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Updated: Feb 5, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
Published on: February 28, 2013
Impaired glucagon secretion in patients with fulminant type 1 diabetes mellitus
Hisako Komada1, Yushi Hirota2, Kazuhiko Sakaguchi1,3
1Division of Diabetes and Endocrinology, Kobe University Graduate School of Medicine, Kobe, 650-0017, Japan.
Purpose:
Fulminant type 1 diabetes mellitus (FT1DM), characterized by rapid and almost complete destruction of pancreatic β-cells, is a newly identified subtype of type 1 diabetes mellitus. Although, the pathophysiology of this condition remains still unclear, histological evidence suggests that not only β-cells but also α-cells of pancreatic islets are reduced in number in FT1DM. However, the ability of glucagon secretion in patients with this condition has remained largely uncharacterized. We therefore examined glucagon secretion in patients with FT1DM and compared that with patients with other types of diabetes mellitus.
Methods:
Fasting glucagon levels as well as glucagon secretion induced by intravenous administration of arginine were measured in hospitalized 83 patients with diabetes mellitus, including 4 with FT1DM, 18 with type 1 diabetes mellitus (T1DM), 40 with type 2 diabetes mellitus (T2DM), 5 with slowly progressive insulin-dependent diabetes mellitus (SPIDDM), and 16 with pancreatic diabetes mellitus (PDM).
Results:
The area under the curve for serum glucagon levels after arginine infusion in FT1DM patients was significantly smaller than that in T1DM, T2DM, or SPIDDM patients but was similar to that in PDM patients. The fasting serum glucagon level of FT1DM patients was lower than that of T1DM or T2DM patients but did not significantly differ from that of SPIDDM or PDM patients.
Conclusions:
These results suggest that glucagon secretion is impaired in patients with FT1DM.
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