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2015 ; 2015
(ä): 626019
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Role of the Insulin-Like Growth Factor Type 1 Receptor in the Pathogenesis of
Diabetic Encephalopathy
#MMPMID26089889
Zhang D
; Jiang S
; Meng H
Int J Endocrinol
2015[]; 2015
(ä): 626019
PMID26089889
show ga
Defective cognitive function is common in patients with diabetes, suggesting that
insulin normally exerts anabolic actions in neuron, namely, diabetic
encephalopathy. However, because insulin can cross-activate the insulin-like
growth factor type 1 receptor (IGF-1R), which also functions in most of tissues,
such as muscle and bone, it has been difficult to establish the direct
(IGF-1-independent) actions of insulin in the pathogenesis of diabetic
encephalopathy. To overcome this problem, we examined insulin signaling and
action in primary PC-12 cells engineered for conditional disruption of the IGF-1
receptor (?IGF-1R). The results showed that the lower glucose metabolism and high
expression of IGF-1R occurred in the brain of the DE rat model. The results also
showed the defect of IGF-1R could significantly improve the ability of glucose
consumption and enhance sensitivity to insulin-induced IR and Akt phosphorylation
in PC12 cells. And meanwhile, IGF-1R allele gene knockout (IGF-1R(neo)) mice
treated with HFD/STZ had better cognitive abilities than those of wild mice.
Those results indicate that insulin exerts direct anabolic actions in neuron-like
cells by activation of its cognate receptor and prove that IGF-1R plays an
important role in the pathogenesis of diabetic encephalopathy.