Problema 2

Paciente joven que presenta TSH aumentada, T3 y T4 aumentadas tambien

1.-Como podemos explicar lo anterior

2.-cual es el diagnóstico del paciente

Problema

Paciente joven que presenta la TSH aumentada

1.- Que signos y sintomas esperan encontrar
2.- Que mecanismos fisiopatológicos estan implicados en la sintomatología del paciente
2.- Cual es el diagnóstico probable

Estimados todos
Leí sus comentarios y me congratulo de su interes, volveremos sobre estos transportadores cuando veamos páncreas endocrino, sin embargo no hemos resuelto el problema, que pasa con estos transportadores en cerebro
Les envío la referencia de este artículo (lo pueden consultar en la Biblioteca Digital de la UNAM) para lo que esten interesados y podemos discutirlo en este espacio


Journal of Cerebral Blood Flow & Metabolism (2007) 27, 1766–1791
& 2007 ISCBFM All rights reserved 0271-678X/07 $30.00

Review Article
Supply and demand in cerebral energy
metabolism: the role of nutrient transporters
Ian A Simpson1, Anthony Carruthers2 and Susan J Vannucci3
1Department of Neural and Behavioral Sciences College of Medicine, Pennsylvania State University, Hershey,
Pennsylvania, USA; 2Department of Biochemistry and Molecular Pharmacology, University of Massachusetts
Medical School, Worcester, Massachusetts, USA; 3Department of Pediatrics, Morgan Stanley Childrens’
Hospital of New York, Columbia University, New York, New York, USA
Glucose is the obligate energetic fuel for the mammalian brain, and most studies of cerebral energy
metabolism assume that the majority of cerebral glucose utilization fuels neuronal activity via
oxidative metabolism, both in the basal and activated state. Glucose transporter (GLUT) proteins
deliver glucose from the circulation to the brain: GLUT1 in the microvascular endothelial cells of the
blood–brain barrier (BBB) and glia; GLUT3 in neurons. Lactate, the glycolytic product of glucose
metabolism, is transported into and out of neural cells by the monocarboxylate transporters (MCT):
MCT1 in the BBB and astrocytes and MCT2 in neurons. The proposal of the astrocyte–neuron lactate
shuttle hypothesis suggested that astrocytes play the primary role in cerebral glucose utilization
and generate lactate for neuronal energetics, especially during activation. Since the identification
of the GLUTs and MCTs in brain, much has been learned about their transport properties, that
is capacity and affinity for substrate, which must be considered in any model of cerebral glucose
uptake and utilization. Using concentrations and kinetic parameters of GLUT1 and -3 in BBB
endothelial cells, astrocytes, and neurons, along with the corresponding kinetic properties of the
MCTs, we have successfully modeled brain glucose and lactate levels as well as lactate transients in
response to neuronal stimulation. Simulations based on these parameters suggest that glucose
readily diffuses through the basal lamina and interstitium to neurons, which are primarily
responsible for glucose uptake, metabolism, and the generation of the lactate transients observed
on neuronal activation.
Journal of Cerebral Blood Flow & Metabolism (2007) 27, 1766–1791; doi:10.1038/sj.jcbfm.9600521; published online 20
June 2007
Keywords: glucose and lactate; glucose transporter proteins; mathematical

FISIOLOGIA ENDOCRINA

Grupo 2212

Pueden empezar a subir a este espacio las preguntas que están realizando de opción múltiple para que entre todos podamos discutirlas e ir formando nuestro acervo de preguntas corregidas.

También pueden subir sus presentaciones siempre y cuando traigan figuras originales creadas por ustedes no se valen copias

BIENVENIDOS

ESTE ESPACIO FUE CREADO PARA LOS ALUMNOS DE LA FACULTAD DE MEDICINA UNAM

En el podemos discutir los temas de:

FISIOLOGIA ENDOCRINA

FISIOLOGIA DIGESTIVA

ESTRÉS OXIDATIVO Y MEDICINA

ESTRÉS OXIDATIVO Y PLASTICIDAD CEREBRAL

También a nivel de Maestría y Doctorado podemos incluir a la materia de:

ESTRÉS OXIDATIVO Y NEURODEGENERACION