ABSTRACT
Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this dysfunction. In this regard, adiponectin, with important metabolic functions (e.g. insulin-sensitizer and anti-inflammatory), has been recently described as a myokine that acts in an autocrine/paracrine manner. Earlier studies reported that muscle adiponectin could be induced by pro-inflammatory mediators (e.g. lipopolysaccharide), cytokines, and high-fat diets, providing a protective mechanism of this tissue against metabolic insults. However, when metabolic insults such as high-fat diets are sustained this protective response becomes dysregulated, making the skeletal muscle susceptible to metabolic impairments. Recent studies have suggested that exercise could prevent or even reverse this process. Considering that most scientific knowledge on adiponectin dysregulation in obesity is from the study of adipose tissue, the present review summarizes and discusses the literature available to date regarding the effects of obesity on skeletal muscle adiponectin induction, along with the potential effects of different exercise prescriptions on this response in an obesity context.
Subject(s)
Adiponectin/metabolism , Exercise/physiology , Muscle, Skeletal/metabolism , Obesity/metabolism , Adiponectin/genetics , Animals , Humans , Insulin Resistance/physiology , Muscle, Skeletal/physiology , Obesity/genetics , Up-Regulation/geneticsABSTRACT
Objetivo: determinar la tasa de muerte celular al exponer fibroblastos humanos (FBH) a concentraciones de BisGMA: IE-6[M], 6E-5[M], IE-5[M] y 4,8E-4[M], con el fin de determinar la citotoxicidad de BisGMA presente en materiales de uso odontológico. Material y métodos: las concentraciones de BisGMA se aplicaron en el cultivo FBH durante 24, 48 y 96 horas. La viabilidad celular se determinó mediante ensayos de reducción metabólica del Bromuro de 3-(4,5dimetiltiazol-2-ilo)-2,5-difeniltetrazol (MTT). Resultados: las concentraciones de BisGMA generan una disminución en la viabilidad celualr, de una forma dosis y tiempo dependiente. Conclusión: la disminución de la viabilidad celular es dependiente de la concentración de BisGMA presente en los cultivos celulares.
