11. Gluconeogenesis Flashcards by Jesus Alberto Martínez Rivera

Q

Glucogeno heparico

A

Sirve en 24horas

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Q

Deficiencia de enzimas gluconeogenicas

A

Hipoglucemia

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Q

Precursores gluconeogenicos

A

Glicerol
Lactato
α-cetoacidos

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Q

Aminoácidos no glucogenicos

A

Leucina y lisina

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Q

Glicerol viene de

A

Hidrolisis de TAG

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Q

Glicerol cinasa

A

Fosforila glicerol a glicerol 3-fosfato

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Q

Glicerol 3- fosfato a digphidroxiacetoma fosfato por

A

Glicerol 3 fosdato deshidrogenasa

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Q

Lactato oxidado a piruvato

A

Ciclo de cori

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Q

Hidrolisis de proteinas en ayuno dan

A

α-cetoacidos(piruvato)

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Q

Compuestos que dan CoA

A

Acetoacetato
Lisina
Leucina

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Q

Precursor directo de PEP

A

OAA

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Q

PEP a Piruvato

A

Reaccion irreversible por piruvato cinasa (PK)

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Q

Piruvato carboxilasa (PC)

A

Piruvato a OAA

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Q

OAA a PEP por

A

PEP-Carboxicinasa (PEPCK)

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Q

Piruvato carboxilasa requiere

A

Biotina como coenzima

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Q

Biotina se une a

A

Grupo ε - amino de lisina

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Q

Se hidroliza ATP para

A

Carboxilar piruvato a OAA

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Q

Reaccion de piruvato carboxilasa

A

En mitocondrias de hepatocitos y renales

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Q

CO2 viene de

A

HCO3 para transferirse a grupo prostetico de biotina

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Q

CO2 + Piruvato da

A

OAA

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Q

Oxalacetato se hace malato para

A

Atravesar menmbrana mitocondrial

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Q

Malato se reoxida en citosol a

A

Oxalacetato

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Q

El OAA se descarboxla por PEPCK a

A

Fosfoenolpiruvato(PEP)

Q

Carboxilasas que requieren biotina

A

PC
AcetilCoA Carboxilasa
Propionil CoA carboxilasa
Metilcrotonil CoA carboxilasa

Q

PC se activa alostericamente por

A

Acetil CoA

Q

Elevado Acetil CoA

A

En ayuno

Q

OAA a malato por

A

Malato deshidrogenasa(MD)

Q

Malato a OAA se reoxida por

A

Malato deshidrogenasa citosolica

Q

En reoxidacion de OAA

A

El NAD se reduce a NaDH

Q

OAA puede convertirse a

A

PEP

Aspartato

Q

GTP impulsa

A

OAA a PEP

Q

Hidrolisis de fructosa 1,6 bifosfato por

A

Fructosa 1,6 bisfosfatasa

Q

PKF-1 inhibida por

A

Fructosa 1,6 bisfosfato

Q

Glucagon aumenta

A

AMPc que activa Proteina cinasa A

Q

Proteina cinasa A fosforila

A

PFK-2 inactivandola

Q

PFK-2 inactivada activa a

A

FBP-2 que crea fructosa 6-fosfato

Q

FBP-1 hace frectosa 6-fosfato

A

Desfosforilando fructosa 1,6 bisfosfato

Q

Fructosa 1,6 bisfosfatasa(FBP-1) se inhibe oor

A

AMP/ATP(baja energia)

Q

Altos ATP impulsan

A

Gluconeogenesis

Q

Fructosa 2,6 bisfosfato inhibe

A

Fructosa 1,6 bisfosfatasa(FBP-1)

Q

Glucosa 6-fosfatasa por hidrolisis

A

Desfosforila glucosa 6-fosfato

Q

Glucosa 6 fosfato a traves de RER por

A

Glucosa 6 fosfato translocasa

Q

Produce glucosa libre

A

Glucosa 6-fosfatasa

Q

Almacenamiento de glucogeno por deficiencia de

A

Fosfatasa(1a) y traslocasa(1b)

Q

Reacciones irreversibles de gluconeogenesis

A

Hexicinasa/glucosijasa
PFK-1
PK

Q

Regulacion de gluconeogenesis por

A

Glucagon

Sustratos glucogenicos

Q

Glucagon disminuye

A

Fructosa 2,6 bifosfato(activando FBP-1 e inhibiendo PFK-1)

Q

Glucagon unido a proteina G

A

Suelta AMPc inactivando PK( fosforilada)

Q

Glucagon incrementa

A

Trascripcion de gen lara PEPCK

Q

Cortisol incrementa

A

Trascripcion de gen de PEPCK

Q

Activacion en ayuno de PC hepatica por

A

AcetilCoA

Q

Acetil CoA inhibe

A

PDHC( activando PDH cinasa)

Q

FBP-1 inhibida por

A

AMP y activa PFK-1

Q

Complejo PDH con AcetilCoA

A

Mo entra a ciclo d krebs

Q

Piruvato con piruvato carboxilasa

A

Se hace OAA que da Glucosa