1,721,098 research outputs found
The p66Shc isoform is essential for induction and maintenance of a normal skeletal muscle cell phenotype in response to growth factors.
No full text
Strategie per la prevenzione della disfunzione beta-cellulare nel diabete mellito tipo 2.
No full textThe IGF-I signaling pathway
No full textThe insulin-like growth factor (IGF)-I is implicated in the regulation of protein turnover and exerts potent mitogenic and differentiating effects on most cell types. IGF-I biological actions are mediated by the IGF-I receptor, comprised of two extra-cellular α-subunits, containing hormone binding sites, and two membrane-spanning β-subunits, encoding an intracellular tyrosine kinase. Hormone binding activates the receptor kinase, leading to receptor autophosphorylation and tyrosine phosphorylation of multiple substrates, including the IRS and Shc proteins. Through these initial tyrosine phosphorylation reactions, IGF-I signals are transduced to a complex network of intracellular lipid and sersine/threonine kinases that are ulitmately responsible for cell proliferation, modulation of tissue differentiation, and protection from apotosis. This review will focus on the IGF-I receptor structure and function, its intracellular signaling pathways, and some important implications of the activation of the IGF-I transduction system in specific tissues. © 2007 Bentham Science Publishers Ltd
The p66Shc isoform inhibits MAP kinase signaling and regulates IGF-mediated proliferation and differentiation in skeletal muscle cells.
No full text
The p66Shc isoform is essential for induction and maintenance of a normal skeletal muscle cell phenotype in response to insulin-like growth factors.
No full textp66Shc plays a key role in maintenance of a normal skeletal muscle cell phenotype in response to growth factors.
No full textGLP-1: a new approach for type 2 diabetes therapy
No full textβ-cell dysfunction is an early pathophysiological defect in type 2 diabetes mellitus. Conventional secretagogues, although effective in increasing insulin secretion, may be associated with undesirable side effects, including hypoglycemia, abnormalities in cardiovascular responses, and β-cell apoptosis. Glucagon-like peptide(GLP)-1 is an incretin hormone displaying glucose-dependent stimulation of insulin secretion, trophic effects on the pancreatic β-cells, and inhibitory effects on gastrointestinal motility, which has been shown to ameliorate hyperglycemia and reduce glycemic excursions. However, after parenteral administration native GLP-1 is rapidly degraded by plasma dipeptydil peptidase (DPP)-IV. Hence, degradation-resistant, long-acting GLP-1 receptor agonists have been proposed as novel agents for diabetes therapy. Alternatively, inhibitionof DPP-IV-mediated GLP-1 degradation represents another approach for exploiting GLP-1 beneficial effects on metabolic control. This review will summarize the biological effects of GLP-1, the general features of GLP-1 mimetics and DPP-IV inhibitors, and the promising results of recently published clinical trials testing these compounds for the treatment of type 2 diabetes. © 2006 Elsevier Ireland Ltd. All rights reserved
Cross-Talk between PPARgamma and Insulin Signaling and Modulation of Insulin Sensitivity
No full textPPARgamma activation in type 2 diabetic patients results in a marked improvement in insulin and glucose parameters, resulting from an improvement of whole-body insulin sensitivity. Adipose tissue is the major mediator of PPARgamma action on insulin sensitivity. PPARgamma activation in mature adipocytes induces the expression of a number of genes involved in the insulin signaling cascade, thereby improving insulin sensitivity. PPARgamma is the master regulator of adipogenesis, thereby stimulating the production of small insulin-sensitive adipocytes. In addition to its importance in adipogenesis, PPARgamma plays an important role in regulating lipid, metabolism in mature adipocytes by increasing fatty acid trapping. Finally, adipose tissue produces several cytokines that regulate energy homeostasis, lipid and glucose metabolism. Disturbances in the production of these factors may contribute to metabolic abnormalities, and PPARgamma activation is also associated with beneficial effects on expression and secretion of a whole range of cytokines
- …
