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Gastroenterology > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

Glycogenesis definition

A

Synthesis of glycogen from glucose

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2
Q

Glycogenolysis definition (2)

A

Breakdown of glycogen to form glucose

Fluctuates dependent upon meal times

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3
Q

Gluconeogenesis definition (2)

A

Synthesis of glucose from precursor substrates (lactate, amino acids, glycerol)
Primary source of glucose when hepatic glycogen is depleted

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4
Q

Main storage forms of glucose (2)

A

Liver glycogen

Muscle glycogen

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5
Q

Liver glycogen use

A

Released to maintain blood glucose levels for RBCs and brain - Glucose 6-phosphate can be dephosphorylated here

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6
Q

Muscle glycogen uses (2)

A

Not available for blood glucose maintenance levels - Glucose 6-phosphate CANNOT be dephosphorylated here
Provides energy via glycolysis and Krebs cycle during exercise

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7
Q

Glycogen structure (4)

A

Polymer of glucose molecules
Joined by alpha 1-4 glycosidic bonds
Branches are introduced by alpha 1-6 glycosidic links
Accomplished from phosphorolysis NOT hydrolysis

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8
Q

Glycogen and Glycogenin (3)

A

Glucose residues can only be added to an existing glycogen chain
A glycogen primer containing at least 4 glucose residues is required
The primer is covalently attached to an enzyme - Glycogenin

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9
Q

Glycogen synthesis pathway (5)

A

Glucose => Glucose-6-phosphate => Glucose-1-phosphate => UDP-glucose => [Glucose]n+1 + UDP

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10
Q

Uridine diphosphate glucose (2)

A

An activated form of glucose

The phosphate ester linkage in UDP (a nucleotide sugar) releases free energy on hydrolysis

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11
Q

Transglycosylase

A

A branching enzyme introducing alpha 1-6 glycosidic branches every 10 glucose residues into glycogen

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12
Q

Glycogenolysis reaction (3)

A

Catalysed by glycogen phosphorylase
[Glucose]n + Pi => Glucose-1-phosphate + [Glucose]n-1 - Rate limiting step of glycogenolysis
One glucose molecule is cleaved off the ends of glycogen at a time

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13
Q

Gluconeogenesis characteristics (6)

A

Occurs in prolonged starvation
Energy is obtained from fatty acid oxidation from adipose tissue
Happens in liver and kidney
IT IS NOT THE REVERSE OF GLYCOLYSIS - Requires unique enzymes to overcome energetically unfavorable steps
Proceeds via the synthesis of oxaloacetate in mitochondria - Vital for accepting acetyl groups from fat breakdown
Rate limiting step by passing pyruvate kinase

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14
Q

Gluconeogensis formula

A

2 pyruvate + 4ATP + 2GTP + 2NADH + 4 H+ + 6H2O

=> glucose + 4ADP + 2GDP + 6Pi + 2NAD+ + 2H+

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15
Q

Cori cycle (Lactic Acid cycle) (6)

A

Lactate is precursor of gluconeogenesis
Blood transports lactate to liver
Liver converts lactate back to glucose
Glucose released into bloodstream
Cycle buys time and shifts metabolic burden from muscle to other organs
Amino acids and glycerol can act as precursors too

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16
Q

Reciprocal regulation (4)

A

High AMP or ADP - Low energy
High ATP - High energy
Fructose 2,6-bisphosphate - High in fed state and low in starved state
Citrate, alanine, acetyl-CoA - High when intermediates or building blocks are abundant

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17
Q

Insulin hormonal regulation effects (3)

A

Promotes glycolysis

Inhibits gluconeogenesis and glycogenolysis

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18
Q

Glucagon hormonal regulation (2)

A

Inhibits glycolysis

Promotes gluconeogenesis

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19
Q

Hormones inhibiting glycogen phosphorylase

A

Insulin

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20
Q

Hormones promoting glycogen phosphorylase (3)

A

Glucagon
Adrenaline
Cortisol

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21
Q

Hormones increasing glycogen synthase

A

Insulin

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22
Q

Hormones decreasing glycogen synthase

A

Glucagon

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23
Q

Rate limiting enzymes in gluconeogenesis (3)

A

Glucose-6-phosphate
Fructose 1,6 biphosphate
PEP carboxykinase

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24
Q

Increased fat intake without appropriate energy expenditure leads to (2)

A

Increase in numbers of adipocytes

More fat in adipocytes

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25
Q

Fat is needed for (3)

A

Energy source
Some PUFAs cant be made in body - Deficiencies can lead to membrane disorders, increased skin permeability, mitochondrial damage
Uptake of lipid soluble vitamins A, D, E and K

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26
Q

Lipids characteristics (4)

A

3 types - Simple, compound and steroids
Predominantly hydrocarbon
Usually contain long chain fatty acids
Insoluble in water

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27
Q

Triglycerides/Triacylglycerols properties and structure (5)

A 
Main energy storage form in adipose tissue
Compact - Don’t require storage of water
Hydrophobic
High energy yield per gram
Structure is glycerol with 3 fatty acids
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28
Q

Fatty acids property and structure (6)

A

Mainly straight chains
Aliphatic (no rings)
Usually contain an even number of carbon atoms (2 - 20 or more)
Branched chains and odd numbers of carbon are rare
Can be saturated, unsaturated, polyunsaturated
Double bonds usually in cis configuration

29
Q

PUFAs (4)

A

More than 1 double bond
Only in small amounts but essential
Cant be synthesised in body
Example is linoleic acid

30
Q

Fatty acids nomenclature (2)

A

Carbon adjacent to carboxyl group is alpha carbon

Carbon furthest away is omega carbon

31
Q

Fatty acid melting point variation (2)

A

Fatty acids with 8 carbons are liquid at room temperature - Longer ones are solid
Double bonds lower melting point

32
Q

Fat absorption (5)

A

Main products of fat digestion are glycerol, fatty acids, monoglycerides
They are absorbed into mucosal cells of intestine
Short and medium-length fatty acids enter portal blood
Longer chain FA and monoglycerides are re-synthesised to triglycerides
Coated with a layer of protein, phospholipid, cholesterol - Chylomicrons

33
Q

Chylomicrons pathways (3)

A

Enter lymph, then the blood stream
At muscle and adipose tissue, chylomicrons are attacked and cleaved by lipoprotein lipases
Free fatty acids are resynthesised into TAGs in adipose tissue or oxidised for energy

34
Q

Lipolysis (2)

A

Breakdown of lipids

Initial cleavage by hormone sensitive lipases - Releases free fatty acids and glycerol when energy is needed

35
Q

Activation of fatty acid oxidation (3)

A

Occurs in cytoplasm
Requires 2 ATP
Fatty acid + CoA => Acyl-CoA

36
Q

Carnitine shuttle (4)

A

In cytoplasm, fatty acids are transferred from acyl-CoA to carnitine
Acyl-carnitine transporter in inner membrane - Facilitates antiport of acyl-carnitine into the mitochondrion and carnitine out
Net result is acyl-CoA in mitochondrial matrix
Rate limiting step of fatty acid conversion to ATP

37
Q

Beta oxidation (3)

A

Occurs in mitochondrial matrix
4 steps in each cycle
Products are 1 acetyl-CoA, 1 FADH2, 1 NADH + H+, 1 fatty acyl-CoA shortened by 2 carbon atoms

38
Q

Yield of beta oxidation for stearic acid (C18) (5)

A

Cycle is repeated 8 times - For even numbered fatty acids follows (n/2)-1
8 FADH2, 8 NADH + 8 H+
9 acetyl-CoA which is oxidised in Krebs cycle - Makes 9 FADH2, 27 NADH + 27 H+, 9 GTP
P/O ratio is 1.5 for FADH2 and 2.5 for NADH + H+
Total yield is 17 x 1.5 + 35 x 2.5 + 9 – 2 = 120 ATP (Minus 2 from activation step)

39
Q

Glycerol breakdown (2)

A

Activated to glycerol-3-phosphate by glycerol kinase

Dehydrogenated to dihydroxyacetone phosphate

40
Q

Ketone bodies production and function

A

Formed in liver mitochondria from acetyl-CoA from beta oxidation
Vital for energy metabolism for heart muscle and renal cortex - Converted back to acetyl-CoA which enters Krebs cycle

41
Q

Ketosis in starvation and diabetes (8)

A

Oxaloacetate is consumed for gluconeogenesis
Fatty acids are oxidised to provide energy
Acetyl-CoA is converted to ketone bodies
High levels in blood
Too much for extrahepatic tissue (heart, brain)
Accumulation leads to severe acidosis
Impairs tissue function, particularly CNS
Smell of acetone can be detected in breath

42
Q

Lipogenesis definition and characteristics (4)

A

Fatty acid synthesis
Occurs in liver, kidney, glands, brain and adipose tissue
Takes place during excess energy intake
A reductive process as electrons are needed

43
Q

Excess carbohydrates and fatty acids (3)

A

Conversion to fatty acids and triglycerides in the liver
Free fatty acids are transported in plasma bound to albumin
Triglycerides are transported to adipose tissue by VLDL for storage

44
Q

Generation and transport of acetyl-CoA for lipogenesis (3)

A

Generated by pyruvate dehydrogenase complex in mitochondria
Inner mitochondrial membrane is impermeable to acetyl-CoA
Citrate transports acetyl groups into the cytoplasm - Citrate is formed by condensation of acetyl-CoA with oxaloacetate (1st Krebs cycle step)

45
Q

Malonyl-CoA (2)

A

Direct precursor of Acetyl-CoA activation - Formed by Acetyl-CoA carboxylase
Donates carbon atoms to new lipid

46
Q

Acetyl-CoA carboxylase (2)

A

Expressed in liver and adipose tissue

Essential regulatory enzyme for Acetyl-CoA activation

47
Q

Fatty acid synthase (4)

A

Catalyses synthesis of saturated long-chain fatty acids from malonyl-CoA, acetyl-CoA, and NADPH
Exists as a single polypeptide chain with 7 distinct enzyme activities
Catalyses fatty acid synthesis in 4 steps - Condensation, reduction, dehydration, reduction and release
Contains an acyl-carrier protein (ACP)

48
Q

Lipogenesis by fatty acid synthase (5)

A

Using acetyl-CoA and malonyl-CoA as precursors, one cycle of reactions adds 2 carbon atoms to the growing acyl chain
Derived from malonyl-CoA
Growing acyl chain is attached to ACP
Requires NADPH as electron donor
When a length of C-16 is reached, the fatty acid is released

49
Q

Essential enzyme in regulating fatty acid synthesis and degradation

A

Acetyl-CoA carboxylase

50
Q

Acetyl-CoA carboxylase regulation (4)

A

Insulin signals fed state - Stimulates fuel storage and protein synthesis
Glucagon signals starved signals (epinephrine signals required for energy) - Mobilizes glycogen stores
Citrate levels are high when acetyl-CoA and ATP are abundant
Antagonised by palmitoyl-CoA - Abundant in fatty acids excess

51
Q

Triglyceride synthesis requirements (4)

A

Requires glycerol-3-phosphate
Liver produces G-3-P from glycerol
Adipose tissue produce G-3-P from glucose - Only during fed state
Involves esterification

52
Q

Where and why are amino acids degraded (2)

A

Occurs in liver

Due to no storage form for amino acids if not used as building blocks

53
Q

Protein turnover (3)

A

Damaged proteins have to be removed
Tightly regulated by AMP kinase
Takes place at various rates

54
Q

Amino acids and nitrogen (2)

A

Amino acid breakdown produces ammonia (NH3) and ammonium ions (NH4+)
NH4+ is toxic at high concentrations

55
Q

Major nitrogen-containing excretory molecules (4)

A

Urea
Uric acid
Creatinine
Ammonium ion

56
Q

Synthesis of urea steps (3)

A

Transamination
Deamination
Urea cycle

57
Q

Transamination (3)

A

Aminotransferases move the amino group from alpha-amino acids to alpha-keto acids - Usually alpha-ketoglutarate giving glutamate
For transport to liver, amino group of glutamate is transferred to pyruvate, giving alanine or glutamine synthase adds NH4+ to glutamate giving glutamine
Alanine and glutamine are major carriers of nitrogen in the blood to liver

58
Q

Deamination (3)

A

Occurs in liver
Amino group of glutamate is converted to free ammonium ion
Urea is synthesised in complex reactions - One nitrogen from free ammonium, the other from aspartic acid and carbon from CO2

59
Q

Identify precursors of urea cycle (2)

A

Ornithine

Carbamoyl phosphate

60
Q

Urea cycle overall reaction

A

CO2 + NH4+ + Asperate + 2H2O => Urea + 2ADP +2Pi + AMP + PPi + Fumarate

61
Q

Fumarate in urea cycle function

A

Its conversion to malate enables its carbon to be transported back to the mitochondrial matrix via malate-aspartate shuttle

62
Q

Degradation of carbon skeletons of amino acids

A

After alpha amino group removal remaining carbon skeleton are converted to glucose or oxidised in Krebs cycle

63
Q

Ketogenic amino acids (2)

A

Degraded to acetyl-CoA or acetoacetyl-CoA

Gives rise to ketone bodies or fatty acids

64
Q

Glucogenic amino acids (2)

A

Degraded to pyruvate or Krebs cycle intermediates

Can be converted into phosphoenolpyruvate (PEP) and then glucose

65
Q

Alcaptonuria disorder

A

Degradation of phenylalanine and tyrosine is blocked

66
Q

Maple syrup urine disease (4)

A

Degradation of valine, isoleucine, and leucine is blocked
Urine smells like maple syrup
Causes mental and physical retardation
Prevented by appropriate diet

67
Q

Phenylketonuria disorder (3)

A

Phenylalanine accumulates in all body fluids
Leads to severe mental retardation
Therapy is low phenylalanine diet

68
Q

Urea cycle disorders (4)

A

Caused by defect in urea cycle enzyme
Leads to accumulation of urea cycle intermediates and glutamine in circulation
Alpha-ketoglurarate is no longer regenerated as levels become too low to fix more free ammonium ions
Treatment is gene therapy, low-protein diet or drugs that remove nitrogen by forming complexes

69
Q

Glycogen synthase (5)

A 
Synthesises glycogen from UDP-glucose
Adds one glucose molecule to glycogen at a time
Can only extend the chains of glycogen
Can not introduce branches
Rate limiting enzyme of glycogenesis

Gastroenterology (11 decks)

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