preguntas Flashcards
pasos regulacion glucagon con adrenalina
- union catecolamida con el receptor de glucagon
2.activacion prot G - activacion adenilato ciclasa por la sb alfa d la prot G
- cataliza reaccion : ATP –> cAMP + PPi. cAMP
5.cAMP binds to protein kinase A (PKA)
6.) PKA phosphorylates phosphorylase kinase,–> activa glycogen
phosphorylase.
efectos pka activa
ÿ Increase in glycogenolysis.
ÿ Reduction of glycogen synthesis.
PKA phosphorylates the PP1 inhibitor, which prevents protein phosphatase 1 from converting glycogen
phosphorylase and phosphorylase kinase back to their dephosphorylated and thus inactive state. The phosphorylated PP1
inhibitor also prevents the dephosphorylation of glycogen synthase, leaving it in its inactive state.
q es el glutamato , efecto en el cerebro, como lo obtienen las celulas cerebrales, si no puede ser transtado x la sangre hasta el cerebro ?
Glutamate is the brain’s leading excitatory transmitter.
brain cells :synthesizing glutamate from glucose.
glutamine cycle
que es el gaba y como se forma, con que enzima y a partir de que producto.
GABA is an inhibitory neurotransmitter and is formed from glutamate by glutamate decarboxylase in the
presynaptic neurons.
What is hepatic encephalopathy?
Hepatic encephalopathy is a dysfunction of the CNS (liver-brain disorder).
What is the main metabolite that causes it, where is it formed
and what effect does it have?
hepatic encephalopathy?
In chronic liver disease, the liver’s detoxification function is insufficient and the serum concentration
of toxic degradation of aminoacids in the intestine products increases.
The main actor in the pathophysiology is ammonia.
se acumula en los astrocytes (glial cells), esto causa desequilibrio osmotico al metabolizarse a glutamina, edema cerebral.
terapia para hepatic encephalopathy?
- Administration of lactulose or lactitol. They are both disaccharides that are not absorbed and thus reduce the amount of toxic amines produced by the MOs in the intestine. *
refaximin
) How is starch broken down?
hydrolytic amylases –> glucosa y maltosa (saliva )
maltose -> glucose (alfa-D-glucosidase.) ´
en el duodeno : pancreatic ÿ-amylase ( no puede romper amilopectina )
oligoÿ(1ÿ6)-glucosidase (para la amilopectina ) –> di- and trisaccharides–> broken down by oligosaccharidases (lactase, maltase, sucrase and isomaltase)
transportadores
- SGLT1: uptake of glucose and galactose.
- GLUT2: uptake of all monosaccharides.
- GLUT5: Fructose absorption.
What is the difference between fructose intolerance and malabsorption?
In fructose intolerance, a distinction is made between a genetic enzyme deficiency
(fructose intolerance) and a fructose transport defect (fructose malabsorption).
q causa fructose intolerance.
falta de aldolase B para partir la fructosa 1,3 en gliceraldehido e dihidroxiacetona
que pasa si la fructosa 1P se acumula en el cuerpo, por no poder partirla, en la intolerancia a la fructosa ?
hepatotoxic and hypoglycaemic substances
toxic effect on the liver, kidneys and small intestine. In addition, the increased fructose-1-
phosphate level inhibits glycolysis and gluconeogenesis.
(hepatomegalia, fallo higado )
massive activation of glycolysis bc low atp in liver : hypoglycemia and lactate
accumulation
a que se debe la Fructose Malabsorption
This is due to a limited transport capacity of the GLUT5 transporter in the small intestinal mucosa.
efecto fructose malabsortion
fructose is insufficiently absorbed in the small intestine and Fructose accumulates in the large intestine.
This is broken down by bacteria x fermentacion, creando methane, short-chain fatty acids, CO2 and hydrogen.
desequilibrio osmotico y gases .
Tryptophan deficiency ÿ reduced serotonin
synthesis ÿ depression/cravings for sweets x falta d absorcion de fructosa
11) Name molecules in which tyrosine is the most important building block and their function in the body.
dopamina
adrenalina y noradrenalina
melanina
t3 y 4
decarboxylation products of the tyrosine
