Abstract
Fulminant type 1 diabetes mellitus (FT1DM) is a subtype of type 1 diabetes mellitus and is characterized by a remarkably abrupt onset and almost complete destruction of β-cells within a few days. Here, we report a case of diabetic ketoacidosis in a 63-year-old man with no history of hyperglycemia. The patient was diagnosed with FT1DM and had almost no insulin secretion. We examined his insulin and glucagon secretions induced by a liquid meal test at the onset of FT1DM and 1 year later. The results suggested severely attenuated insulin secretion and an undetectable level of serum insulin 1 year after onset. In contrast, glucagon secretion, which was highly impaired at onset, increased in response to food intake. Although previous reports have suggested that both β- and α-cells of pancreatic islets are damaged in patients with FT1DM, the number of α-cells may increase over time after the onset of FT1DM.
Similar content being viewed by others
References
Imagawa A, Hanafusa T, Uchigata Y, Kanatsuka A, Kawasaki E, et al. Fulminant type 1 diabetes: a nationwide survey in Japan. Diabetes Care. 2003;26:2345–52.
Sayama K, Imagawa A, Okita K, Uno S, Moriwaki M, et al. Pancreatic beta and alpha cells are both decreased in patients with fulminant type 1 diabetes: a morphometrical assessment. Diabetologia. 2005;48:1560–4.
Shibasaki S, Imagawa A, Tauriainen S, Iino M, Oikarinen M, et al. Expression of toll-like receptors in the pancreas of recent-onset fulminant type 1 diabetes. Endocr J. 2010;57:211–9.
American Diabetes Association. Glycemic targets: standards of medical care in diabetes-2021. Diabetes Care. 2021;44(Suppl 1):S73–84.
Shibasaki S, Imagawa A, Terasaki J, Hanafusa T. Endogenous insulin secretion even at a very low level contributes to the stability of blood glucose control in fulminant type 1 diabetes. J Diabetes Investig. 2010;1:283–5.
Komada H, Hirota Y, Sakaguchi K, Okuno Y, Ogawa W, et al. Impaired glucagon secretion in patients with fulminant type 1 diabetes mellitus. Endocrine. 2019;63:476–9.
Lee Y, Wang MY, Du XQ, Charron MJ, Unger RH. Glucagon receptor knockout prevents insulin-deficient type 1 diabetes in mice. Diabetes. 2011;60:391–7.
Hayashi Y, Yamamoto M, Mizoguchi H, Watanabe C, Ito R, et al. Mice deficient for glucagon gene-derived peptides display normoglycemia and hyperplasia of islet α-cells but not of intestinal L-cells. Mol Endocrinol. 2009;23:1990–9.
Kawamori D, Katakami N, Takahara M, Miyashita K, Sakamoto F, et al. Dysregulated plasma glucagon levels in Japanese young adult type 1 diabetes patients. J Diabetes Investig. 2019;10:62–6.
Kawamori D, Katakami N, Takahara M, Miyashita K, Takebe S, et al. Consistency of plasma glucagon levels in patients with type 1 diabetes after a 1-year period. J Diabetes Investig. 2020;11:337–40.
Longuet C, Robledo AM, Dean ED, Dai C, Ali S, et al. Liver-specific disruption of the murine glucagon receptor produces α-cell hyperplasia: evidence for a circulating α-cell growth factor. Diabetes. 2013;62:1196–205.
Cigliola V, Thorel F, Chera S, Herrera PL. Stress-induced adaptive islet cell identity changes. Diabetes Obes Metab. 2016;18(Suppl1):87–96.
Chung CH, Hao E, Piran R, Keinan E, Levine F. Pancreatic β-cell neogenesis by direct conversion from mature α-cells. Stem Cells. 2010;28:1630–8.
Talchai C, Xuan S, Lin HV, Sussel L, Accili D. Pancreatic β cell dedifferentiation as a mechanism of diabetic β cell failure. Cell. 2012;150:1223–34.
Ishida E, Kim-Muller JY, Accili D. Pair feeding, but not insulin, phloridzin, or rosiglitazone treatment, curtails markers of β-cell dedifferentiation in db/db mice. Diabetes. 2017;66:2092–101.
Takahashi N, Chujo D, Tsujimoto T, Kajio H. Short-term changes in pancreatic α-cell function after the onset of fulminant type 1 diabetes. J Diabetes Investig. 2018;9:636–7.
Acknowledgements
This work was carried out in cooperation with the Clinical Examination Unit, Hiroshima City Asa Citizens Hospital.
Author information
Authors and Affiliations
Contributions
NH and TM analyzed and interpreted patient data. NH performed data collection and wrote the manuscript with support from TM and MY. All authors have commented on previous versions of the manuscript. All authors have read and approved the final manuscript.
Corresponding author
Ethics declarations
Conflict of interest
Author Himeno, Matsuda, and Yoneda declare that they have no conflicts of interest.
Human rights statement
All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1964 and its later versions.
Informed consent
Informed consent was obtained from the patient for this case report.
Additional information
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
About this article
Cite this article
Himeno, N., Matsuda, T. & Yoneda, M. Changes in glucagon secretion induced by food intake in fulminant type 1 diabetes mellitus: a case report. Diabetol Int 13, 304–308 (2022). https://doi.org/10.1007/s13340-021-00527-0
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s13340-021-00527-0