1,720,984 research outputs found
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
Cytochrome P4502E1 participate to the oxidative stress in the kidney of the diabetic rat, Antioxidant effects of taurine and N-acetylcysteine
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The in vitro pentosidine effects on human osteoblasts.
No full textOsteoporosis, a multifactorial and progressive skeletal metabolic disease, is characterized by low-mass density and structural deterioration of bone micro-architecture that leads to enhanced bone fragility and increased susceptibility to fractures. Recently, it has been proposed that age-related bone loss could be correlated with the glycoxidative process. The aim of the present study was to investigate the in vitro effects of pentosidine, a glycoxidative end product, on human osteoblasts (HOb). The mineralization rate, the specific bone markers (alkaline phosphatase [ALP], collagen Iα1 [COL Iα1], osteocalcin [BGP]), and the human receptor for advanced glycation end products (RAGE) gene expression have been evaluated. Pentosidine incubation of HOb caused a significant decrease in ALP, Col Iα1, and RAGE mRNA levels, but only the RAGE gene expression decreased with no dose dependency. Moreover, pentosidine incubation of osteoblasts hampered the formation of bone nodules. No effect was observed on BGP gene expression under all experimental conditions. Our data gives further support to a detrimental effect of AGEs on bone that leads to functional alterations of osteoblasts. This study addresses a crucial role of protein glycoxidation in the bone mineralization process. AGEs formation and accumulation in bone may be one of the first pathogenetic steps of bone remodeling in aging and in age-related diseases, leading to enhanced bone mass los
Il citocromo P450E1 nello stress ossidativo nel rene di ratto diabetico e sua modulazione da parte di una associazione di antiossidanti
No full textDiabetologia, Vol 46: 1175, Supplement 2. August 200
Ruolo della pentosidina sulla cascata pro infiammatoria in colture primarie di osteoblasti umani
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