Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients
Pfeffer, F. ; Nauck, M. A. ; Benz, S. ; Gwodzinski, A. ; Zink, R. ; Büsing, M. ; Becker, H.-D. ; Hopt, U. T.
Springer
Published 1996
Springer
Published 1996
| ISSN: |
1432-0428
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|---|---|
| Keywords: |
Keywords Pancreas transplantation ; insulin secretion ; pancreatic hormones ; oral glucose tolerance ; glucagon stimulation
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| Source: |
Springer Online Journal Archives 1860-2000
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| Topics: |
Medicine
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| Notes: |
Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468]
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| Type of Medium: |
Electronic Resource
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| URL: |
| _version_ | 1798295381094694914 |
|---|---|
| autor | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| autorsonst | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| book_url | http://dx.doi.org/10.1007/BF00400678 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM199937443 |
| issn | 1432-0428 |
| journal_name | Diabetologia |
| materialart | 1 |
| notes | Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468] |
| package_name | Springer |
| publikationsjahr_anzeige | 1996 |
| publikationsjahr_facette | 1996 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1996 |
| publisher | Springer |
| reference | 39 (1996), S. 462-468 |
| schlagwort | Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation |
| search_space | articles |
| shingle_author_1 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| shingle_author_2 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| shingle_author_3 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| shingle_author_4 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. |
| shingle_catch_all_1 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468] 1432-0428 14320428 Springer |
| shingle_catch_all_2 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468] 1432-0428 14320428 Springer |
| shingle_catch_all_3 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468] 1432-0428 14320428 Springer |
| shingle_catch_all_4 | Pfeffer, F. Nauck, M. A. Benz, S. Gwodzinski, A. Zink, R. Büsing, M. Becker, H.-D. Hopt, U. T. Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Keywords Pancreas transplantation insulin secretion pancreatic hormones oral glucose tolerance glucagon stimulation Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468] 1432-0428 14320428 Springer |
| shingle_title_1 | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| shingle_title_2 | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| shingle_title_3 | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| shingle_title_4 | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:35:18.010Z |
| titel | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| titel_suche | Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM199937443 |