Lina Carlbom1, Daniel Espes2,3, Mark Lubberink1, Olof Eriksson4, Lars Johansson1, Leif Jansson2, Olle Korsgren5, Håkan Ahlström1, Per-Ola Carlsson6,7. 1. Department of Surgical Sciences, Radiology, Uppsala University, Uppsala, Sweden. 2. Department of Medical Cell Biology, Uppsala University, Husargatan 3, SE-751 23, Uppsala, Sweden. 3. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. 4. Department of Medicinal Chemistry, Preclinical PET Platform, Uppsala University, Uppsala, Sweden. 5. Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. 6. Department of Medical Cell Biology, Uppsala University, Husargatan 3, SE-751 23, Uppsala, Sweden. per-ola.carlsson@mcb.uu.se. 7. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. per-ola.carlsson@mcb.uu.se.
Abstract
AIMS/HYPOTHESIS: The aim of this study was to investigate pancreatic perfusion and its response to a glucose load in patients with type 1 diabetes mellitus compared with non-diabetic ('healthy') individuals. METHODS: Eight individuals with longstanding type 1 diabetes and ten sex-, age- and BMI-matched healthy controls underwent dynamic positron emission tomography scanning with (15)O-labelled water before and after intravenous administration of glucose. Perfusion in the pancreas was measured. Portal and arterial hepatic perfusion were recorded as references. RESULTS: Under fasting conditions, total pancreatic perfusion was on average 23% lower in the individuals with diabetes compared with healthy individuals. Glucose increased total pancreatic and portal hepatic blood perfusion in healthy individuals by 48% and 38%, respectively. In individuals with diabetes there was no significant increase in either total pancreatic or portal hepatic perfusion. CONCLUSIONS/ INTERPRETATION: Individuals with type 1 diabetes have reduced basal pancreatic perfusion and a severely impaired pancreatic and splanchnic perfusion response to intravenous glucose stimulation.
AIMS/HYPOTHESIS: The aim of this study was to investigate pancreatic perfusion and its response to a glucose load in patients with type 1 diabetes mellitus compared with non-diabetic ('healthy') individuals. METHODS: Eight individuals with longstanding type 1 diabetes and ten sex-, age- and BMI-matched healthy controls underwent dynamic positron emission tomography scanning with (15)O-labelled water before and after intravenous administration of glucose. Perfusion in the pancreas was measured. Portal and arterial hepatic perfusion were recorded as references. RESULTS: Under fasting conditions, total pancreatic perfusion was on average 23% lower in the individuals with diabetes compared with healthy individuals. Glucose increased total pancreatic and portal hepatic blood perfusion in healthy individuals by 48% and 38%, respectively. In individuals with diabetes there was no significant increase in either total pancreatic or portal hepatic perfusion. CONCLUSIONS/ INTERPRETATION: Individuals with type 1 diabetes have reduced basal pancreatic perfusion and a severely impaired pancreatic and splanchnic perfusion response to intravenous glucose stimulation.
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