schliessen

Filtern

 

Bibliotheken

Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action

Aims/hypothesis The impact of strategies for prevention of type 2 diabetes in isolated impaired fasting glycaemia (i-IFG) vs isolated impaired glucose tolerance (i-IGT) may differ depending on the underlying pathophysiology. We examined insulin secretion during OGTTs and IVGTTs, hepatic and peripher... Full description

Journal Title: Diabetologia 2008-03-04, Vol.51 (5), p.853-861
Main Author: Færch, K
Other Authors: Vaag, A , Holst, J. J , Glümer, C , Pedersen, O , Borch-Johnsen, K
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Berlin/Heidelberg: Springer-Verlag
ID: ISSN: 0012-186X
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: cdi_proquest_miscellaneous_70483197
title: Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action
format: Article
creator:
  • Færch, K
  • Vaag, A
  • Holst, J. J
  • Glümer, C
  • Pedersen, O
  • Borch-Johnsen, K
subjects:
  • Article
  • Biological and medical sciences
  • Blood Glucose - metabolism
  • Body Composition
  • Body Weight
  • C-Peptide - blood
  • Dextrose
  • Diabetes Mellitus, Type 2 - prevention & control
  • Diabetes. Impaired glucose tolerance
  • Endocrine pancreas. Apud cells (diseases)
  • Endocrinopathies
  • Etiopathogenesis. Screening. Investigations. Target tissue resistance
  • Fasting
  • Gastric Inhibitory Polypeptide - blood
  • Glucagon
  • Glucagon-Secreting Cells - physiology
  • Glucose
  • Glucose Intolerance - blood
  • Glucose metabolism
  • Glucose Tolerance Test
  • Glucose tolerance tests
  • Human Physiology
  • Humans
  • Incretins - physiology
  • Insulin
  • Insulin - blood
  • Insulin - physiology
  • Insulin resistance
  • Insulin-Secreting Cells - physiology
  • Internal Medicine
  • Medical sciences
  • Medicine
  • Medicine & Public Health
  • Metabolic Diseases
  • Myocardial Ischemia - prevention & control
  • Pancreatic beta cells
  • Peptide hormones
  • Prediabetic state
  • Prediabetic State - blood
  • Prediabetic State - physiopathology
  • Prediabetic State - therapy
  • Prevention
  • Type 2 diabetes
ispartof: Diabetologia, 2008-03-04, Vol.51 (5), p.853-861
description: Aims/hypothesis The impact of strategies for prevention of type 2 diabetes in isolated impaired fasting glycaemia (i-IFG) vs isolated impaired glucose tolerance (i-IGT) may differ depending on the underlying pathophysiology. We examined insulin secretion during OGTTs and IVGTTs, hepatic and peripheral insulin action, and glucagon and incretin hormone secretion in individuals with i-IFG ( n  = 18), i-IGT ( n  = 28) and normal glucose tolerance (NGT, n  = 20). Methods Glucose tolerance status was confirmed by a repeated OGTT, during which circulating insulin, glucagon, glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) levels were measured. A euglycaemic–hyperinsulinaemic clamp with [3– 3 H]glucose preceded by an IVGTT was performed. Results Absolute first-phase insulin secretion during IVGTT was decreased in i-IFG ( p  = 0.026), but not in i-IGT ( p  = 0.892) compared with NGT. Hepatic insulin sensitivity was normal in i-IFG and i-IGT individuals ( p  ≥ 0.179). Individuals with i-IGT had peripheral insulin resistance ( p  = 0.003 vs NGT), and consequently the disposition index (DI; insulin secretion×insulin sensitivity) during IVGTT (DI IVGTT) ) was reduced in both i-IFG and i-IGT ( p  
language: eng
source:
identifier: ISSN: 0012-186X
fulltext: no_fulltext
issn:
  • 0012-186X
  • 1432-0428
url: Link


@attributes
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
RANK2.5162568
LOCALfalse
PrimoNMBib
record
control
sourceidgale_proqu
recordidTN_cdi_proquest_miscellaneous_70483197
sourceformatXML
sourcesystemPC
galeidA177528153
sourcerecordidA177528153
originalsourceidFETCH-LOGICAL-1580t-8e6bde0df993da86ff572cbf37e41128d6689aee43d85aba48927b81529d0880
addsrcrecordideNqNkstu1TAQhiMEoofCA7BBFgh2Kb7k4rCrKi6VKrHpgp018eXUleMcbKdqX4znwyYHChVUKItInu__PZ75q-o5wUcE4_5txJjQtsaY13hoSX39oNqQhtEaN5Q_rDalXBPefTmonsR4iTFmbdM9rg4IZ6Tvabepvp1OO7BBK2QgJuu3aOtuJOjJArqKyP6sbt0i56hRmp0O4KV-h6KdrIOwZybtE5oN2uVi0JCsROB2F4DAKzTqBEhq55BZvEx29mhcElLWGB2y0IJDITvH4mCLQW4FXcxhmn0-LBbWx8XlQ_ghf1o9MuCifrb_H1bnH96fn3yqzz5_PD05PqtJy3Gque5GpbEyw8AU8M6YtqdyNKzXDSGUq67jA2jdMMVbGKHhA-1HTlo6KMw5PqzerLa7MH9ddExisrG8A7yelyh63ORJDn0GX94BL-cl-NyaoITxhnasuL1aoS04Law3cwogi6M4ZpSzjuOW3EvlpbU0t8cydfQXKn8qr07mqRmbz_-w_S_B7zeQVSDDHGPQRuyCnSDcCIJFiZ9Y4ydy_ESJn7jOmhf7MSzjpNWtYp-3DLzeAxAlOFOiZOMvjmLaDpQVrr9zubQJyuZz19bd2wJdlTGb-q0Ot5v4t-g7hRAFag
sourcetypeAggregation Database
isCDItrue
recordtypearticle
pqid213842638
display
typearticle
titleImpaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action
creatorFærch, K ; Vaag, A ; Holst, J. J ; Glümer, C ; Pedersen, O ; Borch-Johnsen, K
creatorcontribFærch, K ; Vaag, A ; Holst, J. J ; Glümer, C ; Pedersen, O ; Borch-Johnsen, K
descriptionAims/hypothesis The impact of strategies for prevention of type 2 diabetes in isolated impaired fasting glycaemia (i-IFG) vs isolated impaired glucose tolerance (i-IGT) may differ depending on the underlying pathophysiology. We examined insulin secretion during OGTTs and IVGTTs, hepatic and peripheral insulin action, and glucagon and incretin hormone secretion in individuals with i-IFG ( n  = 18), i-IGT ( n  = 28) and normal glucose tolerance (NGT, n  = 20). Methods Glucose tolerance status was confirmed by a repeated OGTT, during which circulating insulin, glucagon, glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) levels were measured. A euglycaemic–hyperinsulinaemic clamp with [3– 3 H]glucose preceded by an IVGTT was performed. Results Absolute first-phase insulin secretion during IVGTT was decreased in i-IFG ( p  = 0.026), but not in i-IGT ( p  = 0.892) compared with NGT. Hepatic insulin sensitivity was normal in i-IFG and i-IGT individuals ( p  ≥ 0.179). Individuals with i-IGT had peripheral insulin resistance ( p  = 0.003 vs NGT), and consequently the disposition index (DI; insulin secretion×insulin sensitivity) during IVGTT (DI IVGTT) ) was reduced in both i-IFG and i-IGT ( p  < 0.005 vs NGT). In contrast, the DI during OGTT (DI OGTT ) was decreased only in i-IGT ( p  < 0.001), but not in i-IFG ( p  = 0.143) compared with NGT. Decreased levels of GIP in i-IGT ( p  = 0.045 vs NGT) vs increased levels of GLP-1 in i-IFG ( p  = 0.013 vs NGT) during the OGTT may partially explain these discrepancies. Basal and post-load glucagon levels were significantly increased in both i-IFG and i-IGT individuals ( p  ≤ 0.001 vs NGT). Conclusions/interpretation We propose that differentiated preventive initiatives in prediabetic individuals should be tested, targeting the specific underlying metabolic defects.
identifier
0ISSN: 0012-186X
1EISSN: 1432-0428
2DOI: 10.1007/s00125-008-0951-x
3PMID: 18317726
languageeng
publisherBerlin/Heidelberg: Springer-Verlag
subjectArticle ; Biological and medical sciences ; Blood Glucose - metabolism ; Body Composition ; Body Weight ; C-Peptide - blood ; Dextrose ; Diabetes Mellitus, Type 2 - prevention & control ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fasting ; Gastric Inhibitory Polypeptide - blood ; Glucagon ; Glucagon-Secreting Cells - physiology ; Glucose ; Glucose Intolerance - blood ; Glucose metabolism ; Glucose Tolerance Test ; Glucose tolerance tests ; Human Physiology ; Humans ; Incretins - physiology ; Insulin ; Insulin - blood ; Insulin - physiology ; Insulin resistance ; Insulin-Secreting Cells - physiology ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Myocardial Ischemia - prevention & control ; Pancreatic beta cells ; Peptide hormones ; Prediabetic state ; Prediabetic State - blood ; Prediabetic State - physiopathology ; Prediabetic State - therapy ; Prevention ; Type 2 diabetes
ispartofDiabetologia, 2008-03-04, Vol.51 (5), p.853-861
rights
0Springer-Verlag 2008
12008 INIST-CNRS
2COPYRIGHT 2008 Springer
lds50peer_reviewed
citedbyFETCH-LOGICAL-1580t-8e6bde0df993da86ff572cbf37e41128d6689aee43d85aba48927b81529d0880
citesFETCH-LOGICAL-1580t-8e6bde0df993da86ff572cbf37e41128d6689aee43d85aba48927b81529d0880
links
openurl$$Topenurl_article
thumbnail$$Usyndetics_thumb_exl
backlink
0$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20259236$$DView record in Pascal Francis
1$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18317726$$D View this record in MEDLINE/PubMed
search
creatorcontrib
0Færch, K
1Vaag, A
2Holst, J. J
3Glümer, C
4Pedersen, O
5Borch-Johnsen, K
title
0Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action
1Diabetologia
addtitle
0Diabetologia
1Diabetologia
descriptionAims/hypothesis The impact of strategies for prevention of type 2 diabetes in isolated impaired fasting glycaemia (i-IFG) vs isolated impaired glucose tolerance (i-IGT) may differ depending on the underlying pathophysiology. We examined insulin secretion during OGTTs and IVGTTs, hepatic and peripheral insulin action, and glucagon and incretin hormone secretion in individuals with i-IFG ( n  = 18), i-IGT ( n  = 28) and normal glucose tolerance (NGT, n  = 20). Methods Glucose tolerance status was confirmed by a repeated OGTT, during which circulating insulin, glucagon, glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) levels were measured. A euglycaemic–hyperinsulinaemic clamp with [3– 3 H]glucose preceded by an IVGTT was performed. Results Absolute first-phase insulin secretion during IVGTT was decreased in i-IFG ( p  = 0.026), but not in i-IGT ( p  = 0.892) compared with NGT. Hepatic insulin sensitivity was normal in i-IFG and i-IGT individuals ( p  ≥ 0.179). Individuals with i-IGT had peripheral insulin resistance ( p  = 0.003 vs NGT), and consequently the disposition index (DI; insulin secretion×insulin sensitivity) during IVGTT (DI IVGTT) ) was reduced in both i-IFG and i-IGT ( p  < 0.005 vs NGT). In contrast, the DI during OGTT (DI OGTT ) was decreased only in i-IGT ( p  < 0.001), but not in i-IFG ( p  = 0.143) compared with NGT. Decreased levels of GIP in i-IGT ( p  = 0.045 vs NGT) vs increased levels of GLP-1 in i-IFG ( p  = 0.013 vs NGT) during the OGTT may partially explain these discrepancies. Basal and post-load glucagon levels were significantly increased in both i-IFG and i-IGT individuals ( p  ≤ 0.001 vs NGT). Conclusions/interpretation We propose that differentiated preventive initiatives in prediabetic individuals should be tested, targeting the specific underlying metabolic defects.
subject
0Article
1Biological and medical sciences
2Blood Glucose - metabolism
3Body Composition
4Body Weight
5C-Peptide - blood
6Dextrose
7Diabetes Mellitus, Type 2 - prevention & control
8Diabetes. Impaired glucose tolerance
9Endocrine pancreas. Apud cells (diseases)
10Endocrinopathies
11Etiopathogenesis. Screening. Investigations. Target tissue resistance
12Fasting
13Gastric Inhibitory Polypeptide - blood
14Glucagon
15Glucagon-Secreting Cells - physiology
16Glucose
17Glucose Intolerance - blood
18Glucose metabolism
19Glucose Tolerance Test
20Glucose tolerance tests
21Human Physiology
22Humans
23Incretins - physiology
24Insulin
25Insulin - blood
26Insulin - physiology
27Insulin resistance
28Insulin-Secreting Cells - physiology
29Internal Medicine
30Medical sciences
31Medicine
32Medicine & Public Health
33Metabolic Diseases
34Myocardial Ischemia - prevention & control
35Pancreatic beta cells
36Peptide hormones
37Prediabetic state
38Prediabetic State - blood
39Prediabetic State - physiopathology
40Prediabetic State - therapy
41Prevention
42Type 2 diabetes
issn
00012-186X
11432-0428
fulltextfalse
rsrctypearticle
creationdate2008
recordtypearticle
recordideNqNkstu1TAQhiMEoofCA7BBFgh2Kb7k4rCrKi6VKrHpgp018eXUleMcbKdqX4znwyYHChVUKItInu__PZ75q-o5wUcE4_5txJjQtsaY13hoSX39oNqQhtEaN5Q_rDalXBPefTmonsR4iTFmbdM9rg4IZ6Tvabepvp1OO7BBK2QgJuu3aOtuJOjJArqKyP6sbt0i56hRmp0O4KV-h6KdrIOwZybtE5oN2uVi0JCsROB2F4DAKzTqBEhq55BZvEx29mhcElLWGB2y0IJDITvH4mCLQW4FXcxhmn0-LBbWx8XlQ_ghf1o9MuCifrb_H1bnH96fn3yqzz5_PD05PqtJy3Gque5GpbEyw8AU8M6YtqdyNKzXDSGUq67jA2jdMMVbGKHhA-1HTlo6KMw5PqzerLa7MH9ddExisrG8A7yelyh63ORJDn0GX94BL-cl-NyaoITxhnasuL1aoS04Law3cwogi6M4ZpSzjuOW3EvlpbU0t8cydfQXKn8qr07mqRmbz_-w_S_B7zeQVSDDHGPQRuyCnSDcCIJFiZ9Y4ydy_ESJn7jOmhf7MSzjpNWtYp-3DLzeAxAlOFOiZOMvjmLaDpQVrr9zubQJyuZz19bd2wJdlTGb-q0Ot5v4t-g7hRAFag
startdate20080304
enddate20080304
creator
0Færch, K
1Vaag, A
2Holst, J. J
3Glümer, C
4Pedersen, O
5Borch-Johnsen, K
general
0Springer-Verlag
1Springer
2Springer Nature B.V
scope
0IQODW
1CGR
2CUY
3CVF
4ECM
5EIF
6NPM
7AAYXX
8CITATION
9BSHEE
103V.
117T5
127X7
137XB
1488E
158AO
168C1
178FI
188FJ
198FK
20ABUWG
21BENPR
22FYUFA
23GHDGH
24H94
25K9.
26M0S
27M1P
28PQEST
29PQQKQ
30PQUKI
31PRINS
327X8
sort
creationdate20080304
titleImpaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action
authorFærch, K ; Vaag, A ; Holst, J. J ; Glümer, C ; Pedersen, O ; Borch-Johnsen, K
facets
frbrtype5
frbrgroupidcdi_FETCH-LOGICAL-1580t-8e6bde0df993da86ff572cbf37e41128d6689aee43d85aba48927b81529d0880
rsrctypearticles
prefilterarticles
languageeng
creationdate2008
topic
0Article
1Biological and medical sciences
2Blood Glucose - metabolism
3Body Composition
4Body Weight
5C-Peptide - blood
6Dextrose
7Diabetes Mellitus, Type 2 - prevention & control
8Diabetes. Impaired glucose tolerance
9Endocrine pancreas. Apud cells (diseases)
10Endocrinopathies
11Etiopathogenesis. Screening. Investigations. Target tissue resistance
12Fasting
13Gastric Inhibitory Polypeptide - blood
14Glucagon
15Glucagon-Secreting Cells - physiology
16Glucose
17Glucose Intolerance - blood
18Glucose metabolism
19Glucose Tolerance Test
20Glucose tolerance tests
21Human Physiology
22Humans
23Incretins - physiology
24Insulin
25Insulin - blood
26Insulin - physiology
27Insulin resistance
28Insulin-Secreting Cells - physiology
29Internal Medicine
30Medical sciences
31Medicine
32Medicine & Public Health
33Metabolic Diseases
34Myocardial Ischemia - prevention & control
35Pancreatic beta cells
36Peptide hormones
37Prediabetic state
38Prediabetic State - blood
39Prediabetic State - physiopathology
40Prediabetic State - therapy
41Prevention
42Type 2 diabetes
toplevelpeer_reviewed
creatorcontrib
0Færch, K
1Vaag, A
2Holst, J. J
3Glümer, C
4Pedersen, O
5Borch-Johnsen, K
collection
0Pascal-Francis
1Medline
2MEDLINE
3MEDLINE (Ovid)
4MEDLINE
5MEDLINE
6PubMed
7CrossRef
8Academic OneFile (A&I only)
9ProQuest Central (Corporate)
10Immunology Abstracts
11Health & Medical Collection
12ProQuest Central (purchase pre-March 2016)
13Medical Database (Alumni Edition)
14ProQuest Pharma Collection
15Public Health Database
16Hospital Premium Collection
17Hospital Premium Collection (Alumni Edition)
18ProQuest Central (Alumni) (purchase pre-March 2016)
19ProQuest Central (Alumni Edition)
20ProQuest Central
21Health Research Premium Collection
22Health Research Premium Collection (Alumni)
23AIDS and Cancer Research Abstracts
24ProQuest Health & Medical Complete (Alumni)
25Health & Medical Collection (Alumni Edition)
26Medical Database
27ProQuest One Academic Eastern Edition
28ProQuest One Academic
29ProQuest One Academic UKI Edition
30ProQuest Central China
31MEDLINE - Academic
jtitleDiabetologia
delivery
delcategoryRemote Search Resource
fulltextno_fulltext
addata
au
0Færch, K
1Vaag, A
2Holst, J. J
3Glümer, C
4Pedersen, O
5Borch-Johnsen, K
formatjournal
genrearticle
ristypeJOUR
atitleImpaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action
jtitleDiabetologia
stitleDiabetologia
addtitleDiabetologia
date2008-03-04
risdate2008
volume51
issue5
spage853
epage861
pages853-861
issn0012-186X
eissn1432-0428
abstractAims/hypothesis The impact of strategies for prevention of type 2 diabetes in isolated impaired fasting glycaemia (i-IFG) vs isolated impaired glucose tolerance (i-IGT) may differ depending on the underlying pathophysiology. We examined insulin secretion during OGTTs and IVGTTs, hepatic and peripheral insulin action, and glucagon and incretin hormone secretion in individuals with i-IFG ( n  = 18), i-IGT ( n  = 28) and normal glucose tolerance (NGT, n  = 20). Methods Glucose tolerance status was confirmed by a repeated OGTT, during which circulating insulin, glucagon, glucose-dependent insulinotrophic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) levels were measured. A euglycaemic–hyperinsulinaemic clamp with [3– 3 H]glucose preceded by an IVGTT was performed. Results Absolute first-phase insulin secretion during IVGTT was decreased in i-IFG ( p  = 0.026), but not in i-IGT ( p  = 0.892) compared with NGT. Hepatic insulin sensitivity was normal in i-IFG and i-IGT individuals ( p  ≥ 0.179). Individuals with i-IGT had peripheral insulin resistance ( p  = 0.003 vs NGT), and consequently the disposition index (DI; insulin secretion×insulin sensitivity) during IVGTT (DI IVGTT) ) was reduced in both i-IFG and i-IGT ( p  < 0.005 vs NGT). In contrast, the DI during OGTT (DI OGTT ) was decreased only in i-IGT ( p  < 0.001), but not in i-IFG ( p  = 0.143) compared with NGT. Decreased levels of GIP in i-IGT ( p  = 0.045 vs NGT) vs increased levels of GLP-1 in i-IFG ( p  = 0.013 vs NGT) during the OGTT may partially explain these discrepancies. Basal and post-load glucagon levels were significantly increased in both i-IFG and i-IGT individuals ( p  ≤ 0.001 vs NGT). Conclusions/interpretation We propose that differentiated preventive initiatives in prediabetic individuals should be tested, targeting the specific underlying metabolic defects.
copBerlin/Heidelberg
pubSpringer-Verlag
pmid18317726
doi10.1007/s00125-008-0951-x