Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.

The development of type 2 diabetes is associated with the impairment of insulin secretion. To evaluate the evolution of the secretory response, a chronological study comparing normal Wistar (W) vs Goto-Kakizaki (GK) rats, an animal model of non obese type 2 diabetes, was done. Glucose and arginine w...

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Main Authors: Raquel M Seiça, K I Suzuki, Rosa M Santos, Luis M Do Rosário
Format: Article
Language:English
Published: Ordem dos Médicos 2004-02-01
Series:Acta Médica Portuguesa
Online Access:https://www.actamedicaportuguesa.com/revista/index.php/amp/article/view/1755
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author Raquel M Seiça
K I Suzuki
Rosa M Santos
Luis M Do Rosário
author_facet Raquel M Seiça
K I Suzuki
Rosa M Santos
Luis M Do Rosário
author_sort Raquel M Seiça
collection DOAJ
description The development of type 2 diabetes is associated with the impairment of insulin secretion. To evaluate the evolution of the secretory response, a chronological study comparing normal Wistar (W) vs Goto-Kakizaki (GK) rats, an animal model of non obese type 2 diabetes, was done. Glucose and arginine were tested in collagenase isolated islets of Langerhans with perfusion and ELISA immunoassay techniques. Fasting glycaemia and insulinemia and glucose tolerance were also evaluated. We have seen, in W rats, a mild glucose intolerance in the first two weeks of age. GK rats were always glucose intolerant with hyperglycaemia and hyperinsulinemia at fasten after one month old. Wistar islets had a characteristic biphasic response to glucose after the first two weeks of age. GK islets were always glucose irresponsive. Arginine induced an increase in insulin secretion in both animal models, independent of age, although GK rats had always a smaller response when compared to W rats. We concluded that 1) in W rats, a biphasic insulin secretion in response to glucose is observed after the first two weeks of age, simultaneously with glycaemia stabilization 2) in GK rats, both first and second phases of glucose-induced insulin release are significantly reduced and a smaller reduction in response to arginine is observed. This beta-cell disfunction is a primary event in this model of type 2 diabetes, preceding fasting hyperglycaemia and hyperinsulinemia.
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spelling doaj.art-a6ca88ff8ef54ee4b13d7a16ae3e3c1e2022-12-22T04:12:59ZengOrdem dos MédicosActa Médica Portuguesa0870-399X1646-07582004-02-0117110.20344/amp.1755Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.Raquel M Seiça0K I SuzukiRosa M SantosLuis M Do RosárioInstituto de Fisiologia, Faculdade de Medicina da Universidade de Coimbra.The development of type 2 diabetes is associated with the impairment of insulin secretion. To evaluate the evolution of the secretory response, a chronological study comparing normal Wistar (W) vs Goto-Kakizaki (GK) rats, an animal model of non obese type 2 diabetes, was done. Glucose and arginine were tested in collagenase isolated islets of Langerhans with perfusion and ELISA immunoassay techniques. Fasting glycaemia and insulinemia and glucose tolerance were also evaluated. We have seen, in W rats, a mild glucose intolerance in the first two weeks of age. GK rats were always glucose intolerant with hyperglycaemia and hyperinsulinemia at fasten after one month old. Wistar islets had a characteristic biphasic response to glucose after the first two weeks of age. GK islets were always glucose irresponsive. Arginine induced an increase in insulin secretion in both animal models, independent of age, although GK rats had always a smaller response when compared to W rats. We concluded that 1) in W rats, a biphasic insulin secretion in response to glucose is observed after the first two weeks of age, simultaneously with glycaemia stabilization 2) in GK rats, both first and second phases of glucose-induced insulin release are significantly reduced and a smaller reduction in response to arginine is observed. This beta-cell disfunction is a primary event in this model of type 2 diabetes, preceding fasting hyperglycaemia and hyperinsulinemia.https://www.actamedicaportuguesa.com/revista/index.php/amp/article/view/1755
spellingShingle Raquel M Seiça
K I Suzuki
Rosa M Santos
Luis M Do Rosário
Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
Acta Médica Portuguesa
title Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
title_full Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
title_fullStr Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
title_full_unstemmed Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
title_short Deficiência primária da secreção de insulina de ilhéus isolados de ratos Goto-Kakizaki. Um modelo animal de diabetes tipo 2 não obesa.
title_sort deficiencia primaria da secrecao de insulina de ilheus isolados de ratos goto kakizaki um modelo animal de diabetes tipo 2 nao obesa
url https://www.actamedicaportuguesa.com/revista/index.php/amp/article/view/1755
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AT kisuzuki deficienciaprimariadasecrecaodeinsulinadeilheusisoladosderatosgotokakizakiummodeloanimaldediabetestipo2naoobesa
AT rosamsantos deficienciaprimariadasecrecaodeinsulinadeilheusisoladosderatosgotokakizakiummodeloanimaldediabetestipo2naoobesa
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