Journal
DIABETES
Volume 67, Issue 11, Pages 2389-2396Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db18-0279
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Funding
- Universita Cattolica del Sacro Cuore (Fondi Ateneo Linea D.3.2)
- Ministero dell'Istruzione, dell'Universita e della Ricerca [PRIN 2015373Z39_006]
- European Foundation for the Study of Diabetes (EFSD)/Novo Nordisk
- EFSD/Eli Lilly
- EFSD/AstraZeneca awards
- EFSD award - AstraZeneca
- Fondazione Diabete Ricerca
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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 beta-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 beta-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 beta-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.
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