ECE2015 Eposter Presentations Obesity and cardiovascular endocrinology (108 abstracts)
1Endocrinology Laboratory, Organisms Biology and Physiology Department, FSB, USTHB, Algies, Algeria; 2Departement of Endocrinology, EPH Bologine Ibn Ziri, Algies, Algeria; 3Bioenergitic and Intermediate Metabolism Laboratory, FSB USTHB, Algies, Algeria.
Introduction: The frequency of obesity is increasing in Algeria, insulin resistance is one of the consequences pathological of the abdominal obesity. The purpose of this work is to study the implication of the abdominal obesity in the insulinorésistance and the complications which arise by the latter.
Materials and methods: The study is realised on 105 obese (85 women and 20 men) (BMI >30) and 55 thin (40 women and 15 men) with mean age 37.60±1.18 and 31.03±1.73 years respectively. Glycaemia, lipidaemia, cortisol, insulin and the leptin are analysed. The resistance and the sensibility in the insulin are estimated by the index HOMA-R and QUIKI. The obesity android was held in the criteria of the US NCEP ATP III Defines by a WHR ≥0.85 for women and WHR ≥1.00 for men.
Results: 92% sick suffer from an obesity android associated with critical insulin resistance (HOMA-IR: HOMAR-R: 12.88±1.03 vs 5.17±0.86 P<0.001.QUIKI: 0.29±0.002 vs 0.31±0.002; P<0.001). Plasma cortisol and leptin were higher in obese group by 16% (P<0.05) and 75% (P<0.001) respectively, compared to control group. According to US NCEP ATP III 52 obese (50%) show lipid disturbances associated to dyslipidaemia and metabolic syndrome. Our results show a negative correlation between QUIKI and TT (r=−0.29 P=0.02).
Conclusion: Abdominal obesity associated with metabolic disorders have led to a metabolic syndrome according to US NCEP-ATP III and a physiological stress which stimulated the secretion of cortisol. Despite the significant increase of leptin, known to inhibit adrenal axis. These data suggest that leptin resistance is developed in obese subjects.