metabolism Flashcards

1
Q

Glycogenesis

A

make glycogen = decrease glucose (& ATP) w/ glycogen synthasae

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2
Q

Glycolysis

A

decrease glucose in blood (bc break glucose for ATP) by insulin

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3
Q

Glycogenolysis

A

break down glycogen w/ glycogen phosphorylase-P @ a1-6 branches = make glucose (increase) by glucagon

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4
Q

Gluconeogenesis

A

make glucose (increase) from non carbohydrate precursors by glucagon

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5
Q

What are the energy stores in the human body?

A

Liver, muscle, fat

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6
Q

Which hormone do you expect to function in case of high concentration of plasma glucose? What do you call this process?

A

Insulin, glycolysis

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7
Q

Which hormone do you expect to function in case of low concentration of plasma glucose? What do you call this process?

A

Glucagon, gluconeogenesis

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8
Q

precursor for gluconeogenesis

A

oxaloacetate

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9
Q

Fasting requires all the glucose to be synthesized from ——–precursors?

A

non-carbohydrate

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10
Q

How many steps is bypassed in gluconeogenesis bc it’s irreversible? WHat are they?

A

3

Step 1, 3, 10

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11
Q

ATP gluconeogenesis consume

A

6 ATP

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12
Q

gluconeogenic precursors & where located in body?

A
  • ALanine from muscle
  • glycerol fromadipose tissue
  • lactate from muscle, RBC, Cori cycle
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13
Q

HOw does liver work during exercise? (cori cycle)

A

Muscle works anaerobic = lactate => liver => glucose via cori cycle

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14
Q

In Cori Cycle, how many phosphates are consumed?

A

4

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15
Q

name of cancer responsible for loss of adipose tissue & skeletal muscle mass. (may work similar to cori cycle)

A

Cachexia (Cachectic cancer)

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16
Q

Difference b/w cori cycle and cachexia in terms of glucose turnover

A

Cori cycle: 20%

Cachexia: 50%

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17
Q

When would the alanine or Cahill cycle be used?

A

presence of NH3 due to muscle degeneration

18
Q

Concept of Alanine or Cahill cycle

A

Muscle degeneration = NH3 -> + pyruvate = alanine -> liver -> gluconeogenesis via alanine cycle

19
Q

conversion of glucose to glycogen and where it’s stored

A

Glucose -> glucose -6-phosphate -> gucose-1-phosphate -> glycogen & stored in muscle and liver as glycogen.

20
Q

Which organs can’t undergo gluconeogenesis and why?

A

brain and muscle bc lack glucose-6-phosphatase enzyme

21
Q

What is GLUT2 function? and how is it upregulated?

A

glucose carrier/transporter which is upregulated when [Glu] >30mM

22
Q

What’s the major e- donor in reductive biosynthesis?

A

NADPH

23
Q

Importance of ketone bodies

A

make energy when starving and no glucose

24
Q

Which AA are ketogenic

A

lysine & leucine

25
Q

Which AA are ketogenic and glucogenic?

A

Isoleucine

Threonine, Tryptophan, Phenylalanine and Tyrosine

26
Q

3 types of ketone bodies and are they soluble or insoluble in water

A
  • acetone, acetoacetate and β-hydroxybutyrate

- soluble

27
Q

downside of ketogenesis

A

ketone bodies make blood acidic (ketocidosis)

28
Q

Can the liver use ketone bodies for energy? why?

A

NO bc lack beta-keotacyl-coa-transferase

29
Q

General process of making ketone bodies and use it for energy

A

Starvation -> FA (adipose tissue) in liver-> oxidise to acetyl coa -> ketone bodies -> acetyl AoA (by B-ketoacyl-coa-transferase) in tissues except in liver-> ATP

30
Q

Glycogen is broken down by?

A
  1. Glycogen phosphorylase-P: remove glucose residues from non-reducing end
  2. Glucan transferase: debranch
  3. Alpha-1,6-glucosidase: cleave a1-6 branch
31
Q

Where is GLUT 2 & GLUT 4 located?

A

2: liver
4: muscle

32
Q

In feeding state how is glycogen stimulated to be made (processes)?

A
  1. insulin released
  2. stimulates protein phosphatase-1 => activate glycogen synthase
  3. glycogen produced
33
Q

in fasting state how is glycogen stimulated to be broken down? (process)

A
  1. glucagon & epiniphrine (adrenaline)
  2. => Inc. cAMP => Inc. protein kinase => phosphorylase kinase => activates glycogen phosphorylase-P
  3. break down glycogen = glucose
34
Q

Name of the disease that’s characterised by accumulation of abnormal amounts or types of glycogen in tissues

A

glycogen storgae disease (GSD)

35
Q

difference of GSD type 1a, 1b, 1c & 1d (deficiency in)

A

1a: G1Pase deficient
1b: Translocase T1 deficient
1c: Translocase T2 deficient
1d: transporter that translocates free glucose molecules

36
Q

GSD type 2 (aka Pompe disease) is due to (a) deficiency and _ _ _ in most tissues is detected

A

a. alpha-1,4-glucosidase

b. normally structured glycogen

37
Q

GSD type 3 has glycogen deposited in _ & _

A

liver & skeletal muscles

38
Q

Diagnosis for people w/ GSD. And how blood glucose levels ae maintained throughout the night (2 ways)

A

a. biopsy of muscle of liver tissue
b. - carbohydrate solutions through a stomach tube
- uncooked cornstarch every 4-6hrs

39
Q

Which organ has the most important site for gluconeogenesis during starvation?

A

kidney

40
Q

Consuming alcohol may lead to diabetic ketoacidosis and accumulation of ——-, inhibit the process of gl_ bc it prevents _

A

NADH
gluconeogenesis
oxidation of lactate to pyruvate