Body Fat Distribution, Serum Leptin, And Insulin Resistance In Obese Subjects With Obstructive Sleep Apnoea.

ZA, Hassan; MF, Attia; AH, Ahmed; HA, Hassan; H, Amer

doi:10.21608/ejhm.2006.18038

Body Fat Distribution, Serum Leptin, And Insulin Resistance In Obese Subjects With Obstructive Sleep Apnoea.

Document Type : Original Article

Authors

¹ Endocrinology Department Alazhar university (boys)

² Departments, Alazhar University (girls), ENT Department Alazhar university (boys)

³ General Medicine Department Alazhar university (boys)

⁴ Clinical pathology Department Ain Shams University.

10.21608/ejhm.2006.18038

Abstract

Obstructive sleep apnoea (OSِA) is strongly associated with obesity and is characterized by endocrine and metabolic changes.
The aim of the present study is to clarify whether there is interrelationship between body fat, serum leptin, glucose-insulin metabolism and OSA.
Subjects and measurements: we studied 23 obese subjects with OSA (13 males,& 10 females; age mean 36 ± 4.4 years; BMI: 31.7 ± 3.6 kg/m2; WHR: 1.2 ± .25 in males and 0.81+.5 in females ;Apnoea Index “AI”( 9.2 ±6.1) event/hour of sleep by means of overnight polysomnography; fasting glucose(109.8 ± 21.4 mg/dL) ; fasting insulin(18.6 ± 7.1 uU/L ); IR(6.7 ± 2.8); fasting leptin(577.69 ± 201.6 ng/ml). Results were compared with those of 10 healthy normal weight subjects(6 males,4 females ;age mean 36.8±4.4 years; BMI: 25 ± 0.24 kg/m2; WHR: 0.86 ± 0.01; AI: 2.1 ± 1.1 event/hour; fasting glucose(71.7 ± 2.8 mg /dL ); fasting insulin(15.3 ± .48 uU/L ); IR(4.6 ± .17); fasting leptin (42.4 ± 11.5 ng/ml).
Results: Anthropometric measurements of OSA subjects were highly significantly greater than controls; body weight (P<0.003); BMI (P<0.00); waist (P<0.000); and WHR (P<0.000). Fasting glucose levels; fasting plasma insulin; IR and leptin levels were significantly higher in OSA subjects than controls (P<0.000, 0.03, 0.002; & 0.000 ) respectively. Overnight polysomnography revealed significant difference between OSA subjects and controls as regards AI (P<0.001).
The major dependent outcome variable was the apnoea index (AI), “the average number of apnoeas per hour of sleep determined by overnight polysomnography”. OSA was defined as AI ≥ 5. Highly significant correlation between AI and WHR (P<0.00); Fasting insulin (P<0.04); IR (P<001) and Leptin (P<0.000) were detected. Also leptin concentrations correlated with fasting insulin (P<0.02); IR (P<0.00) and WHR (P<0.000) besides the AI.
IN CONCLUSION: There is strong bidirectional, feed-forward pernicious correlation detected between OSA in one side and each of visceral obesity, leptin, and IR; also between leptin, obesity, and IR. This association may contribute to the pathological manifestations and somatic sequale of this condition.
Leptin could have major role linking OSA with various metabolic abnormalities detected in obese subjects.
High circulating leptin found in this study, suggests that both obesity and OSA may be caused by a leptin resistant state.
Among obese subjects, it is visceral fat (WHR), rather than generalized obesity (BMI) that predisposes to OSA.