Fulminant type 1 diabetes mellitus observed in insulin receptor substrate 2 deficient mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-06

AUTHORS

T. Arai, H. Hashimoto, K. Kawai, A. Mori, Y. Ohnishi, K. Hioki, M. Ito, M. Saito, Y. Ueyama, M. Ohsugi, R. Suzuki, N. Kubota, T. Yamauchi, K. Tobe, T. Kadowaki, K. Kosaka

ABSTRACT

The objective of this study was to characterise the fulminant type 1 diabetes mellitus (DM) accompanying abrupt hyperglycaemia and ketonuria observed in insulin receptor substrate 2 (IRS2)-deficient mice. IRS2-deficient mice backcrossed onto the original C57BL/6J:Jc1 background (B6J-IRS2−/− mice) for more than 10 generations were used. Eight male IRS2-deficient mice with ketonuria and abrupt increase in plasma glucose concentrations over 25 mmol/l were used as the fulminant type 1 diabetic mice (diabetic mice) and 8 male IRS2-deficient mice (8 weeks old) without glycosuria were used as the control mice. Plasma metabolite, immunoreactive insulin (IRI) and C-peptide concentrations, hepatic energy metabolism related enzyme activities and histopathological change in pancreatic islets were investigated. The diabetic mice showed significantly higher plasma glucose and cholesterol concentrations and lower plasma IRI and C-peptide concentrations than the control mice. In livers of the diabetic mice, glycolytic and malate-aspartate shuttle enzyme activities decreased significantly and gluconeogenic, lipogenic and ketone body synthesis enzyme activities increased significantly compared to those in the control mice. The pancreatic islets of the diabetic mice decreased significantly in size and number of β cells. The diabetic IRS2-deficient mice did not show the islet-related antibodies observed in the diabetic NOD mice in their sera. The characteristics of the diabetic IRS2-deficient mice resembled those of the human nonautoimmune fulminant type 1 DM. IRS2-deficient mice may be a useful animal model for studying the degradation mechanism of pancreatic β cells in the process of development of fulminant type 1 DM. More... »

PAGES

93-99

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10238-008-0163-1

DOI

http://dx.doi.org/10.1007/s10238-008-0163-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1018169586

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18618219


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23 schema:description The objective of this study was to characterise the fulminant type 1 diabetes mellitus (DM) accompanying abrupt hyperglycaemia and ketonuria observed in insulin receptor substrate 2 (IRS2)-deficient mice. IRS2-deficient mice backcrossed onto the original C57BL/6J:Jc1 background (B6J-IRS2−/− mice) for more than 10 generations were used. Eight male IRS2-deficient mice with ketonuria and abrupt increase in plasma glucose concentrations over 25 mmol/l were used as the fulminant type 1 diabetic mice (diabetic mice) and 8 male IRS2-deficient mice (8 weeks old) without glycosuria were used as the control mice. Plasma metabolite, immunoreactive insulin (IRI) and C-peptide concentrations, hepatic energy metabolism related enzyme activities and histopathological change in pancreatic islets were investigated. The diabetic mice showed significantly higher plasma glucose and cholesterol concentrations and lower plasma IRI and C-peptide concentrations than the control mice. In livers of the diabetic mice, glycolytic and malate-aspartate shuttle enzyme activities decreased significantly and gluconeogenic, lipogenic and ketone body synthesis enzyme activities increased significantly compared to those in the control mice. The pancreatic islets of the diabetic mice decreased significantly in size and number of β cells. The diabetic IRS2-deficient mice did not show the islet-related antibodies observed in the diabetic NOD mice in their sera. The characteristics of the diabetic IRS2-deficient mice resembled those of the human nonautoimmune fulminant type 1 DM. IRS2-deficient mice may be a useful animal model for studying the degradation mechanism of pancreatic β cells in the process of development of fulminant type 1 DM.
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31 C57BL/6J
32 Insulin receptor substrate-2-deficient (IRS2(-/-)) mice
33 Irs2-deficient mice
34 NOD mice
35 abrupt increase
36 activity
37 animal models
38 antibodies
39 background
40 cells
41 changes
42 characteristics
43 cholesterol concentrations
44 concentration
45 control mice
46 deficient mice
47 degradation mechanism
48 development
49 diabetes mellitus
50 diabetic NOD mice
51 diabetic mice
52 energy metabolism
53 enzyme activity
54 fulminant type 1 diabetes mellitus
55 generation
56 glucose
57 glucose concentration
58 glycosuria
59 hepatic energy metabolism
60 higher plasma glucose
61 histopathological changes
62 hyperglycaemia
63 immunoreactive insulin
64 increase
65 insulin
66 insulin receptor substrate 2
67 islets
68 ketonuria
69 liver
70 mechanism
71 mellitus
72 metabolism
73 metabolites
74 mice
75 model
76 number
77 objective
78 pancreatic islets
79 pancreatic β-cells
80 plasma glucose
81 plasma glucose concentration
82 plasma immunoreactive insulin
83 plasma metabolites
84 process
85 process of development
86 serum
87 size
88 study
89 substrate 2
90 type 1 diabetes mellitus
91 type 1 diabetic mice
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93 β-cells
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