RESUMO
The excess of uric acid is recognized as a risk factor for diverse metabolic diseases which include gout, urolithiasis, type 2 diabetes, arterial hypertension as well as metabolic syndrome and cardiovascular disease. Current studies suggest that the exaggerated increment in fructose consumption, caused mainly by added suggars, is implicated in the high prevalence of hyperuricemia in the western population.The loss of uricase by mutation of its gene 15 million years ago in the large hominids, including man, has contributed to hyperuricemia, facilitated through the metabolism of fructose the formation of uric acid. It has been proposed that the elevation of uric acid in the remote past was an evolutionary benefit to intensify the lipogenic effects of fructose, allowing humans to survive periods of fruit shortages. However, today the high consumption of fructose and resultant hyperuricemia are a disadvantage, increasing the development of obesity and type 2 diabetes.
El exceso de ácido úrico es reconocido como un factor de riesgo para diversas enfermedades metabólicas, incluyendo: gota, urolitiasis, diabetes tipo 2, hipertensión arterial, síndrome metabólico y enfermedad cardiovascular. Estudios actuales sugieren que el incremento exagerado del consumo de fructosa, proveniente especialmente de los azúcares añadidos, está implicado en la alta prevalencia de hiperuricemia que muestra la población occidental. La pérdida de la uricasa por mutación de su gen hace 15 millones de años atrás en los grandes homínidos, incluyendo el hombre, ha contribuido a la hiperuricemia, facilitando a través del metabolismo de la fructosa la formación de ácido úrico. Se ha propuesto que la elevación del ácido úrico en épocas pasadas, fue una ventaja evolutiva al intensificar los efectos lipogénicos de la fructosa, permitiendo al ser humano sobrevivir en períodos de escasez de frutas. Sin embargo, hoy la alta ingesta de fructosa y su hiperuricemia resultante es una desventaja, promoviendo el desarrollo de obesidad y diabetes tipo 2.
RESUMO
In the last decade, specially after the discovery of leptin, several neuropeptides that regulate energy intake and expenditure have been described in animal models. This has partially unvelied the underlying mechanisms that regulate body composition and weight and therefore a promise of a more effective treatment of obesity and its comorbidities is ad portas
Assuntos
Humanos , Diabetes Mellitus Tipo 2 , Resistência à Insulina , Obesidade , Regulação do Apetite/genética , Ácidos Graxos/genética , Acilação , Diabetes Mellitus Tipo 2 , Dopamina , Fator Natriurético Atrial/farmacologia , Hipertensão/etiologia , Leptina , Lipólise , Biologia Molecular , Mutação/genética , Neuropeptídeos/farmacologia , Obesidade , Peptídeo Natriurético Encefálico/farmacologia , Peptídeo Natriurético Tipo C/farmacologia , Proliferadores de Peroxissomos , Proteínas Tirosina Fosfatases/farmacologia , Receptores Adrenérgicos beta/genética , DesacopladoresAssuntos
Humanos , Metabolismo Energético/fisiologia , Obesidade/fisiopatologia , Regulação do Apetite/fisiologia , Tecido Adiposo Marrom/fisiologia , Tecido Adiposo/fisiologia , Hormônio Liberador da Corticotropina/farmacologia , Leptina/farmacologia , Lipólise/fisiologia , Neuropeptídeos/farmacologia , Neurotransmissores/farmacologia , Obesidade/etiologia , Transtornos do Sono do Ritmo Circadiano/complicaçõesRESUMO
Obesity is a non transmissible chronical disease wich severely imipaires health, and whose prevalence is increasing worldwide. In this context, we hall briefly review some of the main topics concerning the definitions, etiology, diagnosis and treatment of obesity, as well as the relation of distribution of body fat in this and other metabolic diseases
Assuntos
Humanos , Obesidade , Metabolismo Basal , Índice de Massa Corporal , Peso Corporal/fisiologia , Dieta , Ingestão de Alimentos , Exercício Físico , Resistência à Insulina , Exames Médicos , Fatores de Risco , Aumento de PesoRESUMO
The mechanism by which obesity leads to type 2 diabetes mellitus is unknown. It is generally agreed that insulin resistance is an invariable accompaniment of obesity but that normoglycemia is maintained by compensatory hiperinsulinemia until the pancreatic B cells become unable to meet the increased demand for insulin, at which point type 2 diabetes mellitus begins. The precise cause of insulin resistance is yet to be determined, but is association with obesity has long been established. Recent data has implied free fatty acids tumoral necrosis factor - alfa, muscle fiber type II b and leptin, as a link resistance and obesity
