Impaired glucose homeostasis after a transient intermittent hypoxic exposure in neonatal rats

被引:17
|
作者
Pae, Eung-Kwon [1 ]
Ahuja, Bhoomika [1 ]
Kim, Marieyerie [1 ,2 ]
Kim, Gyuyoup [3 ]
机构
[1] Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90095 USA
[2] Univ Calif San Francisco, Sch Dent, San Francisco, CA 94143 USA
[3] Univ Maryland, Sch Dent, Dept Orthodont & Pediat Dent, Baltimore, MD 21201 USA
关键词
Intermittent hypoxia; Diabetes; Neonatal model; Pancreatic beta cells; BETA-CELL FUNCTION; MOUSE MODEL; TYPE-1; EPIGENETICS; MECHANISMS; CYTOKINES; OBESITY; ISLETS; MASS;
D O I
10.1016/j.bbrc.2013.10.102
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This initial report presents a neonatal rat model with exposure to a transient intermittent hypoxia (IH), which results in a persisting diabetes-like condition in the young rats. Twenty-five male pups were treated at postnatal day 1 with IH exposure by alternating the level of oxygen between 10.3% and 20.8% for 5 h. The treated animals were then maintained in normal ambient oxygen condition for 3 week and compared to age-matched controls. The IH treated animals exhibited a significantly higher fasting glucose level than the control animals (237.00 +/- 19.66 mg/dL vs. 167.25 +/- 2.95 mg/dL; P=0.003); and a significantly lower insulin level than the control (807.0 +/- 72.5 pg/mL vs. 1839.8 +/- 377.6 pg/mL; P=0.023). There was no difference in the mass or the number of insulin producing beta cells as well as no indicative of inflammatory changes; however, glucose tolerance tests showed a significantly disturbed glucose homeostasis. In addition, the amount of C-peptide secreted from the islets harvested from the IH animals were decreased significantly (from 914 pM in control to 809 pM in IH; P=0.0006) as well. These observations demonstrate that the neonatal exposure to the IH regimen initiates the development of deregulation in glucose homeostasis without infiltration of inflammatory cells. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:637 / 642
页数:6
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