Información del artículo
Resumen
La diabetes tipo 2 se caracteriza por la presencia de hiperglucemia tanto posprandial como en ayuno. La hemoglobina glucosilada es un marcador de la exposición glucémica global e integra la hiperglucemia tanto en ayunas como posprandial. Los estudios epidemiológicos y de intervención en diabetes tipo 2 y tipo 1 han demostrado que la hiperglucemia crónica está asociada con la aparición de complicaciones diabéticas crónicas. Más importante aún es el hecho de que la reducción de la hemoglobina glucosilada, con el fin de alcanzar el objetivo diana, previene y evita la progresión de las complicaciones, en particular, en los eventos microvasculares. Aunque la hiperglucemia crónica produce una glicación de proteínas excesiva, las fluctuaciones agudas de la glucosa pueden activar el estrés oxidativo y contribuir a la disfunción endotelial, lo que también podría estar implicado en el desarrollo de las complicaciones por diabetes. Por consiguiente, la reducción de la hiperglucemia posprandial y de las variaciones glucémicas se reconoce ahora como una prioridad en el tratamiento de la diabetes tipo 2. Los agentes terapéuticos que actúan sobre la glucosa posprandial son particularmente de interés para disminuir las variaciones glucémicas. Los nuevos agentes terapéuticos, los agonistas del péptido 1 similar al glucagón y los inhibidores de la dipeptidil peptidasa 4 (DPP), son interesantes. Ambos aumentan la secreción de insulina e inhiben la liberación de glucagón como respuesta a una comida de un modo que es dependiente de la glucosa. Este artículo se centrará en la creciente repercusión de la hiperglucemia posprandial y de las variaciones glucémicas en el desarrollo de complicaciones por diabetes y el papel de los inhibidores de la DPP-4 (sitagliptina, vildagliptina, saxagliptina) a la hora de reducir ambos defectos en las personas con diabetes tipo 2.
Palabras clave:
Diabetes tipo 2
Hiperglucemia posprandial
Variación glucémica
Inhibidores DPP-4
Estrés oxidativo
Glucación de proteínas
Abstract
Type 2 diabetes is characterized by the presence of both fasting and postprandial hyperglycaemia. Glycated haemoglobin is a marker of overall glycaemic exposure and integrates both fasting and postprandial hyperglycaemia. Epidemiologic and interventional studies in type 1 and type 2 diabetes have demonstrated that chronic hyperglycaemia is associated with the appearance of chronic diabetes complications. More importantly, reducing glycated haemoglobin to achieve target goals prevents and avoid progression of complications, in particular microvascular outcomes. Although sustained chronic hyperglycaemia produces excessive protein glycation, acute fluctuations of glucose may activate oxidative stress and contribute to endothelial dysfunction, which may also participate in the development of diabetes complications. Therefore, reducing postprandial hyperglycaemia and glucose variability are now recognised as a priority in treatment of type 2 diabetes. Therapeutic agents acting on postprandial glucose excursions are of particular interest to diminish glucose variability. Emerging therapeutic agents such as the glucagon-like peptide 1 agonists and the dipeptidyl peptidase (DPP)-4 inhibitors are very attractive. Both increase insulin secretion and suppress glucagon release in response to meals, in a glucose-dependent manner. This review will focus on the increasing impact of postprandial hyperglycaemia and glycaemic variability in developing diabetes complications and the role of DPP-4 inhibitors (sitagliptin, vildagliptin, saxagliptin) in reducing both defects presenting in people with type 2 diabetes.
Keywords:
Type 2 diabetes
Postprandial hyperglycaemia
Glycemic variability
DPP-4 inhibitors
Oxidative stress
Protein glycation
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