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BIOC192 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

First Law of Thermodynamics

A

Total energy constant

Neither created/destroyed

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2
Q

Anabolism

A

Cellular work

ATP -> ADP + Pi

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3
Q

Catabolism

A

Energy from food

ADP + Pi -> ATP

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4
Q

Eintake =

A

Eexpended + Estored

basal metabolism + activities) + (weight gain

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5
Q

1J =

A

The energy to push 1N of force 1m

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6
Q 
Atwater factors
Fat
Carbohydrates
Protein
Ethanol
A

38
17
17
29

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7
Q

Not all energy available eg

A

Cellulose - loss in faeces as fiber

Nitrogen - not oxidised and excreted in urine

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8
Q

Direct calorimetry

A

Whole body calorimeters
Measure heat output
Good at measuring BMR

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9
Q

Indirect calorimetry

A

O2 and CO2 using respirometer

1 mol O2 at STP = 22.4L

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10
Q

Respiration exchange rate

A

CO2/O2

Determine if fuel used

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11
Q

Basal metabolic rate

A

Energy expenditure at rest

Variation: gender, age, genetics, disease

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12
Q

Increase BMR

A 
Training
Late pregnancy
Fever
Drugs (caffeine)
Hyperthyroidism
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13
Q

Decrease BMR

A

Malnutrition
Sleep
Drug (beta-blockers)
Hypothyroidism

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14
Q

Process of digestion

A

1) Hydrolysis of bonds (b/e connecting monomer units)

2) Absorption of products

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15
Q

Dietary carbonhydrates

A

40 - 50% energy intake

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16
Q

Starch from plants

A

Amylose

Amylopectin

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17
Q

Amylose

A

Linear polymer ⍺(1-4) linked glucose units

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18
Q

Amylopectin

A

Branched polymer ⍺(1-4) & ⍺(1-6) linked units

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19
Q

Cellobiose & lactose =

A

Stereoisomers

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20
Q

Cellobiose

A

Repeating disaccharide unit in cellulose

Mammals don’t have enzyme to hydrolysed β(1-4) bond

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21
Q

Maltase/isomaltase

Maltose/isomaltose ->

A

2 glucose

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22
Q

Sucarse

Surcose ->

A

Fructose + glucose

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23
Q

Lactase

Lactose ->

A

Galactose + glucose

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24
Q

Starch digestion 1

A

Amylase hydrolyse ⍺(1-4) glycosidic bonds = small oligosaccharides
Producing maltose/isomaltose disaccharides

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25
Q

Starch digestion 2

A

At brush border

Disaccharides -> monosaccharides

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26
Q

Digestion of protein

A

65g/day

Source of nitrogen an essential animo acid

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27
Q

Deficiency of dietary protein

A

Kwashiorkor

Osmotic imbalance in GI, retention of water

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28
Q

Protein digestion

A

Hydrolyses specific peptide bonds by several proteases

2 stages

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29
Q

All proteases

A

Secreted as inacitve forms

Activated by cleavage of peptides from their structure

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30
Q

Proteases inactive form

A

Zymogens/ proenzymes

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31
Q

Specificity proteases

A

Adjacent a.a side chain

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32
Q

2 stages of protein digestion

A

Endopeptidases

Exopeptidases

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33
Q

Endopeptidases

A

Attack peptide bond within protein polymer

Pepsin, trysin, chymotrysin

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34
Q

Exopeptidases

A

Attack peptide bonds at the ends of protein polymer
Aminopeptidases = N - terminal
Carboxypeptidase = C - terminal

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35
Q

Zyomgen activation

A

Pepsinogen (zymogen) -> pepsin
HCL = parts of pepsinogen unfolds and activates peptin protease
= hyrolysis of pepsinogen = stably activated pepsin

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36
Q

Sequential hydrolysis of proteases

A 
Peptin (stomach)
Trypsin (s.i)
Chymotrypsin (s.i)
Carboxypeptidase (s.i)
Aminopeptidases (s.i)
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37
Q

Bile salt function

A

Solubilize fats

Forms micelles with TAGs (increase SA)

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38
Q

Bile salt structure

A

Hydrophoic and hydrophillic -ve surfaces

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39
Q

Bile salt produced and secreted regulation

A

Produced from cholesterol in liver and stored in gallbladder

Secreted in response to cholecystokinin

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40
Q

Digestion of lipids

A

Pancreatic lipase/colipase enzyme + lipid/aqueous interface of micelles
= hydrolysis triacylglycerol at 1 & 3 of glycerol backbone

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41
Q

Digestion of lipids products

A

Smaller micelles (bile salt, free fatty acids, 2-monoacylglycerol)

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42
Q

Fat malabsorption

A

Excess fat and fat soluble vits in feces
Caused by interference with bile or pancreatic lipase secretion
eg xenical

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43
Q

4 classes of lipoprotein

A

Chylomicrons
VLDL ( carriers TAGs)
LDL (bad - collects on arteries)
HDL (good - absorbs cholesterol and carries to the liver)

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44
Q

Lipoprotein function

A

Solublise lipid to transport in blood to tissue

Delivery system in/out cell

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45
Q

Apoprotein

A

ApoB
ApoE
ApoCII

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46
Q

ApoB

A

Structural for assembly

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47
Q

ApoE & B

A

Ligands for cell surface receptors

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48
Q

ApoCII

A

Enzymes cofactors

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49
Q

Lipid transport pathways

A 
Exogenous chylomicron (dietary fat)
Endogenous VLDL/LDL (endogenously synthesised fats)
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50
Q

Chylomicron assembly

A

TAG & lipids + apoB (in ER) = chylomicrons
Secreted from intestinal epithelial cells to blood via lymphatic system
Milky after fat rich meal

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51
Q

Lipoprotein lipase

A

Enzyme on endothelial surface
ApoCII actives hydrolyse of TAG in lipoprotein = glycerol and fatty acids
Highest activity in heart & skeletal muscle

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52
Q

Defects in ApoCII or lipoprotein lipase

A

Increase chylomicrons and plasma triacylglycerol

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53
Q

Familial Hypercholesterolemia

A

Premature atherosclerosis (fat build up in arteries)]
Defect in LDL receptor gene
LDL x2-3 normal

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54
Q

Familial Hypercholesterolemia treatment

A

Statins (type of drug)

Decrease LDL and increase HDL

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55
Q

Glucose transporters

A

SGLT1
GLUT2
Na+/K+ ATPase

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56
Q

SGLT1

A

Active
Against conc gradient
ATP needed
Glucose - Na+ symport

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57
Q

GLUT2

A

Facilitative

Down conc gradient

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58
Q

Na+ outside cell

A

120-140 mmol/L

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59
Q

Na+ inside cell

A

20-30 mmol/L

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60
Q

Peptide absorption

A

Di- & tri- con-transported with H+
Membrane transporter PepT1
Further digested into a.a by cytoplasmic peptidase

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61
Q

A.a absorption

A

From lumen of s.i by transepitelial transport

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62
Q

A.a absorption

A

Semispecific Na+ - dependent transporter

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63
Q

Lactose intolerence

A

Lactose enzyme deficiency

Fermentation of lactose by intestinal bacteria

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64
Q

Pancreatitis

A

Inappropriate activation of zyogens

Self-digestion

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65
Q

Stomach ulcers

A

Breakdown mucosa

No protection against protease action

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66
Q

Cystic fibrosis

A

Thick mucous secretions, block pancreatic duct & secretion pancreatic enzymes
Malabsorption

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67
Q

Coeliac disease

A

S.i
Reacts against gluten protein
Antibodies react with transglutaminase = villi flatten and no absorption

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68
Q

Nucleic acid polymers

A

Partically hydrolysed by acidic conditions

Exonuclease enzymes release individual nucleotides

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69
Q

Vitamins characteristics

A 
Essential
Organic molecules
No energy when broken down
Low = symptoms of deficiency
Small amounts required
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70
Q

Minerals characteristics

A

Essential
Non - organic elements
Low = symptoms of deficiency may appear
Small amounts

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71
Q

Bioavailability =

A

Amount absorbed/used

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72
Q

Accessing patients methods

A

Clinical Examination
Anthropometry
Biochemical tests
Dietary assessment

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73
Q

Dietary assessment

A

Measure what you eat

Compare with Nutrient Reference Valves

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74
Q

Vitamins co enzymes

A

Organic carriers

Make catalysis reaction smoother

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75
Q

Vitamins co factors

A

In catalysis - stablise adn help convert
Metabolism (energy)
Synthesis DNA/RNA

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76
Q

Minerals co factors

A

Transfer e- in redox
Structural role
Constituent of molecules
Nerve impulse, electrolyte balance

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77
Q

Niacin Deficient Diet

A

Vit B3
NAD & NADP
To carry redox = synthesis and breakdown carbs, lipids, a.a

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78
Q

Niacin Deficient Diet consequences

A

Low variety diet
4 D’s
Rough skin, rash on areas exposed to sun

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79
Q

4 D’s

A

Dermatitis (eczema)
Diarrhea
Dementia
Death

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80
Q

Mg2+ for muscle cramps

A

No solid evidence

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81
Q

ATP hydrolysis

A

-30kJ/mol

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82
Q

ATP synthesis

A

+30kJ/mol

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83
Q

Reaction coupling

A

G1 + G2 < 0

Energetically favourable

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84
Q

Release of energy

A

Phosphorylation of ADP -> ATP

Redox reaction

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85
Q

Oxidation

A

Energy release
Step - wise
Captures energy for ATP production
Without steps = energy released

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86
Q

Reduction

A

Coenzymes NAD & FAD
H -> H+ + e-
Enzyme > dehydrogenase

87
Q

NAD

A

Carries 2e-, 1H+

Glycolysis, fatty acid oxidation, CAC

88
Q

FAD

A

Carries 2e-, 2H+
Fatty acid oxidation, CAC
Tightly bound to proteins which they interact with

89
Q

CoA

A

Not carrier of e-

90
Q

RBC glucose

A

Essential fuel

Lack of mitochondria = no other pathway

91
Q

Brain glucose

A

Favoured
Readily cross blood/brain barrier
120g per day

92
Q

Eye glucose

A

Blood vessels & mitochondria refract light in optical path

93
Q

White muscle cells glucose

A

Sprinting
Anaerobic
Fast twitch

94
Q

Fatty acid preferred method

A

More reduced = more energy released

Lower space needed for some amount of energy

95
Q

TAG ->

A

Lipase

FFA + glycerol

96
Q

FFA transport into cell

A

In blood binds to albumin (albumin-FFA)
Passive into tissue and cell
In cell as FABP-FFA

97
Q

FABP-FFA

A

FAtty acid binding protein

98
Q

Glycerol transport into cell

A

Passive into liver

99
Q

Beta-oxidation transportation

A

Outer
Fatty acyl-CoA carrier
Inner
Fatty acyl-carnitine

100
Q

Beta-oxidation

A

Even no of carbons
Saturated
No ATP (energy transferred to NAD & FAD)
Cleavage b/w Calpha and Cbeta

101
Q

Beta-oxidation products after 1 round

A

1 NADH
1 FADH
1 acetyl-CoA
eg C16 = 7 round (7 NADH, 7 FADH, 8 acetyl-CoA)

102
Q

Isomerisation of citrate

A

Susceptible to decarboxylation

Aconitase catalyse both steps

103
Q

Synthesis of GTP

A

Energy eq of ATP
Energy from cleavage
P from soln

104
Q

Citric Acid Cycle inhibited by

A

Fluoroacetate

105
Q

Problem with fluoroacetate

A

Cannot undergo dehydration reaction
Inhibit pyruvate & build-up acetyl-CoA
= no metabolism

106
Q

Deamination

A

Carbon skeleton
Free amino group
Cleavage by enzymes into soln

107
Q

Carbon skeleton

A

Catabolic reactions

Energy capture

108
Q

Free amino group

A

Exerected

NH4+

109
Q

Transamination

A

Aminotransferase enzymes cataylse
Transfer amino group to keto acid <=>
P.P

110
Q

P.P1

A 
Pyridonal phosphate (without amino)
Co - enzyme
111
Q

P.P2

A

Pyridoxamine phophate

112
Q

Glucose - alanine cycle

A

Remove NH+ from muslce to liver and expelled as urea

113
Q

Isolate mitochondria step 1

A

Tissue
Homogenisation in buffered surcose
Centrifuge at 1000xg

114
Q

Stpe 1 products

A

Debris & nuclei

Supernatant

115
Q

Isolate mitochondria step 2

A

Supernatant

Contrifuge at 7000xg

116
Q

Spet 2 products

A

Pellet of mitchondria
Supernatant of membranes, ribosomes
and cytoplasm

117
Q

Weak detergent on mitochondria

A

Only outer membrane removed
ETC works
No ATP synthesis

118
Q

Strong detergent on mitochondria

A

Solubilises all membranes

ETC doesn’t work

119
Q

ETC e- movement

A 
Carrier accepts (reduced) or donates (oxidised)
To carrier with higher reduction potential
120
Q

ETC energy usage

A

More protons across inner membrane
Increase intermembrane space
Decrease matrix

121
Q

NADH pathway

A

1 - UQ - 3 - cyt c - 4 - O2

122
Q

FADH pathway

A

2 - UQ - 3 - cyct c - 4 - O2

123
Q

Inhibitors of ETC

A

Rotenone
Cyanide
Carbon monoxide

124
Q

Rotenone

A

Inhibits transfer from 1 to CO-Q

125
Q

Cyanide

A

Bind to carrier in 4

126
Q

Carbon monoxide

A

Binds where O2 binds

127
Q

Inhibitor consequences

A

Stops e- flow
Build-up reduced co-enzymes
No H+ gradient
Reactive oxygen species = damage to cells

128
Q

UQ/COQ

A

2e- from 1/2
Moves within inner membrane
2 redox reactions (only accepts/donate 1e- at a time)
Q - cycles

129
Q

Cytochrome C

A

Move on outer surface of inner membrane
1e- via reversible Fe2+/Fe3+ redox reaction
Heme containing protein

130
Q

NADH no of protons

A

10

131
Q

FADH no of protons

A

6

132
Q

Experiments used to support chemiosmotic theory - ATP synthesis

A

Artifical liposome

DNP

133
Q

Artifical liposome

A

Bacteriorhodopsin - light inducible proton pump
In light = proton gradient
Yes ATP - light on
No ATP - light off

134
Q

DNP

A

Uncoupler
Shuffle H+ from intermembrance space to matirx
Dissipate proton gradient
ETC continue, no ATP synthesis

135
Q

Proton motive force

A 
Chemical gradient/pH gradient due to H+ conc differences
Electrical gradient (+ve in intermembrane, -ve in matrix))
136
Q

F1F0

A

Rotor subunits - turn
Stator subunits - doesn’t turn
Proton flow drive rotor movement = conformational changes in stator

137
Q

O =
T =
L =

A

Open - binding & releasing
Tight - ATP formation
Loose - hold ADP and P for catalysis

138
Q

ATP from no of proton

A

4 protons = 1 ATP

139
Q

Chemiosmotic coupling hypothesis knew

A

Inner membrane impermeable to protons and contains ETC

140
Q

Chemiosmotic coupling hypothesis proposed

A

ETC pumps protons out of matrix

pmf and that it drives ATP synthesis

141
Q

GABA is a….

A

γ - aminobutyrate neurotransmitter transmitter

142
Q

GABAa receptor

A

Membrane bound ligand - gated chloride channel

143
Q

Increased NADH/NAD+ and ATP consequences

A 
Slows: 
CAC 
ETC
Pyravate dehydrogenase
Glycolysis
Fatty acid oxidation
144
Q

Fatty acid oxidation consequences

A

Fatty acid -> TAGs

Fatty liver & hypertriglyceridemia (increase fatty acid in blood)

145
Q

Increased NADH/NAD+ consequences

A

Pyruavate -> lactate (drives reaction)
= decrease pH
Inhibits gluconeogenesis (decrease blood glucose)

146
Q

Alternative wat metabolisming alcohol

A

As toxin

Microsomes ethanol oxidising system

147
Q

Microsomes ethanol oxidising system disadvantages

A

Oxidase = extra e- on O2 = O2-

Super oxidise = damges to tissue

148
Q

Toxic effects from chronic alcohol consumption

A 
Toxic acetaldehyde and reactive oxygen species
Fatty liver inflammation
Alcoholic hepatitis
Necrosis
Cirrhosis (death in liver cells)
Coma &amp; death
149
Q

Need for storing fuels

A

Body cannot store ATP (made when needed at rate needed by oxidising fuels)
Maintain glucose supply b/w meals
Immediate fuel from increase activity
Long periods without food intake

150
Q

Fat storage

A

In adipose tissue
Triacylglycerols (TAGs)
Excess converted to TAGs

151
Q

Fat synthesis

A 
Fatty acids (from chylomicrons)
Glycerol backbone (from glucose)
Stimulated by insulin
152
Q

Fat mobilisation

A

Hydrolysis of TAG
Catalysed by hormone sensitive lipase
Release of FFA and glycerol

153
Q

Fat mobilisation hormones involved

A

Adrenaline and glucagon

154
Q

Glycogen

A

Brushed polysaccharides
⍺ 1-4 & ⍺ 1-6 glycosidic bonds
Stored in liver and muscle
Granules in cytoplasm (stored until needed)

155
Q

Glycogen synthesis

A

Occurs in liver and muscle after meal
ATP & UTP - energy inputs
Activated high - energy precursor, UDP - glucose
Insulin stimulated

156
Q

Glycogen mobilisation

A

Degraded by glycogenolysis
Liver > released as glucose
Muscle > release fuel for glycolysis

Adrenaline binds to β adrenergic receptors on muslce cells

157
Q

Excess glucose ->

A

Converted into fatty acid

Exported as TAGs in VLDLto adipose tissue

158
Q

Fuel for liver, heart

A

FFA

159
Q

Fuel for muscle

A

Resting - FFA

Marathon - FFA and glucose

160
Q

Starvation survival

A

Supply brain with glucose (120g)
Supply other tissues with fatty acids
Conserve protein (maintain structure & function)
Hormone - glucagon

161
Q

Lipolysis

A

Enough fuel for 40 days

Use TAGs in adipose tissue

162
Q

Glycerol movement after lipolysis

A

Into blood to liver

163
Q

FFA movement after lipolysis

A

+ albumin in blood

To all aerobic tissue except brain

164
Q

Glycogenolysis

A

90 - 120g glycogen -> glucose

Enough for brain for 1 day

165
Q

Gluconeogenesis

A

In liver

Energy provided by fatty acid oxidation

166
Q

Gluconeogenesis synthesis of glucose

A

Lactate from muscle glycogen
Alanine from muslce protein
Glycerol from adipose tissue

167
Q

Storage proteins

A

None

Too much functional protein degraded into a.a = structural and functional damage = severe -ve N+ imbalance = death

168
Q

Ketogenesis

A

Synthesised in liver from fatty acids
Can cross blood brain barrier
Reduce proteolysis by 1/2
Limited - make blood acidic so 7mmol = limit

169
Q

Proteolysis

A

Breakdon of proteins & prevent -ve N+ imbalance

170
Q

Ketone bodies levels

A

0mmol/L at start of fasting

171
Q

ATP amount for how long

A

5micromol/g

For 1 second

172
Q

Phosphocreatine

A

20micronmol/g in muscle

High-energy phosphate compound

173
Q

Anaerobic glycoysis

A

ATP generate by substrate - level - phosphorylation
Rapid, short time only
Lactate = decrease pH in muscle = fatigue

174
Q

Regulation in exercising muscle

A

Glycogen mobilisation - Ca2+ and adrenaline
Phosphofructokinase - increase by allosteric regulators
+ AMP & Pi

175
Q

Use of ADP

A

ADP + ADP = ATP + AMP

Adenylate kinase

176
Q

Aerobic generation of ATP

A

Oxidation of glucose and fatty acids

ETC, CAC, oxidative phosphorylation

177
Q

Training consquences

A

Rely less on glycogen “top up”

Muscles different with type of training

178
Q

Marathon runner muscles

A

Type 1 fibres => red, slow - twitch

179
Q

High jumpers muscles

A

Type 2 fibres => white, fast - twitch

180
Q

Endurance type 1

A

Increase:
Capillaries, myoglobin content, no and size of mitochondria, capacity of mitochondria, oxidise lipid and carbohydrate capacity

181
Q

Anaerobic

A

High intensity
Rapid generation of force
Short periods

182
Q

Aerobic

A

Low intensity

Prolonged, sustained force

183
Q

% of anaerobic and aerobic depends on

A

Different durations involving maximal work

Increase aerobic, increase exercise duration

184
Q

Diabetes clinical symptoms

A

Fatigue

Increas thirst and urination

185
Q

Diabetes biochemical symptoms

A

Hyperglycaemia => constant high glucose
Glyucosuria => Overwhelm kidney’s ability to filter glucose
Ketones

186
Q

Insulin - dependent

A 
Juvenile - onset
Type 1
Auto - immune destruction β cells
0.5% whole pop
Genetic and environment factors
Treatment - insulin injections
187
Q

Non - insulin - dependent

A 
Maturity - onset
Type 2
Resistance of insulin
2% whole pop
Genetic and environment factors
Treatment - diet, exercise, drugs
188
Q

Long - term complication

A 
Retinopathy
Neuropathy
Nephropathy
Cardiovascular disease
Peripheral vascular disease
189
Q

Blood glucose high complications

A

Target structural proteins

eg crystalline protein of eye, lens = opaque

190
Q

Blood glucose low complications

A

<1mmolL-1

Sweating
Heartbeat increases
SNS = vomiting
No glucose for brain = convulsions, coma

191
Q

Fluctuations glucose tolerence test

A

Increased plasma glucose vs normal and takes longer to decrease/ return to normal levels for diabetic

192
Q

Fluctuations injected insulin

A

Mimic normal rise

Abnormal decrease and takes longer to respond

193
Q

Type 2 treatment

A

Hypoglycaemic drugs

Impairs TAG usage - forcing glucose usage

194
Q

Body Mass Index

A

= W/h^2

195
Q

Obese
Overweight
Healthy weight
Underweight

A

> 30
25 - 30
20 - 25
<20

196
Q

Energy expenditure =

A

Basal metabolic rate

197
Q

Basal metabolic rate depends on

A

Obligatory energy expenditure
Physical activity
Adaptive thermogenesis

198
Q

Obligatory energy expenditure

A

Cellular and organ function

199
Q

Adaptive thermogenesis

A

Variable, regulated by brain
Responds to temp and diet
In brown apipocyte mitochondria, skeletal muscle…

200
Q

Increases risk of obesity =

A

Culture
Monogenic syndromes
Susceptibility genes

201
Q

Brown fat

A

Special thermogenic tissue
Many mitochondria and fat droplets
Contains UCP

202
Q

Uncoupling protein (UCP)

A

Inner mitochondria membrane
Regulate proton channels -> “couple” ATP synthesis by dissipating H+ gradient
Releases heat , increase metabolic rate, uses more fuels

203
Q

White adipose tissue

A

UCP2, UCP3

Increase metabolic rate and burn off excess energy

204
Q

Lipin

A

Coded by obese gene
Hormoe from “fat” fat cells
Signals the brain to decrease food intake, increase energy expenditure

205
Q

Lipin + ?

A

Lepun receptor in hypothalamus and other tissues

206
Q

Strategies for treatment

A

BAT - oriented
Leptin/leptin - receptor
Anti obesity drugs

207
Q

BAT - oriented

A

Stimulate existing BAT
Switch on brown fat differentiation and growth
Transplantation

208
Q

Leptin

A

Mutant obese mouse doesn’t produce leptin
Injected leptin = lipostat
Decrease appetite, increase energy use

209
Q

Leptin - receptor

A

Obes diabetic mouse and fatty rat
Leptin receptor absent
2 - 6% severe obesity due to defect in MC4R in signalling pathway

210
Q

Anti obesity drugs food breakdowwn

A

Xenical

Pancreatic lipase blocked - less fat absorbed

211
Q

Anti obesity drugs satiety signals

A

Trials underway

Increase leptin levels

212
Q

Anti obesity drugs mitochondria and brown fat

A

Future?
Uncouple oxidative phosphorylation from ETC
Increase functional BAT

213
Q

White adipose tissue

A

Numberous hormones secreted for many pathways

Multifunctional

BIOC192 (6 decks)

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