Effects of insulin-like growth factor I on the development of osteoblasts in hyperglycemia

被引:14
作者
Fang, Y
Wang, ZY
Mao, Y
Xin, HT
Ren, GL
Bai, XF
机构
[1] Fourth Mil Med Univ, Coll Stomotol, Dept Prosthodont, Xian 710032, Shan Xi Prov, Peoples R China
[2] Fourth Mil Med Univ, Tang Du Hosp, State Key Lab Discipline, Xian 710038, Shan Xi Prov, Peoples R China
[3] Fourth Mil Med Univ, Tang Du Hosp, Ctr Infect Dis Chinese People Liberat Army, Xian 710038, Shan Xi Prov, Peoples R China
关键词
Glucose; Glucose transporter 1; Insulin-like growth factor I; Osteoblast;
D O I
10.1016/j.diabres.2005.11.010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The delayed wound healing of tooth extraction, the activation of alveolar absorption and the being hindered bone formation around the implants in diabetes are difficult to be solved for dentists. So, the aim of the study was to investigate the influences of hyperglycemia and insulin-like growth factor I (IGF-I) on osteoblasts. Osteoblasts were cultured in different conditions: normal glucose, mimic hyperglycemia, hyperglycemia with IGF-I, hyperglycemia with insulin. The proliferation and mineralization of osteoblasts were observed. As abnormal transport of glucose involved in the development of chronic complications in diabetes. The expression of glucose transporter I (GLUT1) was further evaluated by RT-PCR, immunofluorescence and Western blot in different groups. These results showed that hyperglycemia increased the proliferation and inhibited the mineralization of osteoblasts, while IGF-I seemed to reverse these effects. The levels of GLUT1 mRNA and protein in hyperglycemia were elevated by 51% and 35%, respectively, compared with that in normal glucose, while the levels in hyperglycemia with IGF-I were almost the same as that in normal glucose. In conclusion, the increased expression of GLUT1 may contribute to the delayed mineralization of osteoblasts in hyperglycemia. Also IGF-I may be a new drug for diabetic bone disease through normalizing the expression of GLUT1. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:95 / 97
页数:3
相关论文
共 5 条
[1]   Glucose-induced inhibition of in vitro bone mineralization [J].
Balint, E ;
Szabo, P ;
Marshall, CF ;
Sprague, SM .
BONE, 2001, 28 (01) :21-28
[2]  
Fernandes R, 2004, MOL VIS, V10, P618
[3]   A role for advanced glycation end products in diminished bone healing in type 1 diabetes [J].
Santana, RB ;
Xu, L ;
Chase, HB ;
Amar, S ;
Graves, DT ;
Trackman, PC .
DIABETES, 2003, 52 (06) :1502-1510
[4]   Bone formation is impaired in a model of type 1 diabetes [J].
Thrailkill, KM ;
Liu, LC ;
Wahl, EC ;
Bunn, RC ;
Perrien, DS ;
Cockrell, GE ;
Skinner, RA ;
Hogue, WR ;
Carver, AA ;
Fowlkes, JL ;
Aronson, J ;
Lumpkin, CK .
DIABETES, 2005, 54 (10) :2875-2881
[5]   Evidence for a novel TGF-β1-independent mechanism of fibronectin production in mesangial cells overexpressing glucose transporters [J].
Weigert, C ;
Brodbeck, K ;
Brosius, FC ;
Huber, M ;
Lehmann, R ;
Friess, U ;
Facchin, S ;
Aulwurm, S ;
Häring, HU ;
Schleicher, ED ;
Heilig, CW .
DIABETES, 2003, 52 (02) :527-535