Resistin in morbidly obese patients before and after gastric bypass surgery.

BACKGROUND AND OBJECTIVES: Resistin was originally suggested to be a potential mediator of obesity-related insulin resistance in rodents. However, in humans, the role of resistin in obesity and insulin resistance has not yet been demonstrated. The present study investigates whether there are differences in resistin levels between patients with morbid obesity and lean subjects, and analyzes changes in resistin levels after significant weight loss secondary to bariatric surgery. METHODS: Sixty-eight patients with morbid obesity (body mass index [BMI] ≥ 40 kg/m2) and 31 lean subjects (BMI < 25 kg/m2) were selected. The study variables were: weight, height, BMI, waist-hip ratio (WHR), fat mass, family history of cardiovascular disease (CVD), type 2 diabetes mellitus (DM), hypertension, dyslipidemia, smoking, glucose, glycated hemoglobin (HbA1c), insulin, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), adiponectin and resistin. Homoeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated. The obese patients underwent gastric bypass surgery, and the above mentioned variables were reassessed after 12 months and major weight loss. RESULTS: There were no significant differences in resistin levels between morbidly obese patients and healthy subjects of normal weight, or between obese patients before and after weight loss. Resistin levels in morbidly obese patients were not correlated to adiposity anthropometric measures, insulin, glucose, HOMA, QUICKI, hsCRP, IL-6 or adiponectin. In the morbid obesity group, after one year of weight loss, the only study parameter correlated to resistin levels was IL-6. CONCLUSION: Our results do not support a relationship among resistin levels, obesity and insulin resistance in humans.

Resistin in morbidly obese patients before and after gastric bypass surgery / Resistina en obesos mórbidos antes y después de un bypass gástrico

Background and objectives: Resistin was originally suggested to be a potential mediator of obesity-related insulin resistance in rodents. However, in humans, the role of resistin in obesity and insulin resistance has not yet been demonstrated. The present study investigates whether there are differences in resistin levels between patients with morbid obesity and lean subjects, and analyzes changes in resistin levels after significant weight loss secondary to bariatric surgery. Methods: Sixty-eight patients with morbid obesity (body mass index [BMI] ≥ 40 kg/m2) and 31 lean subjects (BMI < 25 kg/m2) were selected. The study variables were: weight, height, BMI, waist-hip ratio (WHR), fat mass, family history of cardiovascular disease (CVD), type 2 diabetes mellitus (DM), hypertension, dyslipidemia, smoking, glucose, glycated hemoglobin (HbA1c), insulin, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), adiponectin and resistin. Homoeostasis model assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated. The obese patients underwent gastric bypass surgery, and the above mentioned variables were reassessed after 12 months and major weight loss. Results: There were no significant differences in resistin levels between morbidly obese patients and healthy subjects of normal weight, or between obese patients before and after weight loss. Resistin levels in morbidly obese patients were not correlated to adiposity anthropometric measures, insulin, glucose, HOMA, QUICKI, hsCRP, IL-6 or adiponectin. In the morbid obesity group, after one year of weight loss, the only study parameter correlated to resistin levels was IL-6. Conclusion: Our results do not support a relationship among resistin levels, obesity and insulin resistance in humans (AU)

Introducción y objetivos: inicialmente se sugirió que la resistina era un mediador potencial de la resistencia a la insulina relacionada con la obesidad en roedores. Sin embargo, en seres humanos, el papel de la resistina en la obesidad y la resistencia a la insulina aún no se ha demostrado. El presente estudio investiga si existen diferencias en los niveles de resistina entre pacientes con obesidad mórbida y sujetos con normopeso, y analiza los cambios en los niveles de resistina después de la pérdida significativa de peso debida a cirugía bariátrica. Métodos: se seleccionaron 68 pacientes con obesidad mórbida (IMC ≥ 40 kg/m2) y 31 sujetos normopeso (IMC < 25 kg/m2). Las variables del estudio fueron peso, talla, IMC, relación cintura-cadera (WHR), masa grasa, antecedentes familiares de enfermedad cardiovascular, diabetes mellitus tipo 2 (DM), hipertensión arterial, dislipidemia, tabaquismo, glucosa, hemoglobina glicosilada (HbA1c), insulina, proteína C reactiva de alta sensibilidad (hsCRP), interleucina-6 (IL-6), adiponectina y resistina. Se calcularon la evaluación del modelo de homeostasis (HOMA) y el índice cuantitativo de control de sensibilidad a la insulina (QUICKI). Los pacientes obesos se sometieron a un bypass gástrico, y las variables mencionadas fueron reevaluadas después de 12 meses y una pérdida de peso importante. Resultados: no hubo diferencias significativas en los niveles de resistina entre pacientes obesos mórbidos y sujetos sanos de peso normal, ni entre pacientes obesos antes y después de la pérdida de peso. Los niveles de resistina en pacientes obesos mórbidos no se correlacionaron con medidas antropométricas de adiposidad, insulina, glucosa, HOMA, QUICKI, hsCRP, IL-6 o adiponectina. En el grupo de obesos mórbidos, al año de la pérdida de peso experimentada, el único parámetro del estudio correlacionado con los niveles de resistina fue la IL-6. Conclusión: nuestros resultados no apoyan una relación entre los niveles de resistina, la obesidad y la resistencia a la insulina en los seres humanos (AU)