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1.
Horm Metab Res ; 48(2): 106-11, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26372897

RESUMEN

Changes in diet and eating behavior along with excessive consumption of sugar or fat and a sedentary lifestyle are related to increased obesity and its associated comorbidities. The aim of this study was to investigate the role of the type of macronutrients on specific health benefits associated with the weight loss in treating obesity. A total of 30 obese women (34.89±3.04 kg/m(2) and 43.3±5.34 years) participated in an interdisciplinary therapy approach to lifestyle change, which consisted of nutritional counseling, exercise, and psychological therapy for over a period of 26 weeks. The profile was obtained by anthropometric measurements and body composition by bioelectrical impedance analysis (BIA). Usual food intake was assessed with 3-day food record diaries and blood tests were used to determine metabolic and adipokines parameters. After therapy, there was significant reduction in all anthropometric and body composition variables. Food consumption also decreased while still providing adequate nutrient intake. There was significant improvement in LDL-cholesterol, PAI-1, leptin, CRP, ICAM-1, and VCAM-1. Lower dietary carbohydrate and fat intake led to weight loss. The effect of lower carbohydrate intake on weight loss is related to changes in body composition and leptin levels. Weight loss by reducing fat intake modified the inflammatory process and cardiovascular risk, indicating dietary fat as an independent predictor factor of cell adhesion molecules. Therefore, decreasing dietary fat consumption had greater impact on the inflammatory process on obese individuals. Our results show that the type of macronutrient influences the health benefits associated with weight loss.


Asunto(s)
Grasas de la Dieta/administración & dosificación , Obesidad/sangre , Obesidad/terapia , Adulto , Proteína C-Reactiva/metabolismo , LDL-Colesterol/sangre , Femenino , Humanos , Inflamación , Molécula 1 de Adhesión Intercelular/sangre , Leptina/sangre , Persona de Mediana Edad , Inhibidor 1 de Activador Plasminogénico/sangre , Molécula 1 de Adhesión Celular Vascular/sangre
2.
J Cell Physiol ; 227(7): 2917-26, 2012 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-21938726

RESUMEN

Hepatic insulin resistance is the major contributor to fasting hyperglycemia in type 2 diabetes. The protein kinase Akt plays a central role in the suppression of gluconeogenesis involving forkhead box O1 (Foxo1) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), and in the control of glycogen synthesis involving the glycogen synthase kinase beta (GSK3ß) in the liver. It has been demonstrated that endosomal adaptor protein APPL1 interacts with Akt and blocks the association of Akt with its endogenous inhibitor, tribbles-related protein 3 (TRB3), improving the action of insulin in the liver. Here, we demonstrated that chronic exercise increased the basal levels and insulin-induced Akt serine phosphorylation in the liver of diet-induced obese mice. Endurance training was able to increase APPL1 expression and the interaction between APPL1 and Akt. Conversely, training reduced both TRB3 expression and TRB3 and Akt association. The positive effects of exercise on insulin action are reinforced by our findings that showed that trained mice presented an increase in Foxo1 phosphorylation and Foxo1/PGC-1α association, which was accompanied by a reduction in gluconeogenic gene expressions (PEPCK and G6Pase). Finally, exercised animals demonstrated increased at basal and insulin-induced GSK3ß phosphorylation levels and glycogen content at 24 h after the last session of exercise. Our findings demonstrate that exercise increases insulin action, at least in part, through the enhancement of APPL1 and the reduction of TRB3 expression in the liver of obese mice, independently of weight loss.


Asunto(s)
Insulina/metabolismo , Hígado/metabolismo , Obesidad/metabolismo , Condicionamiento Físico Animal/fisiología , Proteínas Adaptadoras Transductoras de Señales/biosíntesis , Proteínas Adaptadoras Transductoras de Señales/genética , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Animales , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/fisiopatología , Dieta , Proteína Forkhead Box O1 , Factores de Transcripción Forkhead/genética , Factores de Transcripción Forkhead/metabolismo , Gluconeogénesis/genética , Gluconeogénesis/fisiología , Glucosa-6-Fosfatasa/genética , Glucosa-6-Fosfatasa/metabolismo , Glucógeno/genética , Glucógeno/metabolismo , Glucógeno Sintasa Quinasa 3/genética , Glucógeno Sintasa Quinasa 3/metabolismo , Glucógeno Sintasa Quinasa 3 beta , Insulina/genética , Masculino , Ratones , Ratones Obesos , Obesidad/etiología , Obesidad/genética , Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma , Fosforilación , Resistencia Física/fisiología , Proteínas Serina-Treonina Quinasas/genética , Proteínas Serina-Treonina Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Transactivadores/genética , Transactivadores/metabolismo , Factores de Transcripción , Pérdida de Peso/fisiología
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