preguntas 2 Flashcards

1
Q

6) What are the key enzymes of glycogen synthesis and which reactions do they catalyze?

A

1) Glucose-6-phosphate can be converted into glucose-1-phosphate by phosphoglucomutase .
2)Glucose-1-phosphate must be activated with UTP by glucose-1-phosphate-UTP transferase before it can be
incorporated into a glycogen starter molecule.
3.The now activated molecule is transferred to the starter glycogen by glycogen synthase ((ÿ-1,4-glycosidic))
4.From a length of 6-11 glucose residues, the branching enzyme

+proteina glycogenin

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2
Q

rate-limiting enzyme sintesis de glycogen (glucogeno)

A

The rate-limiting enzyme is glycogen synthase.

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3
Q

Glycogen degradation enzymes

A

1.Glycogen phosphorylase
2.Debranching enzyme

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4
Q

what are Glycogenoses

A

Glycogenoses are glycogen storage diseases. There is an accumulation glycogen in the cell.
Example: Cori disease. Cause – ÿ-1,6-glucosidase deficiency. Symptoms – hepatomegaly and
myopathy.

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5
Q

types of autophagy

A
  • Macroautophagy: formation of the autophagosome; fuses with lysosome
  • Microautophagy: material to be degraded is introduced into the lysosome.
  • Chaperone-mediated autophagy: material to be degraded is complexed with Hsc70,
    It is then bound by the lysosomal membrane receptor LAMP2 and degraded in the lysosome.
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6
Q

Steps of autophagy:

A

1) Initiation of Autophagy
2) Membrane nucleation and phagophore ( isolation membrane ) formation
3) Phagophor-Expansion
4) Fusion with the lysosome
5) Dismantling

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7
Q

iniciacion del fagosoma

A

the ULK1 complex inicia. se impide que mtor la fosforile, y se une AMPk, y despues se une el PI3K III complex, y se reclutan las ATG proteins. despues de une el PI3P binding complex.

y asi se empieza a formar la isolated membrane.

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8
Q

¿Qué procesos se activan durante el ayuno?

A

se activa la lipólisis y la gluconeogénesis para liberar ácidos grasos y glucosa almacenada, manteniendo la energía celular, y la autofagia.

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9
Q

¿Cómo influye la restricción calórica en la longevidad?

A

Reduce la producción de radicales libres, disminuye el daño molecular y activa vías de reparación celular como la autofagia.

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10
Q

¿Cuál es el papel de la mTOR en la regulación de la autofagia?

A

mTOR actúa como inhibidor de la autofagia. Cuando los nutrientes son abundantes, mTOR está activo y suprime la autofagia. En condiciones de escasez, mTOR se inhibe y se activa la autofagia.

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11
Q

que activa la AMPk

A

activa rutas metaabolicas para aumentar el ATP:
-Captacion de glucosa, transportador GLUT4 a la membrana
Aumenta la gluconeogenesis, produccion de glucosa en el higado
-aumenta la beta oxidacion de acidos grasos
x ejemplo aumementa la hexoquinasa o fosfofructokinasa, baja acetyl coa carboxilasa o glycogen sintasa.

inhibe la sintesis de acidos grasos, glucogeno, y colesterol.

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12
Q

produccion de T4 y T3

A

Here, tyrosyl residues of thyroglobulin
(a protein of the thyroid gland) are iodinated.
triyodotironina (T3) y tetraiodotironina

El yodo se une a la tiroglobulina (TG) mediante la enzima tiroperoxidasa (TPO), formando monoyodotirosina (MIT) y diyodotirosina (DIT).MIT y DIT se acoplan

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13
Q

SINTESIS SALES biliares

A

Sintetizadas en el hígado a partir de colesterol.
Enzima clave: Colesterol 7α-hidroxilasa.

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14
Q

Lipólisis enzimas

A

-Lipasa Hormono-Sensible (HSL): Rompe triglicéridos en ácidos grasos y glicerol.
-Lipasa de Triglicéridos Adiposa (ATGL): Inicia la lipólisis al convertir triglicéridos en diacilglicerol.

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15
Q

Síntesis de Lípidos, enzimas

A

-Acetil-CoA Carboxilasa (ACC): Convierte acetil-CoA en malonil-CoA.
-Ácido Graso Sintasa (FAS): Cataliza la elongación de ácidos grasos

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16
Q

Regulación Hormonal de la sintesis y degradacion d lipidos

A

Lipólisis:
-Activada por: Adrenalina, glucagón.
-Inhibida por: Insulina.
Síntesis de Lípidos:
-Activada por: Insulina.
-Inhibida por: Glucagón, adrenalina.

17
Q

ejemplos d sales biliares

A

Ácido Cólico: Cholic Acid
Ácido Quenodesoxicólico: Chenodeoxycholic Acid

secunndarios deoxycholic y litocholic acidd