4. Glycogen & Fat Flashcards

1
Q

By what mechanism do adrenaline and glucagon regulate the enzymes in glycogenesis/lysis?

A

Phosphorylation

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2
Q

By what mechanism does insulin regulate the enzymes in glycogenesis/lysis?

A

Dephosphorylation

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3
Q

How is the regulation of muscle glycogen stores different from liver stores?

A

Glucagon has no effect

AMP is an allosteric regulator

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4
Q

What are 2 glycogen storage diseases?

A

McCardle

Von Gierke’s

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5
Q

What enzyme is deficient in McCardle disease?

A

Muscle glycogen phosphorylase

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6
Q

What symptoms would you expect to see in McCardle disease?

A

Exercise intolerance, exhaustion as cannot mobilise skeletal muscle glycogen stores.
Hypoglycaemic.

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7
Q

What enzyme is deficient in Von Gierke’s disease?

A

Glucose - 6 -Phosphorylase

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8
Q

What changes do you see in the liver in patients with Von Gierke’s disease and why?

A

Hepatomegaly as the liver cannot release it’s glycogen stores.
Hypoglycaemic

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9
Q

What enzyme catalyses the conversion of Glucose -1P to UDP- glucose?

A

GTP- uridyltranferase

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10
Q

Which enzyme does muscle lack?

A

Glucose-6- phosphorylase

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11
Q

How long after eating do glycogen stores run out and gluconeogenesis begin?

A

8 hours

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12
Q

Where does gluconeogenesis happen?

A

Liver and kidney cortex

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13
Q

What are the 3 precursors used in gluconeogenesis?

A

Lactate (cori cycle)
Glycerol
Amino acids - alanine particularly

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14
Q

Which 3 enzymes are needed in gluconeogenesis to bypass irreversible steps in glycolysis?

A
  1. PEPCK
  2. Fructose-1,6-bisphosphatase
  3. Glucose-6-phosphatase
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15
Q

What reaction does PEPCK catalyse?

A

Oxaloacetate -> phosphoenolpyruvate

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16
Q

What reaction does fructose-1,6-bisphosphatase catalyse?

A

Fructose-1,6-bisphosphate -> Fructose-6-P

17
Q

What reaction does glucose - 6-phosphatase catalyse?

A

Glucose-6P -> Glucose

18
Q

Which 2 enzymes are more important for the regulation of gluconeogenesis?

A

PEPCK and Fructose-1,6-bisphosphatase

19
Q

What type of receptor is the glucagon receptor?

A

GPCR

20
Q

What type of receptor is the cortisol receptor?

A

Nuclear

21
Q

What type of receptor is the insulin receptor?

A

Tyrosine kinase

22
Q

Which 2 hormones increase gluconeogenesis?

A

Cortisol, Glucagon

23
Q

What effect does insulin have on gluconeogenesis?

A

Inhibits both PEPCK and F-1,6-BP

24
Q

What is the key regulatory enzyme in lipogenesis?

A

Acetyl CoA carboxylase

25
Q

How is AcetylCoA carboxylase regulated?

A

Stimulated by insulin and citrate

Inhibited by glucagon/adrenaline and AMP

26
Q

Why is Acetyl CoA carboxylase inhibited by AMP?

A

Low energy signal - process of lipogenesis requires ATP and NADPH so won’t happen if no energy.

27
Q

Where does fatty acid synthesis occur?

A

Cytoplasm

28
Q

What are the major energy stores and when are they used?

A

Glycogen- overnight fast and as part of the response to stress and exercise. (1-10 hours)
TAGs - starvation, prolonged exercise, stress
Protein - emergency during starvation

29
Q

What happens to the fatty acids once they are taken up by adipose and muscle cells?

A

Re-esterified to triacylglycerols using glycerol phosphate derived from glucose metabolism.

30
Q

Why do individuals with a defect in the enzyme LCAT produce unstable lipoproteins of abnormal structure?

A

The spherical shape of lipoproteins is dependent on the ratio of core:surface lipids. As the core gets depleted, LCAT converts surface lipid cholesterol to cholesterol esters, a core lipid. This maintains stability.

31
Q

What is the clinical consequence of LCAT deficiency?

A

Lipid deposits occur in many tissues and atherosclerosis is a serious problem.