fasting values; P = 0.007). In the lean group, the C-peptide decrease during the clamp (percentage variation) was related to insulin sensitivity, M/FFM (r = 0.56, P = 0.03), even after adjustment for the clamp glucose variation. CONCLUSION: We conclude that, in lean subjects, insulin inhibits its own secretion, and this may be related to insulin sensibility. This response is blunted in morbidly obese patients and may have a role in the pathogenesis of fasting hyperinsulinemia in these patients.
dc.description25
dc.description6
dc.description798
dc.description804
dc.languageen
dc.publisherNature Publishing Group
dc.publisherBasingstoke
dc.publisherInglaterra
dc.relationInternational Journal Of Obesity
dc.relationInt. J. Obes.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectobesity
dc.subjectinsulin secretion
dc.subjectinsulin clamp
dc.subjectinsulin resistance
dc.subjectC-peptide
dc.subjectFeedback Inhibition
dc.subjectC-peptide
dc.subjectSomatostatin Infusion
dc.subjectExogenous Insulin
dc.subjectGlucose Clamp
dc.subjectRisk-factors
dc.subjectBeta-cells
dc.subjectHyperinsulinemia
dc.subjectResistance
dc.subjectClearance
dc.titleLack of insulin inhibition on insulin secretion in non-diabetic morbidly obese patients
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución