Increased β-Cell Workload Modulates Proinsulin-to-Insulin Ratio in Humans
Autor: | Giuseppe Quero, Simona Moffa, Andrea Giaccari, Gian Pio Sorice, Sergio Alfieri, Chiara Maria Assunta Cefalo, Franco Folli, Alfredo Pontecorvi, Pietro Manuel Ferraro, Andrea Mari, Francesca Cinti, Vinsin A. Sun, Teresa Mezza |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
endocrine system medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment 030209 endocrinology & metabolism Type 2 diabetes Insulin secretion proinsulin Hyperproinsulinemia 03 medical and health sciences 0302 clinical medicine Insulin resistance Internal medicine Diabetes mellitus Internal Medicine medicine Hyperinsulinemia Proinsulin business.industry Insulin Settore MED/13 - ENDOCRINOLOGIA Glucose clamp technique medicine.disease 030104 developmental biology Endocrinology business hormones hormone substitutes and hormone antagonists |
Zdroj: | Diabetes. 67:2389-2396 |
ISSN: | 1939-327X 0012-1797 |
DOI: | 10.2337/db18-0279 |
Popis: | Increased proinsulin secretion, which characterizes type 2 diabetes and insulin resistance, may be due to an intrinsic, primitive defect in proinsulin processing or be secondary to increased demand on β-cells (hyperinsulinemia secondary to insulin resistance). An alternative way to investigate the relation between relative hyperproinsulinemia and increased secretory demand is to study the dynamic changes in the proinsulin-to-insulin ratio after partial pancreatectomy, a model of acute increased β-cell workload on the remaining pancreas. To pursue this aim, patients without diabetes, scheduled for partial pancreatectomy, underwent 4-h mixed-meal tests and hyperinsulinemic-euglycemic clamps before and after surgery. After acute β-cell mass reduction, no changes were observed in the fasting proinsulin-to-insulin ratio, whereas the fold change in the proinsulin-to-insulin ratio significantly increased over time after the meal. Further, our data demonstrate that whole-body insulin resistance is associated with underlying defects in proinsulin secretion, which become detectable only in the presence of increased insulin secretion demand. |
Databáze: | OpenAIRE |
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