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Increased plasma amylin in type 1 diabetic patients after kidney and pancreas transplantation: A sign of impaired beta-cell function?
Diabetes Care. 2006 May; 29(5):1031-8.DC

Abstract

OBJECTIVE

In response to hyperglycemia, beta-cells release insulin and C-peptide, as well as islet amyloid pancreatic polypeptide, which is involved in glucose homeostasis. After successful pancreas-kidney transplantation (PKT), type 1 diabetic patients may revert to a nondiabetic metabolism without exogenous insulin therapy and re-secrete all beta-cell hormones.

RESEARCH DESIGN AND METHODS

Using mathematical models, we investigated hormone (amylin, insulin, C-peptide) and metabolite (glucose, free fatty acids) kinetics, beta-cell sensitivity to glucose, and oral glucose insulin sensitivity index (OGIS) in 11 nondiabetic type 1 diabetic patients after PKT (BMI 25 +/- 1 kg/m2, 47 +/- 2 years of age, 4 women/7 men, glucocorticoid-free), 6 matching nondiabetic patients after kidney transplantation (25 +/- 1 kg/m2, 50 +/- 5 years, 3 women/3 men, on glucocorticoids), and 9 matching nondiabetic control subjects (24 +/- 1 kg/m2, 47 +/- 2 years, 4 women/5 men) during a 3-h 75-g oral glucose tolerance test (OGTT).

RESULTS

PKT patients had higher fasting amylin (19 +/- 3 vs. control subjects: 7 +/- 1 pmol/l) and insulin (20 +/- 2 vs. control subjects: 10 +/- 1 microU/ml; each P < 0.01) levels. Kidney transplant subjects showed increased OGTT plasma insulin at 90 min and C-peptide levels (each P < 0.05). In PKT patients, plasma glucose from 90 to 150 min was 9-31% higher (P < 0.05 vs. control subjects). Amylin clearance was comparable in all groups. Amylin's plasma concentrations and area under the concentration curve were up to twofold higher in PKT patients during OGTT (P < 0.05). OGIS was not significantly different between groups. beta-Cell sensitivity to glucose was reduced in PKT patients (-64%, P < 0.009). Fasting plasma amylin was inversely associated with beta-cell sensitivity to glucose (r = -0.543, P < 0.004).

CONCLUSIONS

After successful PKT, type 1 diabetic patients with nondiabetic glycemia exhibit increased fasting and post-glucose load plasma amylin, which appears to be linked to impaired beta-cell function. Thus, higher amylin release in proportion to insulin might also reflect impaired beta-cell function in type 1 diabetic patients after PKT.

Authors+Show Affiliations

Ludwig Boltzmann Institute of Metabolic Diseases and Nutrition, Vienna, Austria.marietta.stadler@wienkav.atNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16644633

Citation

Stadler, Marietta, et al. "Increased Plasma Amylin in Type 1 Diabetic Patients After Kidney and Pancreas Transplantation: a Sign of Impaired Beta-cell Function?" Diabetes Care, vol. 29, no. 5, 2006, pp. 1031-8.
Stadler M, Anderwald C, Karer T, et al. Increased plasma amylin in type 1 diabetic patients after kidney and pancreas transplantation: A sign of impaired beta-cell function? Diabetes Care. 2006;29(5):1031-8.
Stadler, M., Anderwald, C., Karer, T., Tura, A., Kästenbauer, T., Auinger, M., Bieglmayer, C., Wagner, O., Kronenberg, F., Nowotny, P., Pacini, G., & Prager, R. (2006). Increased plasma amylin in type 1 diabetic patients after kidney and pancreas transplantation: A sign of impaired beta-cell function? Diabetes Care, 29(5), 1031-8.
Stadler M, et al. Increased Plasma Amylin in Type 1 Diabetic Patients After Kidney and Pancreas Transplantation: a Sign of Impaired Beta-cell Function. Diabetes Care. 2006;29(5):1031-8. PubMed PMID: 16644633.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased plasma amylin in type 1 diabetic patients after kidney and pancreas transplantation: A sign of impaired beta-cell function? AU - Stadler,Marietta, AU - Anderwald,Christian, AU - Karer,Tina, AU - Tura,Andrea, AU - Kästenbauer,Thomas, AU - Auinger,Martin, AU - Bieglmayer,Christian, AU - Wagner,Oswald, AU - Kronenberg,Florian, AU - Nowotny,Peter, AU - Pacini,Giovanni, AU - Prager,Rudolf, PY - 2006/4/29/pubmed PY - 2006/9/26/medline PY - 2006/4/29/entrez SP - 1031 EP - 8 JF - Diabetes care JO - Diabetes Care VL - 29 IS - 5 N2 - OBJECTIVE: In response to hyperglycemia, beta-cells release insulin and C-peptide, as well as islet amyloid pancreatic polypeptide, which is involved in glucose homeostasis. After successful pancreas-kidney transplantation (PKT), type 1 diabetic patients may revert to a nondiabetic metabolism without exogenous insulin therapy and re-secrete all beta-cell hormones. RESEARCH DESIGN AND METHODS: Using mathematical models, we investigated hormone (amylin, insulin, C-peptide) and metabolite (glucose, free fatty acids) kinetics, beta-cell sensitivity to glucose, and oral glucose insulin sensitivity index (OGIS) in 11 nondiabetic type 1 diabetic patients after PKT (BMI 25 +/- 1 kg/m2, 47 +/- 2 years of age, 4 women/7 men, glucocorticoid-free), 6 matching nondiabetic patients after kidney transplantation (25 +/- 1 kg/m2, 50 +/- 5 years, 3 women/3 men, on glucocorticoids), and 9 matching nondiabetic control subjects (24 +/- 1 kg/m2, 47 +/- 2 years, 4 women/5 men) during a 3-h 75-g oral glucose tolerance test (OGTT). RESULTS: PKT patients had higher fasting amylin (19 +/- 3 vs. control subjects: 7 +/- 1 pmol/l) and insulin (20 +/- 2 vs. control subjects: 10 +/- 1 microU/ml; each P < 0.01) levels. Kidney transplant subjects showed increased OGTT plasma insulin at 90 min and C-peptide levels (each P < 0.05). In PKT patients, plasma glucose from 90 to 150 min was 9-31% higher (P < 0.05 vs. control subjects). Amylin clearance was comparable in all groups. Amylin's plasma concentrations and area under the concentration curve were up to twofold higher in PKT patients during OGTT (P < 0.05). OGIS was not significantly different between groups. beta-Cell sensitivity to glucose was reduced in PKT patients (-64%, P < 0.009). Fasting plasma amylin was inversely associated with beta-cell sensitivity to glucose (r = -0.543, P < 0.004). CONCLUSIONS: After successful PKT, type 1 diabetic patients with nondiabetic glycemia exhibit increased fasting and post-glucose load plasma amylin, which appears to be linked to impaired beta-cell function. Thus, higher amylin release in proportion to insulin might also reflect impaired beta-cell function in type 1 diabetic patients after PKT. SN - 0149-5992 UR - https://www.unboundmedicine.com/medline/citation/16644633/Increased_plasma_amylin_in_type_1_diabetic_patients_after_kidney_and_pancreas_transplantation:_A_sign_of_impaired_beta_cell_function L2 - http://care.diabetesjournals.org/cgi/pmidlookup?view=long&amp;pmid=16644633 DB - PRIME DP - Unbound Medicine ER -