Estimation of glucose utilization in a type 2 diabetes mellitus patient on insulin analogs with tumor hypoglycemia induced by IGF-II

Abstract We present a 38-year-old male patient with insulin requiring type 2 diabetes mellitus (DM) who had fasting hypoglycemia caused by a non-pancreatic-islet-cell mesenchymal tumor producing IGF-II. The evaluation was confounded in that there was pre-existing DM being treated with insulin analog...

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Bibliographic Details
Published in:Growth hormone & IGF research 2016-02, Vol.26, p.8-10
Main Authors: Chode, Suresh, Albert, Stewart G, Shoemaker, James D, Green, Aileen L
Format: Article
Language:English
Subjects:
18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan
Adult
Advanced Basic Science
Diabetes Mellitus, Type 2 - drug therapy
Diabetes Mellitus, Type 2 - metabolism
Endocrinology & Metabolism
Glucose - pharmacokinetics
Humans
Hypoglycemia
Hypoglycemia - etiology
Hypoglycemia - metabolism
Hypoglycemic Agents - therapeutic use
IGF-II
Insulin - analogs & derivatives
Insulin-Like Growth Factor II - adverse effects
Insulin-Like Growth Factor II - secretion
Male
NICTH
Non-islet cell tumor hypoglycemia
Retroperitoneal Neoplasms - complications
Retroperitoneal Neoplasms - metabolism
Tumor induced hypoglycemia
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Summary:Abstract We present a 38-year-old male patient with insulin requiring type 2 diabetes mellitus (DM) who had fasting hypoglycemia caused by a non-pancreatic-islet-cell mesenchymal tumor producing IGF-II. The evaluation was confounded in that there was pre-existing DM being treated with insulin analogs. Insulin levels were assessed with an immunoassay with cross reactivity with the insulin analogs. An 18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan localized the 19.7 × 18.0 × 17.8 cm retroperitoneal mass. A 3.25 kg tumor was resected. Post-operatively insulin treatment was resumed and circulating IGF-II levels returned to normal. The maximum standardized uptake values of FDG (SUVmax ) along with a steady state glucose infusion of 17.5 g/h were used to determine the components of glucose utilization due to IGF-II induced muscle glucose uptake (utilization, 62%) whereas the tumor itself was responsible for approximately 22% of measurable glucose uptake. Whereas tumor induced hypoglycemia has been ascribed to preferential glucose utilization by the tumor, the predominant hypoglycemic effect was due to hormonal IGF-II induced total body glucose uptake.
ISSN:1096-6374
1532-2238
DOI:10.1016/j.ghir.2015.11.004