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Y2 NnD > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Are catabolic processes in metabolism predominantly oxidative or reductive

A

Oxidative

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2
Q

Where is NADP primarily produced?

A

Pentose phosphate pathway

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3
Q

What is the first line of energy in starvation

A

Liver glycogen

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4
Q

What intermediate becomes ketone bodies?

A

Acetyl- CoA

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5
Q

x

A

G-6-P

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6
Q

What do kinases do

A

Catalyse the phosphorylation of an enzyme by removing phosphate from ATP or other molecules

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7
Q

What does phosphatase do

A

Hydrolyse phosphates

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8
Q

Do kinases activate or inactivate degradative and biosynthetic pathways

A

Activat degradative pathways, inactivate biosynthetic pathways

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9
Q

Where are ketone bodies produced

A

Liver

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10
Q

Where are NEFAs metabolised

A

Muscle and Liver

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11
Q

How do desaturases work, which carbons can have double bond introduced

A

NADH reduces FAD which reduces haem containing cytochrome which reduces desaturase, oxidising fatty acid to double bond at C4,5,6,9

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12
Q

What are essential fatty acids in diet

A

Linolenic acid, arachidonic acid

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13
Q

Where does the first lipase work on at,,what is it

A

Pancreatic lipase @SI

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14
Q

Where does the 2nd lipase work on and what is it

A

Lipoprotein lipase @ muscle and adipose tissue ( also found in the heart)

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15
Q

What does lipoprotein lipase break down chylomicrons to

A

Fatty acids and Chylomicron remnants containing ADEK and phospholipid

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16
Q

What liberates TAG to Fatty acids and from where

A

Hormone sensitive lipase, TAG in adipose becomes NEFA

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17
Q

Where can fatty acids be stored as TAG

A

Muscle and adipose tissue

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18
Q

What is the process of digestion of TAG in SI

A

Bile salts act on TAG to emulsify them into micelles, pancreatic lipase then breaks it down into MAG and 2 FA

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19
Q

What happens to the FFA and monoglycerol after being liberated in SI

A

Small proportion of FFAs pass straight into blood stream and go to liver, rest get absorbed by intestinal cells

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20
Q

How do chylomicrons pass into blood stream

A

Chylomicrons pass indirectly into bloodstream ⇒ enter lymphatic system, reach the blood through thoracic duct

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21
Q

Where are lipoprotein lipases found - which organs

A

Heart, fat and muscle

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22
Q

What activates lipoprotein lipase

A

Apoprotein CII

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23
Q

How does insulin affect uptake of glucose in liver

A

It doesn’t, lol

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24
Q

a

A

G-1-P

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25
Q

What converts pyruvate in mitochondria to Acetyl CoA eventually in cytosol and what regulates them

A

Pyruvate Dehydrogenase , citrate lyase , Insulin

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26
Q

What is the intermediate between Acetyl-CoA and Fatty acids and what enzyme is involved

A

Malonyl CoA. Acetyl Co-A carboxylase

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27
Q

What are the substrates involved in fatty acid synthase complex

A

Malonyl-CoA and Acetyl-CoA

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28
Q

What energy stores are glucogenic

A

Lactate, glycerol, glucogenic amino acids

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29
Q

How does glucagon and insulin regulate lipogenesis

A

Activates AMP-activated protein kinase to inactivate acetyl-CoA carboxylase
Insulin- protein phosphatase activates…

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30
Q

What hormones stimulate Hormone sensitive lipase

A

Adrenaline, glucagon and growth hormone

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31
Q

How are fatty acids transported in plasma and cytoplasm

A

Binds to albumin in plasma and fatty acid binding protein in cytoplasm

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32
Q

How are fatty acids transported into mitochondria?

A

Becomes Acyl- CoA which binds to carnitine from intermembrane space. Acyl carnitine then enters through mito inner membrane into matrix via carrier and breaks down back to acyl coa and carnitine

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33
Q

What enaymes are involve in B oxidation

A

Ubiquinone, which gets reduced to oxidise FADH2 which then oxidises to form a double bond in Acyl CoA

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34
Q

How does B oxidation of fatty acids take place and what is the product

A

Oxidation, hydration, second oxidation( By NAD+), splitting, production of acetyl coa

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35
Q

What are the substrates involved in fatty acid synthase complex, what electron transporter involved here

A

Malonyl-CoA and Acetyl-CoA
NADPh

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36
Q

precursor of cholesterol synthesis that is control step

A

HMG-CoA to mevalonate by HMG CoA reductase (NADPH involved)

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37
Q

how do statins control reduce cholesterol synthesis and what enzyme do they work on

A

They work on HMG CoA reductase via AMP activated protein kinase

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38
Q

Where is cholesterol synthesized

A

Made mainly in the liver but also some other tissues

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39
Q

How do primary bile acids get formed and what are they

A

Hydroxylation and sidechain cleavage, chenodeoxycholate and cholate

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40
Q

How do bile salts get formed

A

Conjugation of primary bile acids with taurine or glycine

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41
Q

How do secondary bile acids get formed and where

A

Hydrolysis and partial reduction of bile salts by bacteria, in large intestine

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42
Q

How do primary bile acids get formed and what are they and where

A

Hydroxylation and sidechain cleavage, chenodeoxycholate and cholate, in liver

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43
Q

How do fibrates work

A

They inhibit recirculation of LDL

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44
Q

How does cholestyramine work

A

It binds bile acids in digestive tract and precents its reuptake and recirculation, increasing excretimg

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45
Q

How does cholestyramine work

A

It binds bile acids in digestive tract and precents its reuptake and recirculation, increasing excretion

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46
Q

What are essential amino acids

A

Cannot be synthesized within the body, must be supplied in the diet
Isoleucine, leucine, lysin, methionine, phenylalanine, threonine, tryptophan valine ,

semi- arginine and histidine

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47
Q

Where can glucogenic amino acids be broken down

A

In liver or kidney

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48
Q

Role of chief and parietal cells

A

Chief cells secrete enzymes like pepsinogen, parietal cells secrete gastric acid

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49
Q

What hormones regulate gastric ATPase

A

Gastrin, histamin, Ach

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50
Q

What ion movements follows exit of H+ from Gastric ATPase

A

K+ comes in, Cl- moves out as a counterion for HCO3-

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51
Q

What is pepsinogen activate by

A

H+, which forms pepsin which the catalyses production of more pepsin

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52
Q

What enzyme activates most of the pancreatic zymogens

A

Trypsin

53
Q

What is trypsinogen activated by and what produces it

A

Enteropeptidase activates it and it autoactivates itself

54
Q

What happens to leftover proteins in the small intestine

A

Gets degraded by resident peptidases like aminopeptidase

55
Q

what ions bring aminoacids into the cell

A

Na+

56
Q

Degradation of extracellular proteins

A

Formation of endolysosomes at acidic pH. degradation of proteins
- Bind to receptors and form endosome, then merges with lysosomes

57
Q

How are intracellular proteins broken down

A

They are targeted for destruction by ubiquitin , proteasomes binds to protein and breaks it down

58
Q

9

A

They are targeted for destruction by ubiquitin and broken down by proteasome

59
Q

What does transamination do to aminoacid

A

Breaks it to carbon skeleton (ketoacid) and amino group in glutamate

60
Q

Where does urea get produced

A

Urea cycle takes place in liver

61
Q

What happens to urea in renal failure and liver cirrhosis

A

Rises and falls respectively

62
Q

What happens to ammonia in liver cirrhosis

A

Rises as urea cycle is inhibited

63
Q

What is the process of amino acid breakdown and how is this linked to release of ammonia from amino acids

A

Transamination - Nh3+ removed from amino acid by aminotransferase. oxoglutatarate becomes L-glutamate by addition of amino group, amino acid becomes oxo acid

L- glutamate which has the ammonia gets dehydrogenated by glutamate dehyrdogenase and NAD + to become 2-oxoglutarate again, NH4+ gets removed from glutamate

64
Q

How does ammonia become urea

A

NH4+ reacts with co2 to become carbamoyl phosphate , which reacts with citrulline in mitcohondria to eventually become urea

65
Q

How are amino groups transported to the liver

A

L-Glutamate reacts with pyruvate to become oxoglutarate and alanine to be transported in plasma ( amino group transferred from glutamate). Amino group then returned to oxoglutarate to form glutamate again

66
Q

How are amino groups transported to the kindeys

A

Glutamate converted to gutamine by Glutamine synthetase, an amine of glutamate formed in tissues and kidneys

67
Q

how is glutamine excreted

A

Liberates ammonia, doesnt become urea

68
Q

what is the role of folic acid in synthesis of DNA

A

It gets converted to become FH2 and then FH4, which is needed to produce purines and thymine

69
Q

Role of Vitamin B12 in methylation reactions

A

Needed to convert methyl FH4 into methionine for methylation reactions

70
Q

role of sulphonamides

A

Inhibit bacterial synthesis of folic acid

70
Q

role of sulphonamides

A

Inhibit bacterial synthesis of folic acid

71
Q

How does methothrexate work

A

It is a derivative of folic acid and prevents reduction of FH2 to FH4

72
Q

Difference between red and white muscle fibers
slow or fast contraction rate, myoglobin content, myosin atpase acitivtiy, creatine kinase activity, mitochondrial oxidation rate, glycolytic rate

A

slow vs fast, high vs low, low vs high, low vs high, high vs low, low vs high

73
Q

Fuels for muscle contraction in anaerobic vs aerobic exercise

A

Anaerobic - muscle ATP, creatine phosphate, muscle glycogen
Aerobic - all these but also FFA from muscle and adopose tissue and plasma glucose from liver glycogen and gluconeogenesis

74
Q

What are the main substrates of gluconeogenesis

A

From 3 carbon precursors:

  • Alanine (from ingested protein)
  • Pyruvate (from muscle protein)
  • Lactate (from muscle glycogen)
  • Glycerol (from fat)
75
Q

Where is glucose metabolised vs galactose and fructose

A

by all cells vs mostly liver

76
Q

What is the role of creatine phosphate

A

It tops up ATP store by phosphorylating ADP to ATP

77
Q

What are the two main kinds of starch and which is more common

A

By amylose - unbranched chains, a(1-4) links, vs amylopectin, branched chains, a(1-4) and a(1-6),80-90% amylopectin

78
Q

xx

A

xx

79
Q

What enzymes digest starch

A

Salivary and pancreatic amylase a(1-4) - endo
glucoamylase from luminal side of intestinal wall a(1-4) - exo, oligosaccharides, trisaccharides and maltose
Isomaltase also from lumen a(1-6)

80
Q

What enzymes digest disaccharises

A

glucoamylase a(1-4) exo, lumen , acts on oligosaccharides, trisaccharides and maltose
isolmatase. a(1-6), lumen, hydrolyses isomaltose
B galactosidase - B(1-4), lactose to glucose and galactose
Sucrase- a(1-2), sucrose to glucose and fructose

81
Q

What transporter brings glucose into the intestine and what ion is involved and is capacity high or low

A

Na+ drags glucose through SGLT1 , low capacity

82
Q

What channel allows glucose to leave intestinal cell, passiv or active

A

GLUT 2, passive due to high conc.

83
Q

What glucose transporter is present in pancreas and liver and allows uptake of glucose prop to gluc conc

A

GLUT 2

84
Q

What glucose transporters are responsive to insulin and where are they found

A

GLUT 4 , heart, muscle and fat

85
Q

What are the two pathways including glucose and what are their substrates

A

G-6-P for glycolytic pathway and pentose phosphate pathwat

86
Q

Where does glycogen get formed

A

Liver and muscle, kidney to some extent

87
Q

ATP from glycolysis vs TCA cycle and oxidative phosphorylation

A

2 vs 30

88
Q

Fate of glucose in anaerobic resp

A

Lactate from pyruvate

89
Q

Is acetyl CoA involved in anaerobic respiration

A

NO, it is only made in mito

90
Q

How is glycogen converted to glucose

A

Via G-1-P as an intermediate

91
Q

What hormones stimulate conversion of glycogen to G-1-P

A

Glucagon, adrenalin and AMP

92
Q

How does glucose get converted to lactate and where does it take place. What substrate required.

A

Oxidation of glucose to pyruvate produced NADH which is used for reduction of pyruvate to lactate, takes place in cyto of muscle

93
Q

What is the cori cycle

A

Recycling of glucose from lactate=> lactate gets converted back to pyruvate -> G6P-> glucose

94
Q

What enzymes are involved in phosphorylation of glucose to G6P and how do they differ ( saturation and cells they are present in)

A

Hexokinase and glucokinase, hexokinase is saturated much earlier, hexokinase present in all cells but glucokinase only in liver and B cells

95
Q

What is the glycolytic pathway

A

Glucose gets converted to G6P. then F6P and F-1,6-bisP, then Glyceraldehyde-3P ( broken down to 3C), then phosphorylated to 1,3bisphopshoglycerate by NAD+. then ATP produced when converted to 3PG then when PEP is converted to pyruvate

96
Q

what converts glycogen to G-1-P and what stimulates this process

A

Glycogen phosphorylase, stimulated by adrenaline and glucagon, inhibited by insulun

97
Q

How does glucose can converted intp glycogen

A

G-1-P is converted to UDP glucose, which then becomes glucogen through removal of UDP by glycogen synthase

98
Q

What stimulates action of glycogen phosphorylase

A

Glycogen phosphorylase b activated to a by activated phosphorylase kinase which is in turn activated by :
Ca2+ ( rises during muscle contraction,mediated by Ach) or
protein kinase A, activated by adrenaline

Glycogen phosphorylase also activated by AMP which rises during muscle contraction

99
Q

Role of glucose 6 phosphatase and where is it present in

A

Converts G6P to glucose
Livers and kidneys

100
Q

How do lactate and some amino acids get converted to glucose

A

They get converted to pyruvater, but conversion from PEP is irreversible, requires ATP to convert to oxaloacetate and then GTP to go to PEP

101
Q

How does pentose phosphate pathway work

A

G6PD converts G6P into 6 phosphogluconate, which the gets dehydrogenated to Ribulose 5- phosphate (C5), which becomes ribose 5-P or xyulose 5-P. THese C5 undergo carbon shuttling reactions to eventually from 2 C6 and 1 C3

102
Q

How does fructose and galactose get metabolised

A

Fructose can be phosphorylated by hexokinase, and fructokinase ( produced F-1-P which feeds in normal glycolytic pathway)
Galactose by galactokinase, and UDP glucose involved in converting it to G-1-P

103
Q

Role of glutathione (GSH) in antioxidation

A

G6P oxidised to 6 phosphogluconate as in pentose pathway by G6PD, hydrogenation of NADP+ occurs. NADPH then used to reduce oxidised GSH so it can reduce peroxides (which are reactive) via gluthatione peroxidase

104
Q

Does G6PDH deficiency affect males or females more and why

A

males, as it is x-linked

105
Q

How does G6PDH deficiency affect erythrocytes

A

Results in GSH deficiency and leads to hemoglobin crosslinking and breakdown of erythrocytes

106
Q

How does disulphiram work

A

Treats alcohol addiction by preventing conversion of acetalaldehyde to acetic acid,

107
Q

How does alcohol lead to hypoglycaemia

A

Inhibits glucogenesis in liver due to reduced generation of NAD+ which is needed to oxidise lactate to pyruvate

108
Q

x

A

Inhibits glucogenesis in liver due to reduced generation of NAD+ which is needed to oxidize lactate to pyruvate

109
Q

How are ketone bodies formed

A

Acetyl CoA converted to HMG-COA which is then converted to acetoacetate which can be reduced by NAdh to 3-hydroxybutyrate, or decarboxylated to acetone

110
Q

How does pyruvate get converted to acetyl coA

A

Pyruvate dehydrogenase complex, irreversible dehydrogenation by NAD+

111
Q

What activates PDH kinase and phosphatase?

A

NADH, ATP, Acetyl coA ( eventual products of pyruvate oxidation) avs Ca2+, insulin

112
Q

What coenzymes are involved in TCA cycle

A

2 NADH produced by TCA cycle(isocitrate to 2-oxoglutarate, 2-oxoglutarate to succinyl coA, malate to oxoloacetate), GTP produced when succinyl-CoA gets converted to Succinate

UQH2 produced (also used in fatty acid oxidation)

113
Q

x

A

Ketogenic aminoacids, fatty acids

114
Q

Where do fatty acids and ketogenic amino acids enter the TCA cycle

A

acetyl CoA

115
Q

Where does ketogenesis take place in

A

Only in liver

116
Q

what are the functions of the 5 different compleces in ETC

A

I and II are dehydrogenases, help to reduce ubiquinone, III oxidised reduced ubiquinone and reduces cytochrome C. IV oxidises cytochrome c, V produces ATP

117
Q

What does antimycin and cyanide do to ETC

A

Inhibits electron transport along ETC

118
Q

What does oligomycin do to H+ circuit in mitochondria

A

Acts on ATP synthase so H+ cannot enter

119
Q

What do uncouplers do to mitochondria

A

They transport protons across the membrane (tend to be lipid soluble weak acids) protons bind to weak acid that gets through membrane and loses proton inside

120
Q

Where is ubiquinone involved

A

Fatty acid oxidation, TCA cycle and ETC

121
Q

Where is HMG CoA involved

A

Cholesterol synthesis and ketone body sethesis

122
Q

What does myosin ATPase do

A

Converts ATP to ADP in exercise

123
Q

What does adenylate kinase/ myokinase do

A

converts 2 ADP to AMP and ATP

124
Q

How does insulin affect NEFA circulating

A

decreases due to lipolysis inhibition

125
Q

Effects of AMPPK

A

Glucose uptake, glycolysis, fatty acid oxidation
Inhibits synthesis of glucose, cholesterol, glycogen, protein and fatty acid synthesis

126
Q

which tissues does metabolism of fatty acids occure

A

liver and muscle

127
Q

how do odd C fatty acids join TCA cycle

A

B oxidation to propionyl coa, caborxylation to succinyl coa

128
Q

What inhibits fatty acid oxidation and how

A

Malonyl coa inhibits acyl carnititne

Y2 NnD (10 decks)

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