期刊论文详细信息
NEUROSCIENCE LETTERS 卷:445
Pressure pain precedes development of type 2 disease in Zucker rat model of diabetes
Article
Romanovsky, Dmitry1,4  Walker, James C.1  Dobretsov, Maxim1,2,3 
[1] Univ Arkansas Med Sci, Dept Anesthesiol, Little Rock, AR 72205 USA
[2] Univ Arkansas Med Sci, Dept Neurobiol & Dev Sci, Little Rock, AR 72205 USA
[3] Univ Arkansas Med Sci, Dept Physiol & Biophys, Little Rock, AR 72205 USA
[4] Russian Acad Sci, Lab Regulat Brain Neuron Funct, IP Pavlov Physiol Inst, St Petersburg 199034, Russia
关键词: Pre-diabetes;    Hyperglycemia;    Neuropathy;    Pressure pain;    Insulin resistance;   
DOI  :  10.1016/j.neulet.2008.08.087
来源: Elsevier
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【 摘 要 】

Decreased hind limb pressure pain threshold (PPT) is an early indicator of insulinopenia and neuropathy developing in STZ-rat models of type 1 diabetes and pre-diabetes. To test if pain on pressure is also a hallmark of compensated insulin resistance and type 2 diabetes in this work we measured PPT of Zucker lean (ZL), Zucker fatty (ZF) and Zucker fatty diabetic rats (ZDF; 8 animals per group). Using clinically accepted cut-off values for diagnosis of human diabetes and pre-diabetes, at 6th week of age (the study entry), all animals maintained random blood glucose within a normal range (<7.9 mM). Over the following 4 weeks, the random glucose remained normal in lean and ZF rats; it however crossed 11 mM cut-off for the diagnosis of diabetes in all ZDF rats. With no detectable relation to blood glucose levels or changes throughout the study, lean, ZF and ZDF rats maintained respectively highest, intermediate and lowest PPT levels (83 1, 70 1 and 59 I g; mean values for all tests per group). Thus in Zucker rat model, type 2 diabetes-associated impairment of nerve function precedes the development of hyperglycemia. Furthermore, since normoglycemic, but displaying decreased PPT, ZF rats were strongly hyperinsulinemic (plasma insulin concentration 30 +/- 4 ng/mL vs. 2.4 +/- 0.3 ng/mL in lean rats) these data suggest that hyperinsulinemia compensating for glucose metabolism might not restore compromised nerve function. Published by Elsevier Ireland Ltd.

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