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Hyperglycemic Conditions (hyperglycemic + condition)
Selected AbstractsImpact of glucose levels on advanced glycation end products in hemodialysisHEMODIALYSIS INTERNATIONAL, Issue 3 2007Amy Ruth GODFREY Abstract The current obesity epidemic throughout the western world has resulted in a considerable increase in the condition Type II diabetes mellitus. Recently, the World Health Organization has predicted that the global prevalence of Type II will increase from 175 million patients in 2003 to over 350 million by 2030. One of the major consequences of this disorder is renal failure, which presents itself as chronic kidney disease, and can progress to end-stage renal disease. Once diagnosed, patients are generally treated using dialysis due to a shortage of kidney donors. The fundamental process of dialysis still requires improvement because the survival rate of these patients is relatively poor. This has resulted in considerable research into improvements in hemodialysis membranes, and the challenge to find more suitable marker(s) in assessing the efficacy of the dialysis process. A class of compounds highlighted as a possible accumulative toxin is advanced glycation end products or AGEs. This is an article regarding the impact of hemodialysis and hemodiafiltration on glucose and AGE levels within the body and the consequences of a chronic hyperglycemic condition. It also highlights the negative aspects of using dextrose in conventional dialysis solutions (an area that has already been identified by peritoneal dialysis clinicians as problematic). The review concludes by suggesting several possible topics of future research. [source] Specific dynamic and noninvasive labeling of pancreatic , cells in reporter miceGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 4 2005Ahmi Ben-Yehudah Abstract Noninvasive detection of differentiated cells is increasingly demanded for accurate and reliable assessments of both in vitro and in vivo experimental systems. Here we present an efficient, innovative approach for imaging the , cells of the pancreatic islets of Langerhans. The main physiologic function of , cells is glucose-stimulated insulin secretion. This function is facilitated through the synthesis and storage of insulin in secretory vesicles of , cells, which then release their contents when , cells are exposed to hyperglycemic conditions. To visualize , cells in vivo in the mouse, we used targeted mutagenesis techniques to construct a modified insulin II (InsII) gene allele, InsIIEGFP, that expresses a proinsulin-EGFP (enhanced green fluorescent protein) fusion peptide. The EGFP portion of this fusion is entirely within the C-peptide portion of the proinsulin peptide. This fusion protein is processed in , cells to insulin and EGFP-tagged C peptide, which are stored together in cytoplasmic secretory vesicles. The large amount of vesicular EGFP-tagged C peptide is evident as a characteristic robust and specific fluorescence pattern in the , cells of InsIIEGFP mice. This innovative method of visualizing , cells will be a useful tool in the study of both , cell physiology and the development of the endocrine cells of the pancreas.genesis 43:166,174, 2005. © 2005 Wiley-Liss, Inc. [source] New developments in incretin-based therapies: The current state of the fieldJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 2009CDE Diabetes Nurse Educator, Carolyn Robertson APRN Abstract Purpose: To update readers on developments in incretin therapies since the previous JAANP supplement in 2007; specifically, to describe clinical data for currently available incretin-based therapies as well as those under consideration by regulatory agencies. Data source: Medline search for peer-reviewed publications. Conclusions: Incretin-based therapies have pharmacologic properties that avoid some key limitations of previous treatments, such as hypoglycemia and weight gain. Certain agents also lower blood pressure and have the potential to reduce cardiovascular risk. The insulin-secreting action of incretin-based therapies only occurs under hyperglycemic conditions, thus minimizing the risk of hypoglycemia, unless combined with a sulfonylurea. The DPP-4 inhibitors are orally administered and demonstrate modest A1c reductions (0.6%,0.8%); the best results occur when combined with metformin. Glucagon-like peptide-1 (GLP-1) receptor agonists liraglutide and exenatide have shown greater A1c reductions (typically , 1.1% and as high as 1.7%), and these agents have beneficial ancillary effects, including weight and systolic blood pressure reduction. Both DPP-4 inhibitors and GLP-1 receptor agonists have shown the ability to improve pancreatic beta-cell function in early studies. Implications for practice: Data are provided on the efficacy and tolerability of approved incretin therapies, and on treatments currently in regulatory review, in order to inform readers and guide their practice. [source] The incretin hormones GIP and GLP-1 in diabetic rats: effects on insulin secretion and small bowel motilityNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2009T. Edholm Abstract, Incretin hormones often display inhibitory actions on gut motility. The aim of this study was to investigate if altered responsiveness to glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) as regards insulin release and small bowel motility could bring further clarity to the pathophysiology of diabetes in the Goto-Kakizaki (GK) rat. The isolated perfused pancreas was studied in male GK and Wistar rats (controls) under euglycemic and hyperglycemic conditions. Glucose-dependent insulinotropic peptide (10 nmol L,1) or GLP-1 (10 nmol L,1) were added to the medium and perfusate was collected and analysed for insulin. Moreover, GK and Wistar rats were supplied with bipolar electrodes in the small bowel and myoelectric activity was recorded during intravenous administration of GIP (1,400 pmol kg,1 min,1) or GLP-1 (0.1,20 pmol kg,1 min,1). Finally, tissue was collected from GK and Wistar rats for RNA extraction. Under euglycemia, GIP and GLP-1 stimulated the initial insulin response by 10-fold in GK rats (P < 0.05). At later hyperglycemia, the insulin response to GIP and GLP-1 was blunted to about one-third compared with controls (P < 0.05). In the bowel GLP-1 was about 2.6,16.7 times more potent than GIP in abolishing the migrating myoelectric complex in the GK and control rats. Polymerase chain reaction (PCR) showed GIP and GLP-1 receptor gene expression in pancreatic islets and in small bowel. The initially high, but later low insulin responsiveness to stimulation with GIP and GLP-1 along with inhibition of small bowel motility in the GK rat indicates a preserved incretin response on motility in diabetes type 2. [source] 2125: High glucose sensitizes human retinal endothelial cells for IFN-g-mediated apoptosisACTA OPHTHALMOLOGICA, Issue 2010R NAGARAJ Purpose The biochemical mechanisms by which inflammatory cytokines cause damage in the diabetic retina are poorly understood. Indoelamine 2, 3-dioxygenase (IDO) is an inducible by IFN-, enzyme and is the first enzyme of the kynurenine pathway, which produces cytotoxic kynurenines. In this study we have investigated the role of IDO in apoptosis of human retinal capillary endothelial cells (HREC) under hyperglycemic conditions. Methods HREC were cultured in medium containing high glucose (25 mM) or low glucose (7.5 mM) and incubated with 1-100 U/ml of IFN-,. IDO activity was measured by an HPLC assay. Expression of IFN-, receptor 1, and activation of the JAK-STAT signaling pathway along with activation of PKC-, was assessed by Western blotting. HREC apoptosis was measured by Hoechst staining. The role of IDO in HREC apoptosis was evaluated in the presence specific chemical inhibitors of the kynurenine pathway. Results IFN-, dose-dependently activated JAK-STAT signaling and PKC-,, and upregulated IDO. The IDO-mediated tryptophan oxidation led to formation of kynurenines, which was followed by chemical modification of proteins by kynurenines in HREC. These changes were accompanied by production of reactive oxygen species (ROS) and depletion of protein-free thiols. IFN-, inhibited cell cycle at low concentrations and caused caspase-3-mediated apoptosis and at higher concentrations, and those effects were amplified in the presence of high glucose in HREC. We found that IFN-, mediated cytotoxicity in HREC was primarily due to ROS generated by 3-hydroxykynurenine. Conclusion Our results suggest that high glucose sensitizes HREC to deleterious effects IFN-, and provide a novel mechanistic pathway for retinal capillary endothelial cell death in diabetes. [source] | ||||||||||