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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:
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
Publisher: Berlin/Heidelberg: Springer-Verlag
ID: ISSN: 0012-186X
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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


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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.
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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
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0Færch, K
1Vaag, A
2Holst, J. J
3Glümer, C
4Pedersen, O
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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
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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.
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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
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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
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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
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35Pancreatic beta cells
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39Prediabetic State - physiopathology
40Prediabetic State - therapy
41Prevention
42Type 2 diabetes
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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
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date2008-03-04
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volume51
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issn0012-186X
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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