Sleep Disorders: Sleep Disorders: Effects of Intermittent Hypoxia |

Chronic Intermittent Hypoxia Impairs Glucose Homeostasis and Activates Endoplasmic Reticulum Stress Signaling/c-Jun N-Terminal Kinase Pathway in C57BL6/J Mice FREE TO VIEW

Juan Du, MD; Chenjuan Gu; Min Li; Qing Yun Li
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Shanghai Ruijin Hospital, Medical School of Shanghai Jiao Tong University, Shanghai, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A558. doi:10.1016/j.chest.2016.02.583
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SESSION TITLE: Sleep Disorders: Effects of Intermittent Hypoxia

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Sunday, April 17, 2016 at 04:00 PM - 05:00 PM

PURPOSE: The aim of this study was to explore the effect of chronic intermittent hypoxia (CIH) on glucose metabolism, as well as Akt (protein kinase B kinase, one important kinase in insulin signaling) and markers of endoplasmic reticulum (ER) stress/ JNK in insulin target organs.

METHODS: After acclimating to the environment for one week, thirty SPF male wild C57BL/6J mice were divided into CIH group (n=15) and CIA group (n=15) at random. CIH-exposed mice were kept in customized chambers with varying oxygen (5-21%) for 8 hours every day. Control animals were kept in the same chambers with alternating periods of room air. After 7 weeks’ exposure, IPGTT and insulin of three points during it were conducted. The levels of insulin was measured by enzyme-linked immune-sorbent assay (ELISA) and the insulin resistance index (homeostasis model of assessment for insulin resistance index, HOMA-IR) was calculated. The protein expression of activated Akt and markers of ER stress/JNK in liver and adipose were measured by western blot.

RESULTS: After exposed to CIH or CIA for 7 weeks, fasting blood glucose, fasting serum insulin and HOMA-IR were increased in the CIH group compared with the controls, while glucose tolerance was decreased. Moreover, the expression of phosphorylated Akt was decreased and phosphorylated PERK and eIF2α of liver and adipose were higher in CIH group than that in CIA group. CIH also induced augmentation of the phosphorylation of JNK and p-c-Jun in liver and adipose.

CONCLUSIONS: CIH induces insulin resistance and glucose intolerance. Insulin signaling pathway is disturbed and ER stress/JNK pathway is activated, which may be implicated in the impaired glucose homeostasis.

CLINICAL IMPLICATIONS: This finding adds an intriguing new concept to the assembly of mechanisms proposed to link OSA to glucose metabolic impairment.

DISCLOSURE: The following authors have nothing to disclose: Juan Du, Chenjuan Gu, Min Li, Qing Yun Li

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