dc.creatorGeloneze, Bruno
dc.creatorde Oliveira, Maria da Saude
dc.creatorVasques, Ana Carolina Junqueira
dc.creatorNovaes, Fernanda Satake
dc.creatorPareja, José Carlos
dc.creatorTambascia, Marcos Antonio
dc.date2014-Jul
dc.date2015-11-27T13:42:34Z
dc.date2015-11-27T13:42:34Z
dc.date.accessioned2018-03-29T01:20:49Z
dc.date.available2018-03-29T01:20:49Z
dc.identifierMetabolism: Clinical And Experimental. v. 63, n. 7, p. 922-9, 2014-Jul.
dc.identifier1532-8600
dc.identifier10.1016/j.metabol.2014.04.004
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/24854384
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/201416
dc.identifier24854384
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1301649
dc.descriptionTo estimate the impact of aging and diabetes on insulin sensitivity, beta-cell function, adipocytokines, and incretin production. Hyperglycemic clamps, arginine tests and meal tolerance tests were performed in 50 non-obese subjects to measure insulin sensitivity (IS) and insulin secretion as well as plasma levels of glucagon, GLP-1 and GIP. Patients with diabetes and healthy control subjects were divided into the following groups: middle-aged type 2 diabetes (MA-DM), aged Type 2 diabetes (A-DM) and middle-aged or aged subjects with normal glucose tolerance (MA-NGT or A-NGT). IS, as determined by the homeostasis model assessment, glucose infusion rate, and oral glucose insulin sensitivity, was reduced in the aged and DM groups compared with MA-NGT, but it was similar in the MA-DM and A-DM groups. Insulinogenic index, first and second phase insulin secretion and the disposition indices, but not insulin response to arginine, were reduced in the aged and DM groups. Postprandial glucagon production was higher in MA-DM compared to MA-NGT. Whereas the GLP-1 production was reduced in A-DM, no differences between groups were observed in GIP production. In non-obese subjects, diabetes and aging impair insulin sensitivity. Insulin production is reduced by aging, and diabetes exacerbates this condition. Aging associated defects superimposed diabetic physiopathology, particularly regarding GLP-1 production. On the other hand, the glucose-independent secretion of insulin was preserved. Knowledge of the complex relationship between aging and diabetes could support the development of physiopathological and pharmacological based therapies.
dc.description63
dc.description922-9
dc.languageeng
dc.relationMetabolism: Clinical And Experimental
dc.relationMetab. Clin. Exp.
dc.rightsfechado
dc.rightsCopyright © 2014. Published by Elsevier Inc.
dc.sourcePubMed
dc.subjectAdiponectin
dc.subjectAdipose Tissue
dc.subjectAdult
dc.subjectAged
dc.subjectAging
dc.subjectCross-sectional Studies
dc.subjectDiabetes Mellitus, Type 2
dc.subjectDown-regulation
dc.subjectGastric Inhibitory Polypeptide
dc.subjectGlucagon
dc.subjectGlucagon-like Peptide 1
dc.subjectHumans
dc.subjectIncretins
dc.subjectInsulin
dc.subjectInsulin Resistance
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectPancreas
dc.subjectPostprandial Period
dc.subjectUp-regulation
dc.subjectBeta-cell Function
dc.subjectGlp-1
dc.subjectGlucagon
dc.subjectIncretin
dc.subjectInsulin Sensitivity
dc.titleImpaired Incretin Secretion And Pancreatic Dysfunction With Older Age And Diabetes.
dc.typeArtículos de revistas


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