GI Biochem Flashcards

1
Q

Glycogenesis

A

Synthesis of glycogen from glucose

Main storage form

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2
Q

Liver glycogen

Muscle glycogen

A

Liver glycogen /

• Broken down between meals and released to maintain blood glucose levels for RBCs and brain

Muscle Glycogen /

  • Not available for maintenance of blood glucose levels
  • Provides energy via glycolysis and the TCA during exercise
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3
Q

The liver keeps blood/sugar levels…

A

Constant between meal times

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4
Q

What process happens at night when liver glycogen stores have been depleted?

A

Gluconeogenesis

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5
Q

What is at the centre of glycogen? (protein)

A

Glycogenin

Catalytic activity

Can add up to 4 glucose molecules to itself

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6
Q

Glucose can only be added to…

A

an existing glycogen chain

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7
Q

What is needed for glucose to attach?

A

A glycogen “primer”

This primer is covalently attached to glycogenin

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8
Q

Glucose –> G-6-P catalysed by?

A

Hexokinase

and ATP

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9
Q

G-6-P –> G-1-P

A

By phosphoglucomutase

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10
Q

G-1-P –> UDP glucose

A

UDP glucose is the activated form of glucose

by pyrophosphorylase

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11
Q

UDP glucose acts as a substrate for

A

Glycogen synthase

to gie GLYCOGEN + UDP

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12
Q

How many ATP are used to attach one glucose to glycogen?

A

1 ATP molecule

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13
Q

Glycogen synthase is the ____ limiting enzyme of glycogenesis

A

Rate limiting

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14
Q

Branching enzyme (introduces an alpha 1,6 glycosidic branch into glycogen. Which enzyme

A

Transglycosylase

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15
Q

Glycogenolysis

A

Breakdown of glycogen

Catalysed by glycogen phosphorylase

One glucose molecule is cleaved off the ends at a time

G-1-P –> G-6-P by phosphglucomutase

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16
Q

Fates of glycogenolysis?

A

G-6-P —– g-6-p-atase —> Glucose —> Blood (via GLUT2)

Glycolysis to muscles

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17
Q

INSULIN

A

Stimulates synthesis of glycogen
Stimulates synthase (storage)
Inhibits phosphorylase

inhibits gluconeogenesis

stimulates glycolysis

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18
Q

GLUCAGON

A

Signals lack of glucose in blood stream
Stimulates glycogen phosphorylase (breakdown)
Inhibits glycogen synthase

stimulates gluconeogenesis

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19
Q

Adrenaline & cortisol

A

Both stimulate glycogen phosphorylase (breakdown)

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20
Q

Gluconeogenesis

what is it?
when does it happen?

A

Synthesis of glucose within the body from NON-CARBOHYDRATE precursors

Prolonged starvation (when glycogen stores are depleted)

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21
Q

Gluconeogenesis - precursor molecules

A

Lactate - anaerobi cconditions

Amino acids - derived from muscle protein by proteolysis

Glycerol - derived from triglycerides by lipolysis in adipose tissue

22
Q

Is gluconeogenesis energy consuming?

A

Very much

6 ATP

23
Q

Is gluconeogenesis the reverse of glycolysis?

A

NOOOOOOOOOOOOO

24
Q

How many enzymes does gluconeogenesis require?

A

4

Proceeds via synthesis of OXALOACETATE in mitochondria

25
Q

Lactic acid (cori) cycle - lactate (precursor)

A

Precursor for gluconeogenesis (anaerobic)

Blood transports lactate to liver

Liver converts lactate to glucose

26
Q

Amino acids (precursor molecule)

A

2 classes/

  • Ketogenic - can’t be used for making glucose
  • Glucogenic - CAN be used for making new glucose
27
Q

Lipid catabolism

A

Increased fat intake
↑ No of adipocytes
more fat in adipocytes
–> Disease

28
Q

Lipids

Simple
Compound
Steroid

A

> Simple lipids (fatty acids, triglycerides, waxes

> Compound lipids (phosphor, glycol, lipo-protein)

> Steroids (cholesterol, steroid hormones)

29
Q

Triglycerides

A

Main energy storage form
Hydrophobic

Glycerol + 3 fatty acids

30
Q

Fatty acids can be…

A

Saturated
Unsaturated
Polyunsaturated (Several double bonds)

Usually in cis config. (hydrogen on same side)

31
Q

Unsaturated fats are essential/non-essential

A

ESSENTIAL

32
Q

What is the main product of fat digestion?

A

Glycerol

absorbed into mucosal cells of intestine

33
Q

What happens to short and medium length fatty acids?

A

They enter portal blood

Longer chains and monoglycerides are resynthesised –> triglycerides

34
Q

What happens to triglycerides?

A

Coateed with protein, phospholipid and cholesterol –> CHYLOMICRONS

enter lymph
then blood stream
at muscle and adipose tissue chylomicrons are cleared by lipoprotein lipases

35
Q

Fatty acid oxidation

A

Occurs in cytoplasm

Requires 2 ATP

Fatty acid + CoA —> Acyl -CoA (not acetyl CoA)

Further oxidation in mitochondra

36
Q

What shuttle moves fatty acids from acyl-CoA to the mitochondria

A

Carnitine shuttle

acyl carnitine into mitochondrion

Acyl breaks off and carnitine is carried out of cell.

Acyl binds with CoA in mitochondrion to from acyl CoA again.

37
Q

Beta-oxidation

A

Acyl CoA is substrate

Massive energy gain

38
Q

Ketone bodies

A

Formed in liver mitochondria

Diffuse into bloodstream and peripheral tissues

Molecules of energy metabolism for heart muscle and renal cortex

39
Q

Ketosis

A

Starvation or diabetes

acetyl CoA converted to ketone bodies because oxaloacetate has been used in gluconeogenesis

Leads to acidosis

Impairs CNS –> coma

Smell of acetone on breath

DEATH

40
Q

Lipogenesis

A

Liver
Excess energy intake

reductive process

41
Q

How are free fatty acids transported in the blood?

A

Albumin

42
Q

What enzyme catalyses synthesis of long chain fatty acids?

A

Fatty acid synthase

From malonyl CoA, acetyl CoA and NADPH (electron donor)

43
Q

Palmitic acid is the

A

longest faty acid produced by FAS

44
Q

What happens to amino acids that are not used as building blocks?

A

Degraded (not stored) in LIVER

45
Q

What are the toxic bi products of amino acid breakdown?

A

NH3 and NH4+

Excreted in urea

46
Q

Urea synthesis

3 steps

A
  1. Transamination/
  • amino group of an amino acid is transferred onto a keto acid
  • forms a keto acid and a new amino acid
  1. De-amination/
  • removal of amino group from glutamic acid in liver
  • resulting in formation of alpha-keto gluterate
  1. Urea cycle
  • free ammonium ion is converted to urea
  • second nitrogen is derived from aspartic acid

(Urea N2H4CO)

47
Q

What are the major carriers of nitrogen in the blood?

A

Alanine and glutamine

48
Q

Carbon skeletons

A

Removal of amino group leaves a carbon skeleton.

Converted into major metabolic intermediates

Can be used for gluconeogenesis or oxidised in TCA cycle

49
Q

Alcaptonuria

A

Degradation of phenylalanine and tyrosine is blocked

50
Q

Maple syrup wine disease

A

Degradation of valine, isoleucine and leucine is BLOCKED

urine smells like maple syrup
mental and physical retardation
appropriate diet

51
Q

Phenylketonuria

A

Phenylalanine accumulates in all body fluids

mental retardation

therapy - low phenylalanine diet