Insulin Sensitivity and Negative Insulin Feedback after Pancreas Transplantation in Insulin-Dependent Diabetic Patients
العنوان: | Insulin Sensitivity and Negative Insulin Feedback after Pancreas Transplantation in Insulin-Dependent Diabetic Patients |
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المؤلفون: | Tetsuya Babazono, Taro Wasada, Hiroyuki Kuroki, Hiroko Arii, Akiko Saeki, Yasuke Omori, Kaori Aoki |
المصدر: | Endocrine Journal. 42:747-752 |
بيانات النشر: | Japan Endocrine Society, 1995. |
سنة النشر: | 1995 |
مصطلحات موضوعية: | Adult, Blood Glucose, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Feedback, chemistry.chemical_compound, Endocrinology, Insulin resistance, Internal medicine, Diabetes mellitus, Hyperinsulinemia, medicine, Humans, Insulin, C-Peptide, C-peptide, business.industry, medicine.disease, Combined Modality Therapy, Kidney Transplantation, Insulin oscillation, Transplantation, Diabetes Mellitus, Type 1, Basal (medicine), chemistry, Evaluation Studies as Topic, Case-Control Studies, Female, Pancreas Transplantation, business, Immunosuppressive Agents |
الوصف: | The aims of this study were to determine the change in the rate of insulin-stimulated glucose disposal (insulin sensitivity) and the ability of insulin to inhibit its own secretion in four pancreas-kidney transplant recipients with insulin-dependent diabetes mellitus. Insulin sensitivity (glucose infusion rate, GIR) was measured by a euglycemic hyperinsulinemic clamp technique before and 2, 6 and 12 months after transplantation. The GIR values in the four recipients were normalized within 2 months and remained normal for 12 months after transplantation, despite long-term steroid therapy for immunosuppression. Physiological hyperinsulinemia (50-70 microU/ml) suppressed plasma C-peptide, but its nadirs were still higher than the basal levels in normal controls. Taking into account evidence of a minimal increase in the concentration of circulating insulin that inhibits insulin secretion in healthy subjects and evidence of increased insulin secretion in pancreas recipients, the authors speculate that defective feedback inhibition of insulin secretion could contribute, at least in part, to the disproportionate basal hyperinsulinemia in patients with a denervated, transplanted pancreas in the absence of insulin resistance. |
تدمد: | 1348-4540 0918-8959 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8059dc4b936e990c4899a45332fbec45Test https://doi.org/10.1507/endocrj.42.747Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....8059dc4b936e990c4899a45332fbec45 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 13484540 09188959 |
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