Objectives: 

Obstructive sleep apnoea (OSA) refers to sleep related repetitive episodes of obstruction of upper airways. Blood PO2 decreases in each obstruction. As a whole, OSA causes an intermittent hypoxia (IH) lasting all sleep hours. Frequently, OSA generates cardiovascular, metabolic-liver, and neuropsychiatric pathologies to conform the obstructive sleep apnoea syndrome (OSAS). 60-70% of OSAS patients have body mass indexes (BMI) >25 Kg/m2, with OSAS frecuency paralleling BMI. Commonly, OSAS patients exhibit other alterations conforming the metabolic syndrome (MS). Yet, the cause-effect relationship between OSAS and MS is not known: are obesity and MS causes or effect of OSAS or viceversa? Whatever the intimate loops of the pathogenic mechanisms, our interest has been to clarify the relationships between IH and high fat diet (HFD) to generate or aggravate oxidative, metabolic, and inflammation alterations.

Materials: 

We used male Wistar rats fed for 12 weeks (3-6 months of age) with regular or HFD (10 and 60% fat, respectively). We defined four animal groups: control (C), CIH, O (obese) and OIH. Protocol of IH was: 5% O2, 40s/ 21% O2, 80s, 8h/day, 15 days, from weeks 10-12 of HFD or equivalent age in regular diet animals.

Results: 

Body weights varied with the diet as expected; IH did not modify it. Perirenal and epididymal fat weight doubled in O and OIH groups. Plasma lipid levels (triglycerides and total cholesterol), total liver fat, and glycidic metabolism parameters (basal glycaemia, insulinemia, and HOMA index-equivalent) were also augmented in groups CIH, O and OIH vs. C. Liver lipid peroxides levels were progressively increased and liver SODmit and cyt were progressively diminished in CIH, O and OIH vs. C. In comparison to C, plasma C-reactive protein and liver NFkB were higher in CIH and O, and maximal in OIH.

Conclusions: 

We conclude that indeed HFD and IH seem to interact positively to produce deleterious effects.

Grants: BFU2007-61848, PT2009-0172, JCyL2011 (Sanidad) and CIBERES