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Mechanisms of hyperinsulinaemia in Child’s disease grade B liver cirrhosis investigated in free living conditions

Aims: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. However, whether the hyperinsulinaemia is a consequence of increased pancreatic insulin secretion, decreased hepatic insulin removal, or impaired feedback regulation of insulin secre... Full description

Journal Title: Gut 2002-12, Vol.51 (6), p.870-875
Main Author: Greco, A V
Other Authors: Mingrone, G , Mari, A , Capristo, E , Manco, M , Gasbarrini, G
Format: Electronic Article Electronic Article
Language: English
Subjects:
EHC
FFA
Quelle: Alma/SFX Local Collection
Publisher: London: BMJ Publishing Group Ltd and British Society of Gastroenterology
ID: ISSN: 0017-5749
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title: Mechanisms of hyperinsulinaemia in Child’s disease grade B liver cirrhosis investigated in free living conditions
format: Article
creator:
  • Greco, A V
  • Mingrone, G
  • Mari, A
  • Capristo, E
  • Manco, M
  • Gasbarrini, G
subjects:
  • Abridged Index Medicus
  • Biological and medical sciences
  • Biomarkers - analysis
  • Blood Glucose - analysis
  • C peptide deconvolution
  • C-Peptide - analysis
  • Case-Control Studies
  • Causes of
  • EHC
  • euglycaemic hyperinsulinaemic clamp
  • Female
  • FFA
  • free fatty acid
  • Gastroenterology. Liver. Pancreas. Abdomen
  • Glucose
  • Humans
  • Hyperglycemia
  • Hyperinsulinism - blood
  • Hyperinsulinism - etiology
  • Hyperinsulinism - physiopathology
  • Insulin - metabolism
  • insulin clearance
  • Insulin Resistance
  • Insulin Secretion
  • insulin sensitivity
  • ISI insulin sensitivity index
  • Islets of Langerhans - metabolism
  • Liver - metabolism
  • Liver cirrhosis
  • Liver Cirrhosis - blood
  • Liver Cirrhosis - complications
  • Liver Cirrhosis - physiopathology
  • Liver Disease
  • Liver. Biliary tract. Portal circulation. Exocrine pancreas
  • Male
  • mathematical model
  • Medical sciences
  • Metabolic diseases
  • Middle Aged
  • Models, Biological
  • Monitoring, Physiologic
  • Other diseases. Semiology
  • Physiological aspects
  • Regression Analysis
  • Statistics, Nonparametric
ispartof: Gut, 2002-12, Vol.51 (6), p.870-875
description: Aims: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. However, whether the hyperinsulinaemia is a consequence of increased pancreatic insulin secretion, decreased hepatic insulin removal, or impaired feedback regulation of insulin secretion is still doubtful. To investigate these issues, insulin secretion—during 24 hours of standardised living conditions—insulin sensitivity, and hepatic insulin extraction were assessed in cirrhotic patients compared with matched healthy subjects. Patients: Nine Child’s disease grade B cirrhotic patients and seven healthy volunteers, participated in the study. The subjects were studied on two separate days, one for the assessment of insulin secretion during a standardised 24 hour life period (calorimetric chamber), and one for the determination of insulin sensitivity. Methods: Insulin secretion rates were reconstructed from plasma C peptide concentrations by deconvolution, and indices of β cell function were derived using a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations. Insulin sensitivity was determined using the euglycaemic hyperinsulinaemic clamp technique. Results: Cirrhotic patients showed a marked hypersecretory response, both in absolute terms (mean (SEM) 295 (53) versus 138 (11) nmol/m2, p
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0017-5749
fulltext: fulltext
issn:
  • 0017-5749
  • 1468-3288
url: Link


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titleMechanisms of hyperinsulinaemia in Child’s disease grade B liver cirrhosis investigated in free living conditions
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creatorGreco, A V ; Mingrone, G ; Mari, A ; Capristo, E ; Manco, M ; Gasbarrini, G
creatorcontribGreco, A V ; Mingrone, G ; Mari, A ; Capristo, E ; Manco, M ; Gasbarrini, G
descriptionAims: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. However, whether the hyperinsulinaemia is a consequence of increased pancreatic insulin secretion, decreased hepatic insulin removal, or impaired feedback regulation of insulin secretion is still doubtful. To investigate these issues, insulin secretion—during 24 hours of standardised living conditions—insulin sensitivity, and hepatic insulin extraction were assessed in cirrhotic patients compared with matched healthy subjects. Patients: Nine Child’s disease grade B cirrhotic patients and seven healthy volunteers, participated in the study. The subjects were studied on two separate days, one for the assessment of insulin secretion during a standardised 24 hour life period (calorimetric chamber), and one for the determination of insulin sensitivity. Methods: Insulin secretion rates were reconstructed from plasma C peptide concentrations by deconvolution, and indices of β cell function were derived using a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations. Insulin sensitivity was determined using the euglycaemic hyperinsulinaemic clamp technique. Results: Cirrhotic patients showed a marked hypersecretory response, both in absolute terms (mean (SEM) 295 (53) versus 138 (11) nmol/m2, p<0.02), and in relation to glucose (175 (26) versus 57 (5) pmol/min/m2, p<0.02). In particular, the β cell dose-response function was shifted upward compared with controls. The sensitivity of insulin secretion to the rate of glucose change was also increased. Insulin sensitivity, markedly reduced in cirrhosis (157 (10) versus 296 (30) ml/min/m2, p<0.002), was strongly inversely correlated (r=0.89, p<0.002) in these patients with insulin secretion at 5 mM glucose. Insulin clearance and hepatic insulin extraction were not reduced. A frank hypermetabolism with increased lipid oxidation was found in this series. Conclusions: This study suggests that hyperinsulinaemia, at least in Child’s disease grade B cirrhotic patients, is the consequence of increased β cell sensitivity to glucose, while hepatic insulin extraction does not seem to play a significant part.
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publisherLondon: BMJ Publishing Group Ltd and British Society of Gastroenterology
subjectAbridged Index Medicus ; Biological and medical sciences ; Biomarkers - analysis ; Blood Glucose - analysis ; C peptide deconvolution ; C-Peptide - analysis ; Case-Control Studies ; Causes of ; EHC ; euglycaemic hyperinsulinaemic clamp ; Female ; FFA ; free fatty acid ; Gastroenterology. Liver. Pancreas. Abdomen ; Glucose ; Humans ; Hyperglycemia ; Hyperinsulinism - blood ; Hyperinsulinism - etiology ; Hyperinsulinism - physiopathology ; Insulin - metabolism ; insulin clearance ; Insulin Resistance ; Insulin Secretion ; insulin sensitivity ; ISI insulin sensitivity index ; Islets of Langerhans - metabolism ; Liver - metabolism ; Liver cirrhosis ; Liver Cirrhosis - blood ; Liver Cirrhosis - complications ; Liver Cirrhosis - physiopathology ; Liver Disease ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; mathematical model ; Medical sciences ; Metabolic diseases ; Middle Aged ; Models, Biological ; Monitoring, Physiologic ; Other diseases. Semiology ; Physiological aspects ; Regression Analysis ; Statistics, Nonparametric
ispartofGut, 2002-12, Vol.51 (6), p.870-875
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2Mari, A
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descriptionAims: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. However, whether the hyperinsulinaemia is a consequence of increased pancreatic insulin secretion, decreased hepatic insulin removal, or impaired feedback regulation of insulin secretion is still doubtful. To investigate these issues, insulin secretion—during 24 hours of standardised living conditions—insulin sensitivity, and hepatic insulin extraction were assessed in cirrhotic patients compared with matched healthy subjects. Patients: Nine Child’s disease grade B cirrhotic patients and seven healthy volunteers, participated in the study. The subjects were studied on two separate days, one for the assessment of insulin secretion during a standardised 24 hour life period (calorimetric chamber), and one for the determination of insulin sensitivity. Methods: Insulin secretion rates were reconstructed from plasma C peptide concentrations by deconvolution, and indices of β cell function were derived using a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations. Insulin sensitivity was determined using the euglycaemic hyperinsulinaemic clamp technique. Results: Cirrhotic patients showed a marked hypersecretory response, both in absolute terms (mean (SEM) 295 (53) versus 138 (11) nmol/m2, p<0.02), and in relation to glucose (175 (26) versus 57 (5) pmol/min/m2, p<0.02). In particular, the β cell dose-response function was shifted upward compared with controls. The sensitivity of insulin secretion to the rate of glucose change was also increased. Insulin sensitivity, markedly reduced in cirrhosis (157 (10) versus 296 (30) ml/min/m2, p<0.002), was strongly inversely correlated (r=0.89, p<0.002) in these patients with insulin secretion at 5 mM glucose. Insulin clearance and hepatic insulin extraction were not reduced. A frank hypermetabolism with increased lipid oxidation was found in this series. Conclusions: This study suggests that hyperinsulinaemia, at least in Child’s disease grade B cirrhotic patients, is the consequence of increased β cell sensitivity to glucose, while hepatic insulin extraction does not seem to play a significant part.
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0Abridged Index Medicus
1Biological and medical sciences
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3Blood Glucose - analysis
4C peptide deconvolution
5C-Peptide - analysis
6Case-Control Studies
7Causes of
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15Humans
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17Hyperinsulinism - blood
18Hyperinsulinism - etiology
19Hyperinsulinism - physiopathology
20Insulin - metabolism
21insulin clearance
22Insulin Resistance
23Insulin Secretion
24insulin sensitivity
25ISI insulin sensitivity index
26Islets of Langerhans - metabolism
27Liver - metabolism
28Liver cirrhosis
29Liver Cirrhosis - blood
30Liver Cirrhosis - complications
31Liver Cirrhosis - physiopathology
32Liver Disease
33Liver. Biliary tract. Portal circulation. Exocrine pancreas
34Male
35mathematical model
36Medical sciences
37Metabolic diseases
38Middle Aged
39Models, Biological
40Monitoring, Physiologic
41Other diseases. Semiology
42Physiological aspects
43Regression Analysis
44Statistics, Nonparametric
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authorGreco, A V ; Mingrone, G ; Mari, A ; Capristo, E ; Manco, M ; Gasbarrini, G
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1Biological and medical sciences
2Biomarkers - analysis
3Blood Glucose - analysis
4C peptide deconvolution
5C-Peptide - analysis
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7Causes of
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1Mingrone, G
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3Capristo, E
4Manco, M
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atitleMechanisms of hyperinsulinaemia in Child’s disease grade B liver cirrhosis investigated in free living conditions
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0Correspondence to:
 Dr A V Greco, Istituto di Medicina Interna, Università Cattolica S Cuore, Largo A Gemelli 8, 00168 Rome, Italy;
 agreco@rm.unicatt.it
1Correspondence to: …Dr A V Greco, Istituto di Medicina Interna, Università Cattolica S Cuore, Largo A Gemelli 8, 00168 Rome, Italy; …agreco@rm.unicatt.it
abstractAims: Human liver cirrhosis is commonly associated with increased fasting and glucose induced insulin concentrations. However, whether the hyperinsulinaemia is a consequence of increased pancreatic insulin secretion, decreased hepatic insulin removal, or impaired feedback regulation of insulin secretion is still doubtful. To investigate these issues, insulin secretion—during 24 hours of standardised living conditions—insulin sensitivity, and hepatic insulin extraction were assessed in cirrhotic patients compared with matched healthy subjects. Patients: Nine Child’s disease grade B cirrhotic patients and seven healthy volunteers, participated in the study. The subjects were studied on two separate days, one for the assessment of insulin secretion during a standardised 24 hour life period (calorimetric chamber), and one for the determination of insulin sensitivity. Methods: Insulin secretion rates were reconstructed from plasma C peptide concentrations by deconvolution, and indices of β cell function were derived using a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations. Insulin sensitivity was determined using the euglycaemic hyperinsulinaemic clamp technique. Results: Cirrhotic patients showed a marked hypersecretory response, both in absolute terms (mean (SEM) 295 (53) versus 138 (11) nmol/m2, p<0.02), and in relation to glucose (175 (26) versus 57 (5) pmol/min/m2, p<0.02). In particular, the β cell dose-response function was shifted upward compared with controls. The sensitivity of insulin secretion to the rate of glucose change was also increased. Insulin sensitivity, markedly reduced in cirrhosis (157 (10) versus 296 (30) ml/min/m2, p<0.002), was strongly inversely correlated (r=0.89, p<0.002) in these patients with insulin secretion at 5 mM glucose. Insulin clearance and hepatic insulin extraction were not reduced. A frank hypermetabolism with increased lipid oxidation was found in this series. Conclusions: This study suggests that hyperinsulinaemia, at least in Child’s disease grade B cirrhotic patients, is the consequence of increased β cell sensitivity to glucose, while hepatic insulin extraction does not seem to play a significant part.
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pmid12427792
doi10.1136/gut.51.6.870
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