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Advanced glycation endproducts and diabetes. Beyond vascular complications.
No full textAdvanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs is related with the aging process and is accelerated in diabetes. Type 2 diabetes, the most common form of diabetes, is characterized by hyperglycaemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently other aspects of the detrimental effects of AGEs in type 2 diabetes are emerged: AGEs interfere with the complex molecular pathway of insulin signaling, leading to insulin resistance; AGEs modify the insulin molecule, and, consequently, its function; AGEs decrease insulin secretion and insulin content. In this article we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications.Advanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs are related with the aging process and are accelerated in diabetes. Type 2 diabetes are the most common form of diabetes, which are characterized by hyperglycemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently, other aspects of the detrimental effects of AGEs in type 2 diabetes have emerged: AGEs interfere with the complex molecular pathway of insulin signalling, leading to insulin resistance; AGEs modify the insulin molecule, and consequently, its function; AGEs decrease insulin secretion and insulin content. In this article, we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications. © 2011 Bentham Science Publishers Ltd
Behind beta cell glucotoxicity: a pivotal role of glycoxidative damage?
No full textThis book presents current research from across the globe in the study of Beta-cells, including the induction of pancreatic cancer cell death by elevated concentrations of extracellular zinc; the role of Rab GTPases and their effectors in the insulin secretory pathway of the pancreatic beta cell; In vivo reprogramming of pancreatic A-cells into B-like cells; and the role of glucocortoids, exercise and glucolipotoxicity with regard to stress and pancreatic B-cell function.Type 2 diabetes, which is the most common form of diabetes, is characterized by hyperglycemia and insulin resistance associated with a progressive deterioration of β-cell function and mass. High blood glucose plays a key role in the development of diabetic complications and may contribute to the progressive β-cell failure. Chronic exposure to high glucose levels increases non enzymatic reactions between aldehydic and amino group of molecules like sugars and proteins, lipids or nucleic acids leading to Advanced Glycation End-Products (AGEs) formation. Accumulation of AGEs is related to the aging process and is boosted by diabetes. Although the pathogenic role of AGEs in microvascular complications of diabetes has been widely investigated and recognized, their role in pancreatic β-cell dysfunction remains to be fully elucidated. Evidence of a direct role of AGEs on pancreatic β-cell dysfunction is discussed in this review. Findings show that exposure to high AGE concentration damages the β-cell functionality affecting insulin production and disturbing the insulin secretion machinery. The studies provide solid evidence that AGEs not only may play a causative role in diabetes complications but may be crucial in the onset and maintenance of it
RETINAL PIGMENT EPITHELIAL CELLS EXPRESS A FUNCTIONAL RECEPTOR FOR GLUCAGON-LIKE PEPTIDE-1.
No full textAnti-Inflammatory Effects of GLP-1R Activation in the Retina
No full textGlucagon-like peptide-1 (GLP-1) is an incretin hormone, mainly produced by enteroendocrine L cells, which participates in the regulation of glucose homeostasis, and in reduction in body weight by promoting satiety. Actions of GLP-1 are mediated by activation of its receptor GLP-1R, which is widely expressed in several tissues including the retina. The effects of GLP-1R activation are useful in the management of type 2 diabetes mellitus (T2DM). In addition, the activation of GLP-1R has anti-inflammatory effects in several organs, suggesting that it may be also useful in the treatment of inflammatory diseases. Inflammation is a common element in the pathogenesis of several ocular diseases, and the protective effects of treatment with GLP-1 emerged also in retinal diseases. In this review we highlight the anti-inflammatory effects of GLP-1R activation in the retina. Firstly, we summarized the pathogenic role of inflammation in ocular diseases. Then, we described the pleiotropic effects of GLP-1R activation on the cellular components of the retina which are mainly involved in the pathogenesis of inflammatory retinal diseases: the retinal ganglion cells, retinal pigment epithelial cells and endothelial cells
Bcl-2 family and caspase-3 gene expression in fas-mediated apoptosis of isolated rat islets.
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Pentosidine Reduces Fas Ligand Expression In Pigmented Epithelial Cells: A Possible Involvement In Choroidal Neovascularization
No full textSpecial Issue: “Anti-inflammatory Effects of Glucagon-like Peptide-1”
No full textFrom the failure of gut extracts in diabetic patients’ therapy to the effective action in cardiovascular outcomes [...
Differente effetto ossidativo indotto da pentosidina e siero glicato ed efficacia del trattamento antiossidante con N-acetilcisteina su linee HIT-T15 e ARPE-19
No full textPioglitazone attenuates the detrimental effects of Advanced Glycation End-Products in the pancreatic beta cell line HIT-T15.
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