|
KMID : 0354720070310030208
|
|
Journal of Korean Diabetes Association
2007 Volume.31 No. 3 p.208 ~ p.219
|
|
|
Proliferation and Differentiation of Pancreatic β Cells in L-type Calcium Channel α1D Subunit (Cav1.3) Heterozygous Knock Out Mice After Partial Pancreatectomy
|
|
Choi Yoon-Hee
Yun Il-Hee
Suh Sun-Hee
Lim Dong-Jun
Cho Jae-Hyoung
Kwon Hyeok-Sang
Cha Bong-Yun
Son Ho-Young
Park Chung-Gyu
Yoon Kun-Ho
|
|
|
Abstract
|
|
|
Backgrounds: L-type voltage-dependent calcium channel (LTCC) plays a crucial role in insulin secretion from
pancreatic β cells through Ca2+ influx. In the recent report, LTCC Cav1.3 subtype homozygous knock out mice showed impairment of postnatal pancreatic beta cell development as well as insulin secretion.
Methods: We performed 90% partial pancreatectomy in heterozygous Cav1.3 knock out mice to investigate the effect of partial deficiency of Cav1.3 gene on beta cell regeneration in the adult. Glucose homeostasis, metabolic profiles including serum insulin and lipid levels and morphologic changes of pancreatic islets were studied.
Results: 90% Partial pancreatectomy induced glucose intolerance only in the heterozygous knock out mice
at 8 weeks after surgery. Distribution of islet size was significantly different between two groups after partial pancreatectomy; median value of islet size of heterozygote was larger than that of wild type (642.8 μm2 vs 1459.8 μm2, P < 0.01). The frequency of single beta cell unit, considered as a unit of β cell neogenesis, was much lower in heterozygote than that of wild type (41% vs 23.3%, P < 0.05).
Conclusion: These data suggest that Cav1.3 gene deficiency is specifically associated with impairment of beta
cell regeneration, especially neogensis and eventual glucose intolerance in the 90% partial pancreatectomized mice.
|
|
|
KEYWORD
|
|
|
Beta cell neogenesis, Cav1.3, L-type voltage-dependent calcium channel, LTCC, Partial pancreatectomy
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
 
|