Publications by authors named "Friederike Pfisterer"
Glucose and glucose degradation products (GDPs), contained in peritoneal dialysis (PD) fluids, contribute to the formation of advanced glycation end-products (AGEs). Local damaging effects, resulting in functional impairment of the peritoneal membrane, are well studied. It is also supposed that detoxification of AGE precursors by glyoxalase-1 (GLO1) has beneficial effects on GDP-mediated toxicity.
View Article and Find Full Text PDFObjective: Establishing Caenorhabditis elegans as a model for glucose toxicity-mediated life span reduction.
Research Design And Methods: C. elegans were maintained to achieve glucose concentrations resembling the hyperglycemic conditions in diabetic patients.
Background: Experimental animal models have demonstrated that the interaction of advanced glycation end-products (AGE) with their receptor RAGE is, at least in part, responsible for peritoneal damage. This study investigates the in vivo expression of RAGE in the peritoneal membrane of uraemic human patients.
Methods: Peritoneal biopsies of 89 subjects (48 uraemic and 41 healthy age-matched patients) were examined.
Article Synopsis
- Research shows that the production of reactive oxygen species (ROS) in mitochondria is a key factor in aging, using the organism Caenorhabditis elegans as a model.
- A newly identified mechanism involves the modification of mitochondrial proteins by methylglyoxal (MG), a byproduct of glycolysis, which increases with age when the enzyme glyoxalase-1, responsible for detoxifying MG, becomes less active.
- Enhancing the activity of glyoxalase-1 can reduce these harmful modifications and lower ROS production, leading to an extended lifespan in C. elegans, while reducing its activity has the opposite effect.