Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans
Autor(a) principal: | |
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Data de Publicação: | 2006 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.2337/dc06-0438 http://hdl.handle.net/11449/219396 |
Resumo: | OBJECTIVE - To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS - We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of β-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS - Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased ∼30% (P < 0.05), but clampdetermined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced ∼35% (P < 0.002) and ∼30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but ∼15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced ∼30%. IFG/NGT differed from NFG/IGT by having ∼40% lower HOMA-%B (P < 0.012) and ∼50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS - Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity. © 2006 by the American Diabetes Association. |
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Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humansOBJECTIVE - To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS - We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of β-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS - Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased ∼30% (P < 0.05), but clampdetermined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced ∼35% (P < 0.002) and ∼30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but ∼15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced ∼30%. IFG/NGT differed from NFG/IGT by having ∼40% lower HOMA-%B (P < 0.012) and ∼50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS - Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity. © 2006 by the American Diabetes Association.Department of Endocrinology Carl T. Hayden VA Medical Center, Phoenix, AZDepartment of Clinical Medicine Faculdade de Medicina Botucatu University of Sao Paulo State, Sao PauloDepartment of Internal Medicine II Ludwig-Maximilians University of Munich, MunichDepartment of Internal Medicine University Medical Center Utrecht, UtrechtDepartment of Medicine University of Rochester School of Medicine, Rochester, NYDiabetes/Metabolism Unit Henry Dunant Foundation, AthensCarl T. Hayden VA Medical Center, 650 East Indian School Rd., Phoenix, AZ 85012Carl T. Hayden VA Medical CenterUniversidade de São Paulo (USP)Ludwig-Maximilians University of MunichUniversity Medical Center UtrechtUniversity of Rochester School of MedicineHenry Dunant FoundationMeyer, ChristianPimenta, WalkyriaWoerle, Hans J.Van Haeften, TimonSzoke, ErvinMitrakou, AsiminaGerich, John2022-04-28T18:55:17Z2022-04-28T18:55:17Z2006-08-07info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1909-1914http://dx.doi.org/10.2337/dc06-0438Diabetes Care, v. 29, n. 8, p. 1909-1914, 2006.0149-5992http://hdl.handle.net/11449/21939610.2337/dc06-04382-s2.0-33746617223Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengDiabetes Careinfo:eu-repo/semantics/openAccess2022-04-28T18:55:17Zoai:repositorio.unesp.br:11449/219396Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T16:47:38.105780Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
title |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
spellingShingle |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans Meyer, Christian |
title_short |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
title_full |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
title_fullStr |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
title_full_unstemmed |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
title_sort |
Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans |
author |
Meyer, Christian |
author_facet |
Meyer, Christian Pimenta, Walkyria Woerle, Hans J. Van Haeften, Timon Szoke, Ervin Mitrakou, Asimina Gerich, John |
author_role |
author |
author2 |
Pimenta, Walkyria Woerle, Hans J. Van Haeften, Timon Szoke, Ervin Mitrakou, Asimina Gerich, John |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Carl T. Hayden VA Medical Center Universidade de São Paulo (USP) Ludwig-Maximilians University of Munich University Medical Center Utrecht University of Rochester School of Medicine Henry Dunant Foundation |
dc.contributor.author.fl_str_mv |
Meyer, Christian Pimenta, Walkyria Woerle, Hans J. Van Haeften, Timon Szoke, Ervin Mitrakou, Asimina Gerich, John |
description |
OBJECTIVE - To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS - We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of β-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS - Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased ∼30% (P < 0.05), but clampdetermined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced ∼35% (P < 0.002) and ∼30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but ∼15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced ∼30%. IFG/NGT differed from NFG/IGT by having ∼40% lower HOMA-%B (P < 0.012) and ∼50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS - Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity. © 2006 by the American Diabetes Association. |
publishDate |
2006 |
dc.date.none.fl_str_mv |
2006-08-07 2022-04-28T18:55:17Z 2022-04-28T18:55:17Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.2337/dc06-0438 Diabetes Care, v. 29, n. 8, p. 1909-1914, 2006. 0149-5992 http://hdl.handle.net/11449/219396 10.2337/dc06-0438 2-s2.0-33746617223 |
url |
http://dx.doi.org/10.2337/dc06-0438 http://hdl.handle.net/11449/219396 |
identifier_str_mv |
Diabetes Care, v. 29, n. 8, p. 1909-1914, 2006. 0149-5992 10.2337/dc06-0438 2-s2.0-33746617223 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Diabetes Care |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1909-1914 |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1808128701979688960 |