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Avances en la fisiopatologia de la Diabetes Mellitus tipo 2

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Avances en la fisiopatologia de la Diabetes Mellitus tipo 2

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Avances en la fisiopatologia de la Diabetes Mellitus tipo 2

  1. 1. AVANCES EN LA FISIOPATOLOGIA DE LA DIABETES MELLITUS TIPO 2 <ul><li>Dr. Jorge R. Calderón T. </li></ul><ul><li>Medico Endocrinólogo </li></ul><ul><li>Hospital Nacional Arzobispo Loayza </li></ul>XII CONGRESO INTERNACIONAL DE ENDOCRINOLOGIA
  2. 2. Páncreas Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA
  3. 3. Historia Natural de la DM 2
  4. 4. AUC de Glucosa e Insulina
  5. 5. Etiología de la falla de la celula beta en la DM 2
  6. 6. Genotipo proinflamatorio <ul><li>TNF alfa. </li></ul><ul><li>IL 6. </li></ul><ul><li>gp 130 </li></ul><ul><li>Receptor de IL 6 alfa. </li></ul>Escobar Morreale ett al. Endorine Reviews. 2005: 26: 251-82.
  7. 7. Genes involucrados en la RI <ul><li>Acción y secreción de Insulina: </li></ul><ul><li>INRS: Region de Receptor de Insulina </li></ul><ul><li>VNTR: Tamdem Repetido de Numero Variable de Insulina. </li></ul><ul><li>IRS 1: Sustrato de Receptor de Insulina </li></ul><ul><li>tipo 1. </li></ul><ul><li>IRS 2: Sustrato de Receptor de Insulina tipo 2. </li></ul><ul><li>INS: Insulina </li></ul><ul><li>Sistema IGF. </li></ul><ul><li>PPAR Gamma. </li></ul>Escobar Morreale ett al. Endorine Reviews. 2005: 26: 251-82.
  8. 8. Genes involucrados en la RI en el SOPQ <ul><li>Acción y secreción de Insulina: </li></ul><ul><li>Receptor Beta 3 Adrenergico. </li></ul><ul><li>Calpaina 3. </li></ul><ul><li>Sintetasa de Glucogeno. </li></ul><ul><li>Resistina </li></ul><ul><li>Leptina y receptor de leptina </li></ul><ul><li>Apolipoproteina E. </li></ul><ul><li>Adiponectina. </li></ul>Escobar Morreale ett al. Endorine Reviews. 2005: 26: 251-82.
  9. 9. Etiología de la falla de la celula beta en la DM 2
  10. 10. Efecto de los AGL en la secreción de péptido C
  11. 11. Etiología de la falla de la celula beta en la DM 2
  12. 12. Respuesta de la insulina plasmatica a un clamp hiperglicemico en ratas pancreatectomizadas parcialmente
  13. 13. Etiología de la falla de la celula beta en la DM 2
  14. 14. Etiología de la falla de la celula beta en la DM 2
  15. 15. HIGADO : Producción de Glucosa hepática basal en pacientes con DM2 Relación con la glucosa en ayunas
  16. 16. MUSCULO: Captación de glucosa mediada por insulina esta reducida en la DM2
  17. 17. SEÑAL DE TRANSDUCCION DE LA INSULINA ESTADO NORMAL
  18. 18. SEÑAL DE TRANSDUCCION DE LA INSULINA EN LA DM2
  19. 19. SEÑAL DE TRANSDUCCION DE LA INSULINA EN LA DM2
  20. 20. Tejido Adiposo Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA Lipolisis incrementada
  21. 21. ROL DE LA LIPOTOXICIDAD EN LA DM 2 Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida LIPOTOXICIDAD
  22. 22. Efecto de la infusión de lípidos en la señal intracelular de la insulina en el músculo
  23. 23. ROL DEL MIOCITO EN LA DM 2 Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida LIPOTOXICIDAD
  24. 24. Efecto del tejido adiposo en el miocito
  25. 25. Las Incretinas Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA Lipolisis incrementada Efecto Incretina disminuido
  26. 26. Incretinas <ul><li>GLP-1  Péptido Parecido (Like) a Glucagon </li></ul><ul><li>GIP  Péptido Insulinotrópico Glucosa </li></ul><ul><li>Dependiente </li></ul><ul><li>Regulan la síntesis y liberación de insulina </li></ul><ul><li>GLP-1 producido por células L (íleo distal, colón) </li></ul><ul><li>GIP producido por células K (duodeno, intestino delgado proximal) </li></ul>European Journal of Endocrinology 2000; 143: 717 Endocrinology 2004; 145: 2653
  27. 27. EFECTO INCRETINA El efecto de las incretinas disminuye en la DM2 * p  0,05. Adaptado de Nauck M y cols. Diabetologia 1986;29:46-52. 0 – 10 10 15 20 Glucosa en plasma venoso (mmol/l) 5 60 120 180 Tiempo (min) 0 40 60 80 Insulina (mU/l) 20 Controles sanos Diabetes tipo 2 0 10 15 20 Glucosa en plasma venoso (mmol/l) 5 Tiempo (min) 0 40 60 80 Insulina (mU/l) 20 – 5 – 10 60 120 180 – 5 -10 60 120 180 -5 -10 60 120 180 -5 Glucosa por vía oral Isoglucémicos – glucosa por vía intravenosa * * * * * * * * * * Efecto normal de las incretinas Disminución del efecto de las incretinas
  28. 28. Célula alfa pancreática Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA Lipolisis incrementada Efecto Incretina disminuido Célula alfa Pancreatica Secreción incrementada de glucagon
  29. 29. Equilibrio entre la insulina y el glucagon
  30. 30. Contribución de los niveles basales de glucagon al mantenimiento de la produccion hepática de glucosa en DM2
  31. 31. El Riñon Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA Lipolisis incrementada Efecto Incretina disminuido Célula alfa Pancreatica Secreción incrementada de glucagon Reabsorción de glucosa incrementada
  32. 32. Manejo Renal de la Glucosa
  33. 33. RNAm del transportador de glucosa y los niveles de proteína SGLT2 se hallan incrementadas en DM2
  34. 34. Reabsorción tubular de la glucosa en DM 2 <ul><li>Modelos animales de DM1 y DM2 muestran que la capacidad de reabsorción tubular renal máxima (Tm) esta aumentada. </li></ul><ul><li>En humanos con DM1, la Tm para glucosa esta aumentada </li></ul><ul><li>En humanos con DM2, la Tm para glucosa aun no ha sido examinada sistematicamente </li></ul>
  35. 35. Sistema Nervioso central Secreción de Insulina alterada Producción de glucosa hepatica aumentada Captación de Glucosa disminuida HIPERGLICEMIA Lipolisis incrementada Efecto Incretina disminuido Célula alfa Pancreatica Secreción incrementada de glucagon Reabsorción de glucosa incrementada Disfunción de neurotransmisor
  36. 36. SNC y DM 2 Alimentacion excesiva Inactividad Fisica O B E SI D A D Resistencia a la insulina Proliferacion de las celulas B del pancreas Diabetes Mellitus tipo2 Hiperinsulinemia
  37. 37. Información metabólica con el SNC
  38. 38. Información metabólica con el SNC
  39. 39. Información metabólica con el SNC GASTO DE ENERGIA MEJORA LA OBESIDAD Y LA DM2
  40. 40. comunicación INTERMETABOLICA INTER ORGANOS <ul><li>Señales que regulan la ingesta de alimentos desde el tejido adiposo . </li></ul><ul><li>Señales que mejoran el gasto de energia desde el higado </li></ul><ul><li>Señales que estimulan la proliferacion de las celulas beta desde el higado </li></ul>
  41. 41. Nervios esplacnicos Nervio Vago Activación Hepática Proliferación de las células beta Hipersecreción de insulina
  42. 42. Nervios esplacnicos Nervio Vago Activación Hepática Proliferación de las células beta Hipersecreción de insulina
  43. 43. Estado Ideal
  44. 44. El Ovario <ul><li>Síndrome Ovario Poliquistico </li></ul><ul><li>8 al 20 % de mujeres en edad fertil </li></ul>
  45. 45. Disfunción de Célula Beta en SOPQ Dunaif A. 1996. JCE & M. 96: 942-947 Secreción de Insulina luego de la administración de glucosa 300 mg/kg y 500 mg de Tolbutamida.
  46. 46. Disfunción de Célula Beta en SOPQ Dunaif A. 1996. JCE & M. 96: 942-947 Concentraciones de Glucosa luego de la administración de glucosa 300 mg/kg y 500 mg de Tolbutamida.
  47. 47. Nestler , NEJM 358 (1): 47, January 3, 2008
  48. 48. Fisiopatología Azziz R, JCE & M , 2002. 87: 4055-4059. LH FSH GnRH Estradiol Inhibina Testosterona INSULINA HIGADO SUPRARRENAL LEPTINA GENES
  49. 49. Conclusiones <ul><li>Existen diversos órganos involucrados en la fisiopatología de la DM2 </li></ul><ul><ul><li>Base genética </li></ul></ul><ul><ul><li>Páncreas: Célula beta y célula alfa </li></ul></ul><ul><ul><li>Tejido Adiposo </li></ul></ul><ul><ul><li>Musculo </li></ul></ul><ul><ul><li>Intestino (Incretinas) </li></ul></ul><ul><ul><li>Riñón </li></ul></ul><ul><ul><li>Cerebro </li></ul></ul><ul><ul><li>Ovario </li></ul></ul>
  50. 50. GRACIAS
  51. 51. GRACIAS

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