Article: article from journal or magazin.
The alpha2B adrenergic receptor deletion/insertion polymorphism in morbid obesity.
Clinical Autonomic Research
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
The sympathetic nervous system participates in the regulation of the basal metabolic rate (BMR) and in the manifestation of the obesity-related metabolic syndrome. A deletion/insertion germline polymorphism of the alpha(2B) adrenergic receptor that is associated with reduced agonist-promoted desensitization has been linked to low BMR in obese subjects and to a predisposition to gain weight. This study investigated an association of the alpha(2B) polymorphism with the BMR and metabolic syndrome-related parameters of morbidly obese patients. Genotype frequencies were similar in patients and in a control group. The patients' BMR, adjusted for fat-free mass, fat mass, sex and age, did not differ between alpha(2B) genotypes. The polymorphism was also not associated with the patients' BMI, systolic and diastolic blood pressure, resting heart rate, total and HDL cholesterol, triglycerides, fasting glucose and uric acid levels. These findings do not support a major functional significance of the alpha(2B) adrenergic receptor polymorphism in the present sample of morbidly obese subjects.
Adolescent, Adult, Basal Metabolism/genetics, Female, Gene Deletion, Genotype, Humans, Male, Metabolic Syndrome X/genetics, Middle Aged, Obesity, Morbid/genetics, Obesity, Morbid/metabolism, Polymorphism, Genetic, Receptors, Adrenergic, alpha-2/genetics, Rest, Sympathetic Nervous System/physiology
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