RT info:eu-repo/semantics/bachelorThesis T1 Bioquímica y biología celular de las complicaciones de la hiperglucemia (diabetes tipo II) A1 Castro Díaz, Raquel K1 Diabetes mellitus, AGES, Methylglyoxal, Oxidative stress (ROS), Sorbitol, Protein kinase C, Hexosamines, Insulin resistance, GAPDH, NF-κB, Poly (ADP-ribose) polymerase. AB Diabetes mellitus is a complex disease, where chronic hyperglycemia generatescomplications in different organs. In this circumstance, reactive oxygen species increase dueto its autoxidation and other mechanisms, so that their metabolism favors the accumulation ofmetabolites such as fructose, sorbitol and triose phosphate. The latter generate highly reactiveα-oxoaldehydes with high capacity to bind proteins and generate oxidative stress. In turn,there is an increase in the synthesis of diacylglycerol from the phosphate trioses, whichactivate protein kinase C. In addition, the alteration between the proportions of theniacinamide nucleotides reduced with respect to the oxidized leads to a deficit of antioxidantsystems. These metabolic imbalances cause impaired signal translation, such as abnormalgene expression, and tissue damage, providing a series of complications for patients withdiabetes. But why does damage only occur in certain cells? The answer is that some cells canregulate glucose transport when exposed to hyperglycemia, keeping the glucose concentrationconstant. However; other cells lack this mechanism and suffer damage due to hyperglycemia.So, the explanation of the causes of diabetic complications involves mechanisms that occurwithin cells, rather than outside. On the other hand, the increase of ROS in the mitochondriaproduces DNA damage (chain breaks) activating PARP that breaks down NAD into nicotinicacid and ADP ribose. PARP then proceeds to form polymers that accumulate in GAPDH andother nuclear proteins. Which leads to further accumulation of the phosphate trioses and theproblem worsens. YR 2020 FD 2020 LK http://riull.ull.es/xmlui/handle/915/20483 UL http://riull.ull.es/xmlui/handle/915/20483 LA es DS Repositorio institucional de la Universidad de La Laguna RD 29-mar-2024