Subject(s)
Animals , Humans , Hunger/physiology , Satiation/physiology , Stomach/anatomy & histology , Digestion/physiology , Gastric Emptying/physiology , Glucagon-Like Peptide 1/physiology , Hyperphagia/physiopathology , Intestinal Absorption/physiology , Meals , Organ Size , Stomach/physiology , Stomach/surgeryABSTRACT
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.
Subject(s)
Humans , Male , Female , Diabetes Mellitus, Type 2/therapy , Incretins/physiology , Incretins/therapeutic use , Gastric Inhibitory Polypeptide/physiology , Gastric Inhibitory Polypeptide/metabolism , Glucagon-Like Peptide 1/physiology , Glucagon-Like Peptide 1/metabolism , Incretins/metabolismABSTRACT
Severe obesity is associated with type 2 diabetes mellitus, and both resolve with weight loss after bariatric operations. Intestinal hormones have been identified which are stimulated by rapid nutrient delivery to the lower small bowel after certain weight-loss operations. These incretins stimulate secretion and hypertrophy of the pancreatic beta cells. Surgical procedures are now being performed to treat diabetes in adults of lesser weight, and the importance of ruling out latent autoimmune diabetes in the adult (a variety of type 1) is suggested, before experimenting with these procedures.
A obesidade grau III está francamente associada ao risco e à presença do diabetes tipo 2, sendo as duas condições passíveis de resolução com as cirurgias bariátricas. Hormônios gastrointestinais que formam eixo enteroinsular têm sido identificados, sendo mais intensa e rapidamente liberados após os procedimentos antiobesidade. Esses hormônios, entre os quais as incretinas, estimulam a secreção e a hipertrofia da células betapancreáticas. Novos procedimentos têm sido desenvolvidos para tratar o diabetes tipo 2 em adultos com obesidade em graus menos intensos. No entanto, é necessária a exclusão de pacientes com diabetes autoimune latente do adulto (LADA - uma variedade do diabetes tipo 1) antes da indicação de um procedimento cirúrgico.