ABSTRACT
Neste artigo descrevemos os mecanismos envolvidos na gênese da hiperglicemia do diabetes mellitus tipo 2. Serão analisadas a resistência insulínica, as características da secreção de insulina, a redução da secreção de insulina, a secreção hepática de glicose, a captação e a secreção hepática de glicose, o aumento da secreção de glucagon e da lipólise e a reabsorção da glicose pelos túbulos renais. Também serão revistos os defeitos das incretinas, a resistência insulínica cerebral e as alterações na flora intestinal.
In this article we describe the mechanisms involved in the genesis of hyperglycemia in type 2 diabetes mellitus. Will be analyzed separately insulin resistance, the characteristics of insulin secretion, the decrease in insulin secretion, the liver's secretion of glucose and hepatic uptake of glucose and glucose reabsorption in the kidney. Also will be review defects of the incretins, cerebral insulin resistance and changes in intestinal flora.
Subject(s)
Humans , Male , Female , /etiology , /physiopathology , Hyperglycemia/complications , Fatty Acids, Nonesterified/pharmacology , Insulin-Secreting Cells , Insulin Resistance , Incretins/physiology , Insulin , /metabolismABSTRACT
En los últimos años se reconoce un nuevo mecanismo involucrado en la fisiopatología de la Diabetes Mellitus tipo 2: el déficit de producción y/o acción de las incretinas. Las incretinas son enterohormonas que estimulan la secreción de insulina en respuesta a la ingesta de nutrientes. Glucagon like péptido-1 (GLP1) y Polipéptido insulinotrópico glucosa dependiente (GIP) son las principales incretinas descubiertas hasta hoy. Ambas presentan también efecto trófico sobre las células beta de los islotes pancreáticos. GLP-1 presenta otras acciones como son la inhibición de la secreción de glucagón, enlentecimiento del vaciamiento gástrico e inhibición del apetito. Ambas incretinas son rápidamente clivadas por la enzima dipeptidil peptidasa 4 (DPP-4). Nuevas drogas como los incretinomiméticos, análogos y los inhibidores de DPP-4 se presentan como una terapéutica prometedora para los pacientes con diabetes tipo 2.
Two main patophysiological mechanisms are currently involved in Type 2 Diabetes (T2DM), insulin resistance and impairment of beta cell function. However in the last years a new mechanism was reported: a significant decrease in incretins production and or action. Incretins are gut hormones whose main action is stimulating insulin secretion in response to nutrients. The more known incretins are glucagon like peptide-1 (GLP-1) and Gastric insulinothropic peptide (GIP). GLP-1 and GIP not only increase insulin secretion, nor decrease glucagon secretion, slow gastric emptying and reduce apetite generating weight lose. Both incretins are rapidly clived by the enzyme dipeptidil peptidase 4 (DPP4). In order to emulate incretins action, several drugs where developed: agonists of GLP-1 receptors, GLP-1 mimetics, and inhibitors of the DPP4. All of them seems to became a very promise tool for the treatment of T2DM.