Abstract
Sleep apnea syndrome is characterized by repetitive upper airway collapses during night leading to intermittent hypoxia (IH). The latter is responsible for metabolic disturbances that rely, at least in part, on abdominal white fat inflammation. Besides qualitative alterations, we hypothesized that IH could also modify body fat distribution, a key factor for metabolic complications. C57BL6 mice exposed to IH (21–5% FiO2, 60 s cycle, 8 h/day) or air for 6 weeks were investigated for topographic fat alterations (whole-body MRI). Specific role of epididymal fat in IH-induced metabolic dysfunctions was assessed in lipectomized or sham-operated mice exposed to IH or air. Whereas total white fat volume was unchanged, IH induced epididymal adipose tissue (AT) loss with non-significant increase in subcutaneous and mesenteric fat. This was associated with impaired insulin sensitivity and secretion. Epididymal lipectomy led to increased subcutaneous fat in the perineal compartment and prevented IH-induced metabolic disturbances. IH led to reduced epididymal AT and impaired glucose regulation. This suggests that, rather than epididymal AT volume, qualitative fat alterations (i.e. inflammation) could represent the main determinant of metabolic dysfunction. This deterioration of glucose regulation was prevented in epididymal-lipectomized mice, possibly through prevention of IH-induced epididymal AT alterations and compensatory increase in subcutaneous AT.
Highlights
Obstructive sleep apnea (OSA) is a worldwide public-health problem affecting at least 10% of the middle aged population and representing a main cause of cardiometabolic morbidity and mortality[1]
As we previously observed smaller epididymal fat pads but similar body weight in mice exposed to intermittent hypoxia (IH) compared to normoxic animals[9], we suggest that IH, in addition to structural and inflammatory white adipose tissue (WAT) remodeling, could induce fat redistribution that could participate to cardiometabolic disturbances
The aims of the present study were: (1) to investigate the effects of IH on regional distribution of body fat using magnetic resonance imaging in a non-obese mouse model; (2) to assess whether the IH-related pattern of fat distribution was associated with metabolic alterations; (3) to evaluate whether epididymal lipectomy before IH exposure had a protective role on IH-induced metabolic alterations and influenced the IH-related pattern of fat distribution
Summary
Obstructive sleep apnea (OSA) is a worldwide public-health problem affecting at least 10% of the middle aged population and representing a main cause of cardiometabolic morbidity and mortality[1]. Rather than obesity per se, there are growing evidence that the pattern of fat distribution within the body is a major determinant of the metabolic profile and the severity of complications[6]. As well as alterations of the lipoprotein clearance pathway[12, 13] These WAT alterations contribute to IH-associated cardiovascular complications as epididymal lipectomy before IH exposure partially attenuated IH-induced dyslipidemia and atherogenesis[9]. As we previously observed smaller epididymal fat pads but similar body weight in mice exposed to IH compared to normoxic animals[9], we suggest that IH, in addition to structural and inflammatory WAT remodeling, could induce fat redistribution that could participate to cardiometabolic disturbances. (2) to assess whether the IH-related pattern of fat distribution was associated with metabolic alterations; (3) to evaluate whether epididymal lipectomy before IH exposure had a protective role on IH-induced metabolic alterations and influenced the IH-related pattern of fat distribution
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