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
menciona un sistema en el que los individual genes are responsible for the development of obesity
leptin-melanocortin system.
increase in leptine x a cantidad de grasas almacenadas, reconocido x el receptor d leptina.
This receptor signal is then passed
on to the melanocortin-4 receptor (MC4R) in the neurons. union ded alfa-MSH (proviene d POMC) con mc4r –> SACIEDAD
Mutations in one of these genes (leptin, leptin receptor, POMC or MC4R)
14) Degradation of alcohol with enzymes, cofactors, intermediates and sketch.
etanol–> acetaldehido –> acetato –> acetil coa
enzimas degr alcohol y cofactores.
alchold deshidrogenasa para pasar de etanol a acetaldehido,
aldehido deshidrogenasa para pasar de acetaldehido a acetato
atp y coa para producir acetil coa a partir del acetato .
donde se produce energia en el ciclo del etanol
en el paso de etanol a acetaldehido, y en el paso de acetaldehido a acetato .
funcion kreatinfosfat
s. It is essential for muscle function because it provides its
phosphate for the rephosphorylation of ADP–> atp again available
¿como regulan los acidos grasos la expresion de genes de metabolismo de lipidos y energia?
uniendose con los PPAR (Peroxisomal Proliferator Activator Receptors ) , nucleares , que forman un heterodimero con los retinoid receptors (rxr).
ejemplos de que activa la union de Fatty acids con PPAR+RXR
Activa la transcripcion de genes de:
-la acil coa sintetawsa
la lipoprotein lipasa
transportadores de ac gr
-carnitina palmitol transferasa
-receptor de insulina
-Leptina
todo dirigido a degradar FA
) Pathological effects when bile acid levels are too low.
Cholestasis (bile stasis) –> impaired lipid absorption
Cholelithiasis (gallstones)–> Formation of cholesterol crystals due to high cholesterol levels in the bile.
Diabetes Typ I
Autoimmune disease, se destruyen las celulas de insulina
Diabetes Type II
Insulin resistance of the muscle, liver and fat cells. tissues get increasingly insensitive to insuline
Fullness (Satiety) Stimuli
-Leptin: Produced by adipose (fat) tisse
-Peptide YY (PYY): Released by the small intestine
-Cholecystokinin (CCK): Released by the small intestine,
-Insulin: Secreted by the pancreas
Stomach and Intestinal Distention: vagus nerve
Enteric Nervous System
Hunger Stimuli
-Ghrelin (stomach)
-Neuropeptide Y (NPY)
-Agouti-Related
-Peptide (AgRP): hypothalamus
-Orexins
Stomach Contractions
Gut Stretch Receptors:
