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GI > Metabolic Pathways > Flashcards

Metabolic Pathways Flashcards

1
Q

what is glycogenesis

A

synthesis of glycogen from glucose

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2
Q

what is glycogenolysis

A

breakdown of glycogen to from glucose

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3
Q

what is glycogen

A

major storage molecule of glucose

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4
Q

where is glycogen stored

A

in the liver and in muscle

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5
Q

what is the role of liver glycogen

A

broken down into individual glucose molecules which are released into bloodstream to supply other organs with energy inbetween meal times

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6
Q

what is the role of muscle glycogen

A

can only be used by muscles, not available for maintenance of blood glucose levels.
provides energy via glycolysis and the TCA during bursts of physical activity

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7
Q

what causes glycogenolysis to fluctuate

A

meal times

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8
Q

what is the primary source of glucose overnight when hepatic glycogen is depleted

A

gluconeogenesis

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9
Q

what accounts for the majority of glucose in blood after meals

A

dietary carbohydrates

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10
Q

what is glycogen made of

A

polymer of glucose molecules

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11
Q

how are the glucose molecules in glycogen bonded

A

alpha 1-4 glycosidic links (between carbons 1 and 4)

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12
Q

how are branches introduced into a glycogen molecule

A

via an alpha 1-6 glycosidic chain

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13
Q

what reaction facillitates glycogenolysis

A

phosporolysis

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14
Q

how is glucose added to glycogen

A

can only be added to existing glycogen chain ( a glycogen primer of glycogenin protein with at least four glucoses attached)

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15
Q

how is glucose trapped inside a cell

A

is phosphorylated to form glucose-6-phosphate

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16
Q

what happens to glucose 6 phosphate when energy s recquired

A

glycolysis

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17
Q

what happens to glucose 6 phosphate when there is no need for energy

A

converted to glycogen

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18
Q

describe how glucose 6 phosphate is activated

A

glucose 6 phosphate -> glucose 1 phosphate (phosphate group moved from carbon 6 to 1), UDP- glucose

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19
Q

how is UDP- glucose added to glycogen

A

covalently bonds, UDP left over is phosphorlyated into UTP.

process uses 1 ATP

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20
Q

what are the functional groups of UDP-glucose

A

nucleotide like ATP:

uracil base, ribose sugar, two phosphate groups, attached to second phosphate group is glucose

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21
Q

what are simple precursors converted to

A

activated intermediates

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22
Q

what is the activated forms of phosphate and glucose

A

ATP

acetyle- CoA

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23
Q

what is glucose synthase

A

synthesises glucose from UDP glucose- cannot start new chain or introduce branchd

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24
Q

what is the rate limiting enzyme of glycogenesis

A

glycogen synthase

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25
Q

what is the branching enzyme of glycogen

A

transglyosylase

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26
Q

what catalyses glycogenolysis

A

glycogen phosphorylase

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27
Q

what is the rate limiting step of glycogenolysis

A

when glucose group cleaved from glycogen and adds a phosphate group to it so the product is glucose-1-phosphate

catalysed by glycogen phosphorylase

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28
Q

what is glycogenolysis

A

when glucose removed from its stored form of glycogen

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29
Q

where can glucose be de phosphorlyated

A

in liver NOT skeletal muscle

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30
Q

briefly list the steps of glycogenolysis

A

glycogen-> glucose 1 phosphate-> glucose 6 phosphate -> either:
-glycolysis if energy needed or (in liver only) deposphorlyated -> glucose released into blood via GLUT2 transporter

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31
Q

what regulates both glycogenesis and glycogenolysis

A

hormomes

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32
Q

what stimulates the synthesis of glycogen and how

A

insulin- signals availability of carbs in the bloodstream, stimulates the synthesis of glyocgen

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33
Q

what inhibits the synthesis of glycogen

A

glucagon- hormone of starving state, stimulates the breakdown of glycogen and glycogen phosphorylase,

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34
Q

what stimulates the breakdown of glycogen and how

A

glucagon, adrenaline and cortisol- allow rapid mobilisation of glycogen stores,stimulate glycogen phosphorylase

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35
Q

what inhibits the breakdown of glycogen

A

insulin

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36
Q

what are glycogen storage diseases and what causes them

A

group of disease with increased glycogen deposits in liver or muscle or both

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37
Q

what is glycolysis

A

the breakdown of glucose by enzymes releasing energy and pyruvic acid

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38
Q

what are the three phases of glycolysis

A

stage 1 - glucose is trapped and destabilised

stage 2 - two interconvertible three carbon molecules are formed

stage 3 generation of ATP

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39
Q

what is the overall reaction of glycolysis

A

glucose + 2 ADP + 2 Pi + 2 (NAD+)
->
2 pyruvate + 4 ATP + 2 H2O + 2 NADH + 2 (H+)

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40
Q

describe the process of glycolysis

A

glucose – (2 ATP -> 2 ADP) –> fructose- 1, 6- bisphosphate –> 2 triose phosphates – ( 4 ADP -> 4ATP) (2 NAD+ -> 2NADH + 2H+) –> 2 pyruvate

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41
Q

what is the cellular need for glycolysis

A

production of ATP, provision of building blocks for synthetic reactions

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42
Q

how is glycolysis controlled

A

enzymes catalysing irreversible reactions

  • hexokinase: substrate entry
  • phosphofructokinase: rate of flow
  • pyruvate kinase- product exit
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43
Q

what is the fates of the products of glycolysis

A

4 ATP = energy
2 pyruvate = carbon to fuel TCA in mitochondria
2 NADH +2H+ = electron transport chain and ATP synthesis

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44
Q

what is glucogenesis

A

source for new glucose when glycogen stores are delpeted – generates new glucose from non carbohydrate pre cursor molecules, occurs during prolonged starvation when no dietary carbs or glycogen stores depleted

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45
Q

what are the three precursors for glucose in gluconeogensis

A

lactate (lactic acid), amino acids, glycerol

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46
Q

why is pyruvate converted to lactic acid

A

during anaerobic resp to convert NAD+ to NADH

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47
Q

where is lactate synthesised

A

in skeletal muscle during anaerobic synthesis

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48
Q

where are amino acids derived from

A

muscle protein by proteolysis

49
Q

where is glycerol derived from

A

from triglycerides by lipolysis in adipose tissue

50
Q

does gluconeogenesis require or release energy

A

very energy expensive

51
Q

where does gluconeogenesis happen

A

mainly in the liver, small amounts in the kidney

52
Q

what is gluconeogenesis is relation to glycolysis

A

the reverse

53
Q

what allows gluconeogenesis to be the reverse of glycolysis as this has irreversible reactions

A

special enzymes that are able to bypass the irreversible reactions

54
Q

what does gluconeogensis proceed via

A

the synthesis of oxaloacetate in the mitochondria

55
Q

can all amino acids be precursors for gluconeogenesis

A

no but majority can be

56
Q

what is oxaloacetate

A

immediate in the TCA cycle that accepts acetyl groups, can be synthesised from pryuvate

57
Q

how many pyruvates are needed to make a glucose

A

2 as pyruvate 3 carbon molecule, glucose 6 carbon molecule

58
Q

how much ebergy is needed to make one molcule of glucose in gluconeogensis

A

equivalent of 6 ATP (4 ATP and 2 GTP)

59
Q

how much energy does glycolysis produce from every glcose oxidised

A

2 ATP

60
Q

what is lactate a precursor of

A

gluconeogenesis

61
Q

where is lactate generated

A

in muscles under anaerobic conditions

62
Q

how does lactate reach the liver

A

carried in the blood stream- is a polar molecule

63
Q

what happens to lactate when it reaches the liver

A

enzymes covert it to pyruvate and the glucose using 6 atp

64
Q

why is gluconeogenesis in the liver important

A

Means neither liver or bloodtsream acidifies too much, takes metabolic burden way from the muscle

65
Q

how are amino acids grouped

A

either

  • ketogenic (cannot be used for making glucose)
  • glucogenic (can be used as precursors for gluconeogensis)
66
Q

how can glucogenic amino acids enter the TCA cycle

A

either as amino acids or be converted into pyruvate

67
Q

what can any molecule that can be converted to pyruvate also be converted to

A

oxaloacetate

68
Q

how can ketogenic amino acids enter the tca cycle

A

converted into acetyl CoAor acetyoacetyl CoA and can enter only if oxaloacetate present to accept it

69
Q

at which two levels is glycolysis and gluconeogenesis regulated

A

system level: hormones

individual cells level: allosteric effectors

70
Q

which hormones regulate gluconeogenesis and how

A

, glycagon signals a need for glucose therefore stimulates gluconeogenesis and inhibits glycolysis.

Insulin signals availability of glucose so inhibits gluconeogenesis and stimulates glycolysis

71
Q

what allosteric effectors regulate gluconeogenesis and how

A

amp/ adp signal the requirement for energy, stimulate glycolysis and inhibit glucneogeneis as energetically expensive

ATP singals high availbality of energy inhibits glycolysis and stimulates gluconeogenesis

Fructose 2,6-bisphosphate is a intermediate of glycolysis that is in high con in fed state and low con in starved state. Stimulates glycolysis in high conc and inhibit glucneogensis

72
Q

what are citrate, alanine and acetyl-CoA

A

important pre cursor molecules for biosynthetic processes, all present at high conc when intermediates for building blocks for biosynthetic processes are abundant, high conc stimulate glucoenogensis and inhibit glycolysis

73
Q

what is fat intake and deposit of fat associated with

A

human disease

74
Q

what does increase fat intake without appropriate energy expenditure lead to

A

increase in numbers of adipocytes, more fat deposits in adipocytes (obesity)

75
Q

what does the control of energy balamce depend on

A

genetically linked factors (protein messengers regulating appetite)

environmental factors (food abundance and fashionable food)

76
Q

why is fat required

A

energy source,
for essential fatty acids (required but cannot be synthesised-polyunsaturated),
fat soluble vitamins (A, D, E & K- stored in and up-taken in fat)

77
Q

what can deficiencies in essential fatty acids lead to

A

membrane disorders:

increased skin permeability, mitochondrial damage- reduction in energy generation

78
Q

give examples of simple lipids

A

fatty acids, triglycerides, waxes (protective fats on animal hair)

79
Q

give examples of compound lipids

A

fats associated with other compound groups

phospho-, glyco- lipids, lipoprotein

80
Q

steroids

A

cholesterol, steroid hormones

81
Q

name the different types of lipid

A

simple, compound and steroid

82
Q

describe the structure lipids

A

predominantly hydrocarbon (hydrophobic), usually contain long chain fatty acids, insoluble in water

83
Q

what is the main energy storage form in adipose tissue

A

triglycerides

84
Q

what are triacylglycerols

A

triglycerides

85
Q

what is the main source of energy in our diet

A

triglycerides

86
Q

how are triglycerides stored

A

compact as dont need concomitant storage of water as hydrophobic- high energy yield per gram

87
Q

what is the structure of triglycerides

A

glycerol and three fatty acids
each of the three hydroxyl groups of the glycerol is esterified with the carboxyl of the fatty acid to make a triacylgylcerol

88
Q

what is the structure of fatty acids

A

long, straight chain hydrocarbon with a carboxly (acid) group at one end
aliphatic (no rings)
usually contain an even number of carbon atoms

89
Q

what are the types of fatty acid

A

saturated (no double bonds)
unsaturated (1 double bond)
polyunsaturated (several double bonds)

90
Q

what configuration are double bonds in in fatty acids

A

usually cis (within the same plane) not trans (opposing sides)

91
Q

what is the most common fatty acid in humans

A

plamitic

92
Q

what does the number 16:0 mean in palmitic acid

A

number of carbons: number of double bonds

93
Q

what are the numbers for stearic and oleic acis

A

stearic 18:0

oleic 18:1

94
Q

describe the prevalence of polyunsaturated fatty acids and give an example

A

Occur only in small amounts
many can not be synthesised by the body
essential fatty acids
e.g. linoleic acid (18 : 2):

95
Q

what is the limit for the body making double bonds

A

9 carbons away from the carboxyl group- past this cant make double bond (further than 9= essential fatty acid)

96
Q

what are the two ways of naming the carbons in fatty acids

A

Either: carboxyl group is C-1
Or:
C adjacent to carboxyl group is alpha carbon
C furthest away is omega carbon
(omega 3 fatty acid- double bond away from omega carbon)

97
Q

what short do fatty acids have to be to be liquid at room temp

A

8 or less

98
Q

what does the presence of double bonds do to the melting point

A

reduce it dramatically

99
Q

what is the difference between plant and animal fats

A

plant= large proportions of unsaturated fatty acids- liquid

animals= mostly palmitic and stearic acid- solid

100
Q

what are the main products of fat digestion

A

glycerol, fatty acids, monoglycerides (glycerol molecule with fatty acid still attached)

101
Q

where is glycerol absorbed

A

in intestinal epithelial cells

102
Q

where are the products of fat digestion absorbed

A

into epithelial cells lining the intestine (mucosal cells)

103
Q

what fatty acids can enter the portal blood directly

A

short and medium length ones

104
Q

what has to happen to longer chain fatty acids and monoglycerides so they can be absorbed

A

are re-synthesised to triglycerides

105
Q

what are chylomicrons

A

type of lipo protein that is transportable in the blood stream-made of newly absorbed triglycerides that have been coated with protein, phosholipids and cholesterol

106
Q

where do chylomicrons go after they are formed in mucosal cells

A

Enter lymph, then the blood stream
At muscle and adipose tissue, chylomicrons are attacked and cleaved by lipoprotein lipases
(way of transporting fat to any tissue that need it)

107
Q

what happens when chylomicrons are cleaved at muscle and adipose tissue

A

fatty acids left are

  • resynthesised into triacylglycerols (in adipose tissue, for storage)
  • oxidised to provide energy (in muscle)

(depends on amount of FA available)

108
Q

what is the breakdown of lipids cause and caused by

A

lipolysis

hormone sensitive lipases

109
Q

when does lipolysis of stored fat occur and what happen

A

when energy is needed, releases free fatty acids and glycerol

110
Q

what regulates hormone sensitive lipases

A

hormones e.g. adrenaline sensitive is inhibited by adrenaline

111
Q

what do fatty acids have to converted to before they can be oxidised to make energy, how does this happen

A

CoA derivatives (activated)- this is done by linking the acid to CoA which happens in the cytoplasm and requires equivalent of 2 ATP= making acyl- CoA

112
Q

why and how does acyl-CoA need to be transported to the mitochondrial matrix

A

for further oxidation of the fatty acids

transported there by special carrier mechanism called the carnitine shuttle (as acyl-carnitine)

net result acyl-CoA located in mitochondrial matrix

113
Q

what is beta oxidation

A

a series of reactions that happen in the mitochondrial matrix and produces:
1 acetyl-CoA
1 FADH2
1 NADH + H+
1 fatty acyl-CoA, shortened by 2 carbon atoms

114
Q

why is the beta oxidation reaction repeated 8 times

A

to increased yield for:
- FADH2, NADH and H+ used for ATP generation in oxidative phosphorylation

  • acetyl-CoA oxidised in TCA cycle to CO2
115
Q

what is the P/O ratio

A

amount of ATP that can be generated for the reduction of a single oxygen to water (for complete oxidation of stearic acid 120 ATP compared to glucose 30 ATP)

116
Q

what do additional pathways require

A

additional enzymes

117
Q

what happens to the glycerol in the break down of fatty acids

A

is phosphorylated and activated to glycerol 3 phosphate and enters mainstream metabolism as can be converted to substrate for glycolysis- can present in liver and kidney but absent from adipose tissue, skeletal and heart muscle

118
Q

describe ketone bodies

A

Formed in liver mitochondria
from acetyl-CoA from b oxidation
contain ketone groups (hyrdophillic)
Diffuse into the blood stream and to peripheral tissues
Important molecules of energy metabolism for heart muscle and renal cortex
converted back to acetyl-CoA, which enters TCA cycle

119
Q

why cam ketosis cause problems in starvation or diabetes

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 (i.e. heart, brain, etc.)

ketone bodies are moderate acids

accumulation leads to severe acidosis (blood can’t buffer any more)

impairs tissue function, particularly central nervous system

smell of acetone can be detected in breath

GI (64 decks)

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