title: Relationship between non-genomic actions of estrogens and insulin resistace.
abstract: Numerous experimental and clinical data show that the physiological actions of insulin and sexual steroids interact in target tissues for these hormones. In the other hand, sexual steroids has effects on peripheral tissues, and since the skeletal muscle is the main responsible for peripheral glucose uptake, it would be possible that the sexual steroids induce directly in the muscle a decrease of the sensibility of this tissue to insulin action. Some of the biological actions of the estrogens are too fast like to be compatible with this classical mechanism of action, and this mechanism has been called not classical, non-genomic or rapid actions of the estrogens. Moreover, some experiments have shown that low concentrations of estradiol, induce an increase in the rate of IRS-1 phosphorylation, promotes the association between IRS-1 and the subunit of PI3-k, p85alpha, causes a decrease in the rate of IRS-1 serine phosphorylation and increases the rate of Akt phosphorylation. Therefore, the evidences suggest the existence of a narrow interrelation between the estrogens and insulin sensitivity, but relatively few studies have tried to resolve the molecular base of this relation in insulin-dependent tissues. The resolution of these unknown questions would be able to have a great long-term therapeutic repercussion. In this sense, we should not forget that insulin resistance is the underlying cause of several associated pathologies to the female aging, as Type 2 diabetes, cardio-circulatory pathology or neurodegenerative disease.
authors.affiliation: Department of Functional Biology, Physiology Area, Oviedo University, Oviedo, Spain.
authors.forename: Ana
authors.initials: A
authors.lastname: Alonso
authors.forename: Celestino
authors.initials: C
authors.lastname: González
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000503:physiopathology; D004958:Estradiol / Q000494:pharmacology / Q000502:physiology; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology*; D005260:Female; D006801:Humans; D055504:Insulin Receptor Substrate Proteins; D007333:Insulin Resistance; D008297:Male; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000503:physiopathology; D010766:Phosphorylation
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D004967:Estrogens; C526292:IRS1 protein, human; D055504:Insulin Receptor Substrate Proteins; D004958:Estradiol