Intermittent hypoxia in obese Zucker rats: cardiometabolic and inflammatory effects

Obstructive Sleep Apnea (OSA) is associated with obesity with a high prevalence, and both co-morbidities are independent cardiovascular risk factors. Intermittent hypoxia (IH) is thought to be the main factor responsible for the OSA-related cardiometabolic alterations. This study aimed at assessing the respective impact of obesity and IH on the inflammatory and cardiometabolic state in rats. Lean and obese Zucker rats were exposed to normoxia or chronic IH, and metabolic and inflammatory parameters were assessed such as plasma lipids and glucose, serum leptin and adiponectin, liver cytokines, NF-κB activity and cardiac endothelin-1 levels. Myocardial infarct size was also evaluated following in vitro ischemia-reperfusion. Circulating lipids, insulin, HOMA-IR, leptin and adiponectin levels were higher in obese versus lean rats. Chronic IH did not have a significant impact on metabolic parameters in lean rats. In obese rats, IH increased glycaemia and HOMA-IR. Liver IL-6 and TNF-α levels were elevated in lean rats exposed to IH; obesity prevented the increase in IL-6 but not in TNF- α. Finally, IH exposure enhanced myocardial sensitivity to infarction in both lean and obese rats and increased cardiac endothelin-1 in lean but not obese rats. In conclusion, this study shows that the dyslipidemia and insulin resistance induced by obesity of genetic origin does not enhance the deleterious cardiovascular response to IH and may even partially protect against IH-induced inflammation.

This article is protected by copyright. All rights reserved

from Physiology via xlomafota13 on Inoreader http://ift.tt/2c5l1rV
via IFTTT