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Biochemistry year 1 > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Name the 3 non carbohydrate precursors of glucose :

A

1 lactate
2 amino acids (alanine in skeletal muscle)
3 glycerol (triacylglycerols in fat tissue )

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2
Q

Which organs are involved in gluconeogenesis :

A

Liver (90%), kidney and small intestine

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3
Q

Where in the cells does gluconeogenesis occur?

A

Cytosol (except for the first reaction )
Most of the same glycolysis enzymes involved

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4
Q

Summarise how gluconeogenesis occurs:

A

Reversal of glycolysis except for 3 steps

  1. Pyruvate converted to PEP
  2. F1,6BP converted to F6P
  3. G6P converted to glucose
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5
Q

Explain the importance of pyruvate carboxylate

A

Catalyses an important anapleurotic reaction
This means it maintains the conc of Krebs cycle intermediates, allowing it to be a continuous process

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6
Q

Name the reactions involved in gluconeogenesis and the enzymes involved

A
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7
Q

How do the 3 glucose precursors join the gluconeogenesis pathway ?

A

Lactate —> pyruvate
Lactate DH

Amino acids —> oxaloacetate + pyruvate
Transamination

Glycerol —>dihydroxyacetone phosphate —>glyceraldehyde 3-phosphate

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8
Q

State the 2 condition for gluconeogenesis

A

Low [glucose] and high [ATP]

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9
Q

glycolysis and gluconeogenesis can occur simultaneously

true or false

A

False

when one pathway is active, the other must be inactive

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10
Q

What conditions inhibit Gluconeogenesis

A

High AMP/F1,6P/ADP

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11
Q

What conditions stimulate gluconeogenesis

A

High acetyl CoA / citrate

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12
Q

What conditions inhibit glycolysis

A

High ATP/Citrate/H+/alanine

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13
Q

What conditions stimulate glycolysis

A

High F2,6P as this stimulate PFK-1 involved in the irreversible step; high AMP (as this indicate there is low ATP); insulin secretion

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14
Q

Describe the effects of insulin

A

Promote synthesis of glycolysis enzymes e.g. PFK/PK/PFK2
Inhibit synthesis of PEPCK ; this inhibits gluconeogenesis

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15
Q

Describe the effects of glucagon

A

Increases expression of PEPCK/F1,6BPase

increased gluconeogenesis

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16
Q

Draw the Krebs cycle

A

citrate is krebs special substrate for making oxaloacetate.

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17
Q

What is the PDH reaction

A

the link reaction

converts pyruvate to acetyl CoA

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18
Q

Name the4 5 coenzymes of PDH

A

Thiamine pyrophosphate (TPP)

Lipoamide

CoA

FAD+

NAD+

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19
Q

draw the mechanism of the PDH reaction

A
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20
Q

Name the 3 enzymes found within the PDH complex

A

E1 pyruvate decarboxylase

E2 hydrolipoyl transacetylase

E3 dihydrolipoyl dehydrogenase

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21
Q

What conditions cause activation of PDH

A

Increased [insulin] and [Ca2+]

this cause dephosphorylation of PDH

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22
Q

What conditions cause the inhibition of PDH

A

Increased ATP/NADH/Acetyl CoA

results in phosphorylation of PDH via kinase

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23
Q

Name the 3 enzymes needed for glycogen formation

A

Glycogenin

glycogen synthase

branching enzyme

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24
Q

State the role of glycogenin

A

Combine UDP-glucose (activated form of glucose) to tyrosine

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25
Q

describe the role of glycogen synthase

A

Make alpha 1,4 glycosidic bond cause the chain to extend

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26
Q

describe the role of the branching enzyme

A

Breaks off part of the amylose chain and branches it via the formation of alpha 1,6 glycosidic bonds

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27
Q

When does glycogenesis occur in the liver and skeletal muscle

A

In the liver - during well fed periods

in skeletal muscle : during rest periods

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28
Q

Describe the hormonal regulation of glycogenolysis

A

Glucagon bind to receptors on hepatocytes / adrenaline binds to myocyte/hepatocytes

adenylyl cyclase activated by G proteins ; makes cAMP

cAMP activates protein kinase A ; phosphorylates glycogen

inhibition of glycogen synthesis

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29
Q

Characteristics of high energy state

A
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30
Q

Characteristics of low energy state

A
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31
Q

Breakdown of adipose tissue forms:

A

Triacylglycerol which is converted to free fatty acid (FFA) and glycerol

glycerol acts as a gluceneogenic substrate

FFA form acetyl CoA

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32
Q

describe the structure of triacylglycerol

A

glycerol backbone with 3 fatty acid chains attached

the fatty acid chains may be saturated or unsaturated

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33
Q

Describe the mobilisation of fatty acids

A

In response to glucagon or adrenaline , hormone-sensitive lipase hydrolyses triacylglycerol in adipose tissue to free fatty acids and glycerol

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34
Q

How are fatty acids transported to the skeletal muscle from adipose tissue?

A

Free fatty acids(FFA) bind to albumin in blood and travel via circulation to muscle

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35
Q

Describe mitochondrial beta oxidation of fatty acids

A

Long Chain fatty acids (LCFA) activated in cytosol to form fatty acyl CoA

these are then transported to mito where beta oxidation in matrix occurs to form NADH, FADH2 and acetyl CoA

2C removed from fatty acids in each round ; this continues until the LCFAs are fully broken down

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36
Q

State the energy yield starting with a C16 saturated fatty acid (typical fatty acid)

A

7FADH2 = 14 ATP (beta-oxidation occurs 7 times)

7NADH = 21 ATP

8 acetyl CoA = 96 ATP via the TCA cycle

Net yield of 129 ATP (2 needed to form LC fatty acylCoA)

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37
Q

Describe the pathway of fatty acid synthesis

A

Acetyl CoA (2C-CoA) ⇒ malonyl CoA (3C-CoA) ⇒ 16C-CoA ⇒TAG

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38
Q

state the two functions of acetyl CoA

A

Fed into TCA cycle

form ketone bodies

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39
Q

What are Ketone bodies

A

Alternate fuel for cells during starvation/uncontrolled diabetes ; especially important for brain

made from acetyl CoA in liver mitochondria

occur when high [AcCoA]

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40
Q

Name the ketone bodies

A

Acetoacetate ⇒ beta-hydroxybutyrate + acetone

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41
Q

Utilisation of ketone bodies

A

preferentially metabolised in brain/heart during starvation to preserve glucose for use elsewhere

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42
Q

Ketoacidosis - what is this

A

when [ketone body] is too high , ketones are secreted in urine (ketonuria)

ketone bodies are acidic so lower blood pH which can be life threatening

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43
Q

what is cholesterol

A

essential molecule

component of cell membrane

precursor to bile acids, steroid hormones and vitamin D

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44
Q

Biosynthesis of cholesterol

A
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45
Q

what is the purpose of lipoproteins

A

Allow transport of lipids around the body

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46
Q

Structure of lipoproteins

A

Globular shape

outer layer of unesterified cholesterol and phospholipid

inside cholesteryl ester and TAG

apoprotein wrapped around the outside

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47
Q

Function of apoproteins

A

Interact with cellular receptors

activate and inhibit enzymes involved in lipoprotein metabolism

48
Q

Function of chylomicrons

A

Secreted into lymph and reach blood plasma via thoracic duct

they are then transported to adipose tissue or muscle where they are converted to FFA so they can cross the capillary endothelium

the FFA are then converted back into TG once inside the adipose/muscle tissue

49
Q

describe the intestinal uptake of dietary lipids

A

Triacylglycerides broken down fatty acids + monocyglycerols just outside cell then recombined once they enter the cell

triacylglycerides are combined with other lipids and proteins to form chylomicrons which are transported to circulatory system via the lymph system

50
Q

What is the importance of the apoprotein CII

A

Activates lipoprotein lipase (LPL)

LPL catalyses the reaction TG⇒FFA + glycerol

LPL found on surface of endothelial cells

this means FFA are liberated when chylomicrons reach their end destination in the blood

51
Q

What are chylomicron remnants ?

what is their function ?

A

They are also formed when the CM are converted to FFA to allow exit from the plasm a

CM remnant deliver dietary cholesterol to the liver

52
Q

What are endogenous lipids ?

A

Formed when there is excess carbohydrate and lipids in diet

excess carbs/lipids ⇒ TAG (in liver)

53
Q

What are endogenous lipids ?

A

Formed when there is excess carbohydrate and lipids in diet

excess carbs/lipids ⇒ TAG (in liver)

54
Q

What is VLDL

A

Transports endogenous TAGs to peripheral tissues

55
Q

What are IDLs

A

Intermediate density lipoprotein

formed by removal of triacylglycerol from VLDL

they can either be sent to the liver and be destroyed or lose more triacylglycerol and become LDL such as cholesterol

56
Q

What is LDL

A

Formed via the removal of TG from IDL

contains apoB-100, esterified cholesterol and normal cholesterol

major cholesterol carrier to tissues

high levels of LDL associated with CHD

57
Q

Compare metabolism of dietary lipid vs endogenous lipids

A

Digestive lipids absorbed in liver; endogenous in liver

digestive lipids converted to CMs; endogenous to VLDL

both VLDL and CM catalysed by LPL to release FFA

VLDL broken down to form FFA and IDL ; CM broken down to form FFA and CM remnants

CM remnants go to liver ; IDL can either be converted to LDL or be destroyed in liver

58
Q

What is HDL

A

Transports cholesterol from peripheral tissue to liver ; this is called reverse cholesterol transport

it helps protect against CHD

59
Q

Define anabolism

A

Synthesise large molecules

60
Q

What are the 4 types of metabolic pathways

A

fuel oxidative pathways (breakdown substrates)

fuel storage and mobilisation

bio synthetic pathways

detoxification and waste disposal pathways

61
Q

What is catabolism

A

Breakdown on large molecules

62
Q

What is metabolic homeostasis

A

Control of the balance between substrate availability and need caused by anabolic and catabolic pathways

63
Q

Glucagon :

Where does it act

where is it made?

describe its effects

A

Made by alpha cells in islets of lagerhans in pancreas

Glucagon acts to maintain fuel availability

principally acts in liver and adipose tissue not in muscle however

Promotes glycogenolysis and gluconeogenesis/ketogenesis

mobilises fatty acids from adipose triacylglycerols

reduces glycogen synthesis in liver

increasses [adrenaline]

64
Q

how is insulin made?

Describe the action of insulin

A

Polypeptide synthesised as a preprohormone

degraded by liver, kidney and skeletal muscle where its converted to its final form

Acts on liver, muscle and adipose tissue

65
Q

How is glucagon made

A

Produces as preprohormone in RER

degraded by liver and kidneys

66
Q

What promotes glucagon release?

A

release of catceholamines (such as adrenaline)

high amino acid conc

low blood glucose

67
Q

Describe the 2 types of signal transduction

A

Receptor coupled to adenylate cyclise to produce cAMP

receptor/kinase activity

receptor couples to hydrolysis of PIP2

68
Q

intracellular effects of insulin

A

overall has an anabolic effect

effect on carb metabolism:

  • stimulates uptake of glucose from blood
    • incorporation of vesicles with GLUT4 receptors into membrane
  • stimulates storage of glucose in liver primarily
    • phosphorylation of glucose/PFK/glycogen synthase = increased glycogen synthesis
  • cells driven to preferentially oxidise carbs over fatty acids/AA

effect on lipid metabolism:

  • promotes synthesis of FAs in liver from excess glucose which are then used to make lipoproteins which travel in blood
  • promotes accumulation of TGs in adipose tissue by inhibiting hydrolysis of TGs

effect on protein metabolism

  • increased uptake of amino acids/ protein synthesis
69
Q

intracellular events of glucagon

A

Secondary messenger activation

glucagon binds to G-protein coupled receptor

G protein dissociates = cAMP formed = protein kinase activated

protein kinase phosphorylase’s regulatory enzymes in order to control lipid/carb metabolism

70
Q

Complete this table

A
71
Q

what is the fed state ?

A

Period of 2-4 hrs after a meal

characterised by an anabolic state : increased TAG and glycogen synthesis

72
Q

How is the liver adapted for metabolism

A

Blood containing nutrients and hormones from gut and pancreas directly passes through liver before returning to heart

the liver absorbs the carbs/lipids/aa to be broken down, stored or redistributed

73
Q

Excess glucose is converted to ….

A

TAG which is then packages into very low density lipoproteins (VLDL)

74
Q

What happens after carb intake occurs

A

Increased glucose uptake by hepatocytes ; insulin independent glucose transporters (GLUT-2) have high Km

increased phosphorylation of glucose

excess glucose to form TAG

increased glycogenesis

increased activity of the pentose phosphate pathway/hexose monophosphate (uses up to 10% of glucose)

75
Q

When does glycolysis mainly occur ?

A

Glycolysis mainly occurs during the absorptive period after a carb rich meal

76
Q

Where is the primary site of fatty acid synthesis

A

The liver

77
Q

Describe the degradation of amino acids

A

Deamination of amino acids to form urea

carbon skeleton will be degraded to pyruvate, acetyl CoA, or TCA cycle intermediates

78
Q

What is the function of the pentose phosphate pathway

A

Produce NADPH which is needed for fat synthesis

79
Q

what occurs in the skeletal muscle during the fed state

A

Glucose used to replenish glycogen stores depleted by exercise

increased uptake of BCAAs

increased insulin:glucagon

FAs are of secondary importance to glucose during resting stage

80
Q

Describe the fuel used by the brain tissue

A

No significant glycogen/TAG stores as they cannot cross the blood-Brian barrier

blood glucose is the fuel used and sometimes ketone bodies

81
Q

Describe the symptoms refeeding syndrome

A

after prolonged starvation, a meal can bring complications

symptoms:

most commonly hypophosphataemia

hypokalaemia(cuases arrhythmias and cardiac arrest) and hypomagnesaemia (cardiac dysfunction)

can be fatal

82
Q

what kind of people at risk of refeeding syndrome

A

malnourished due to anorexia nervosa, dysphagia, alcoholism, depression, old age, uncontrolled diabetes

reduced ability to absorb due to bowel disorders such as IBS, coeliac disease, CF

increased metabolic demands due to cancer or surgery

83
Q

What happens during refeeding syndrome

A

During starved state, ketones and FAs become major fuel source

during prolonged starvation, intracellular minerals become depleted (These are needed as cofactors); with the aim to preserve muscle breakdown, decreased use of FA and ketones, brain switches to ketones

during refeeding, shift back to carb metabolism ;

insulin stimulates macromolecule synthesis which requires minerals

uptake of minerals by cell from blood leads to osmotic issues in cells and lack of PO42-, K+ and Mg2+ in blood

84
Q

Breakdown of carbohydrates

A

digested by alpha-amylase and disaccharidases

glucose is oxidised for energy

glucose forms the carbon skeleton of most compounds

85
Q

Protein breakdown

A

cleaved by pepsin in stomach and proteolytic enzymes in pancreas

proteins used for neurotransmitter and heme synthesis

carbon skeleton may be oxidised

86
Q

How does glucose enter b-cells?

A

GLUT-2 transporter = facilitated diffusion phosphorylated by glucokinase glucose-6-phosphate metabolised via glycolysis

87
Q

what happens after glucose enters Beta cells in islets of langerhans ?

A

ATP levels rise rise in ATP = potassium pump starts working, leaves cell, voltage potential changes, calcium diffuses in, signalling molecules are told to release insulin

88
Q

How does the liver aid in metabolism?

A

connection between digestive tract and circulatory system

venous drainage of gut and pancreas passes through the hepatic portal vein

liver takes up carbohydrates, lipids and amino acids from blood

89
Q

describe carb metabolism during the fed state [7]

A

Increased glucose uptake by hepatocytes (GLUT2),

increased phosphorylation of glucose (glucokinase creates G6P),

Excess glucose is converted to TAG (packaged in VLDL),

increased glycogenesis (glycogen synthase activated),

increased activity of pentose phosphate pathway,

increased insulin-to-glucagon results in increased

glycolytic enzymes (glucokinase, PFK1, pyruvate kinase), decreased production of glucose

90
Q

Import of LCFAs into mitochondria

A

CoA esters cannot cross mitochondrial inner membrane,

long chain fatty acyl group transferred to carnitine,

LCF acyl carnitine transported into mitochondrial matrix (carnitin exported),

LCF acyl group transferred to CoA

91
Q

how do short and medium fatty acids get converted to fatty acylCoAs?

A

short and medium chain fatty acids pass directly into mitochondria where they are activated to fatty acylCoAs

92
Q

describe carbohydrate metabolism (starved state)

A

Liver: Glycogen degradation occurs first, followed by gluconeogenesis. Also produces ketone bodies.

The carbon skeletons from gluconeogenesis are derived from glucogenic aa, lactate from muscle and glycerol from adipose tissue.

93
Q

reaction 1 of glycolysis

A

Irreversible.

Phosphorylation: -traps glucose inside the cell;

-ive charge at physiological pH.

conserves metabolic energy.

phosphates interact with enzyme active sites and lower activation energy.

Catalysed by GLUCOKINASE in the liver or HEXOKINASE in muscle/fat.

94
Q

describe reaction 3 of glycolysis

what are the enzymes involved

what type of reaction is it

A

the phosphorylation of fructose 6-phosPhate

irreversible reaction,

rate limiting,

catalysed by phosphofructokinase-1.

Most important control point

Inhibited by high ATP and citrate

95
Q

how are glycogenolysis and calcium linked

A

calcium is released into cytoplasm after neutral stimulation, released from sarcoplasmic reticulum

this leads to glycogenolysis in the muscle

96
Q

what is the importance of glycerol ?

A

transported to liver, phosphorylated to glycerol-3-phosphate and converted to DHAP: used in glycolysis or gluconeogenesis

97
Q

gluconeogenesis ;

when does it occur and which substrate is used

A

Exercise: lactate Sort term fasting: alanine Diabetes: insulin sensitivity Trauma: peripheral insulin resistance

98
Q

how is metabolic flux controlled?

A

by controlling enzymes involved, hence inhibiting or stimulating different reactions

99
Q

when does the starved state occur?

A

>3 days after last meal

100
Q

Describe the fuel use of muscle

A

Glucose, fatty acids and ketone bodies

glycogen store can be converted to glucose for contraction (glucose prioritised for contraction)

FAs are primarily used by resting muscle

101
Q

Describe the fuel use of the heart

A

Fatty acids

ketone bodies

lactate

no glycogen reserves

102
Q

Describe the fuel use of adipose tissue

A

Needs glycerol 3-phosphate to creat triacylglycerols

needs glucose for glycolytic intermediate dihydroxyacetone phosphate (then it is reduced to G-3-P)

103
Q

Metabolic functions of liver

A

makes fuel for brain, muscle and peripheral organs

metabolises ⅔ of glucose to form glycogen

turns fatty acids to ketone bodies

uses alpha-keto acids from amino acids

104
Q

Describe what occurs in the liver during the starved state

A

in liver:

  • glycogenolysis first then gluconeogenesis
    • increased glucagon:insulin
    • Carbon skeletons of glucose derived from glucogenic amino acids, lactate from muscle and glycerol from adipose
  • ketone body production (conc drops during prolonged starvation due to organ shutdown)
    • NADH produced inhibits TCA cycle
      • Acetyl CoA produced activates pyruvate carboxylase and inhibits pyruvate dehydrogenase
  • Fatty acid Oxidation is the major energy source
105
Q

What occurs in adipose tissue during the starved state

A

TAG lipolysis = releases FAs

decreased uptake of fatty acids and glucose so reduced glycolysis/TAG synthesis

106
Q

role of kidney in fasting state

A

In late fasting 50% of gluconeogenesis occurs here

uses self generated glucose

compensates for acidosis caused by ketone bodies

107
Q

Summary of starved state

A

at first brain uses glucose

beyond 2-3 weeks ketone bodies replace glucose usage

as glucose no longer required, protein catabolism for gluconeogenesis not needed either - lower protein degradation

kidney becomes more important : most gluconeogenesis occurs here now to provide kidneys with glucose to counteract acidosis from ketone bodies

108
Q

Diabetes mellitus

type 1

describe and explain the symptoms

A

early onset - childhood or adolescence; hyperglycaemia causes increased urination/thirst/weight loss/ increased appetite; diabetic ketoacidosis = persistent fatigue, dry or flushed skin, abdominal pain, nausea or vomiting, confusion, trouble breathing, and a fruity breath odor

108
Q

Diabetes mellitus

type 1

describe and explain the pathophysiology

A

caused by autoimmune attack on beta cells in islets of langerhans

hyperglycaemia and ketoacidosis :

  • increased gluconeogenesis
  • increased mobilisation/oxidation of FAs
    • leads to increased 3-hydroxybutyrate and acetoactetate

Hypertriacylglycerolemia:

  • excess FAs are converted to TAG
  • low lipoprotein degradation by LPL
    • reduced enzyme production
      • excess chylomicrons and VLDL
109
Q

Type II diabetes

explain the pathophysiology

A

Caused by a combination of insulin resistance and dysfunctional beta cells

hyperglycaemia

  • increased hepatic production and reduced peripheral use
  • ketosis is minimal as insulin is usually present in small amounts

dislipidemia

  • FAs converted to TAG and secreted as VLDL (can cause plaques)
  • chylomicrons synthesised from dietary lipids in intestine
  • but LPL is low so VLDL/chylomicrons are elevated
110
Q

Describe how ATP is formed from NADH and FADH2

A

TCA cycle produces 1 FADH2 and 3NADH molecules (8 e- in total)

NADH binds to complex I and it transfers its e- to CoQ ; 4 H+ pumped from matrix to IMS

complex II accepts e- from FADH2 and transfers them to CoQ

CoQ transfer all these e- to complex III ; e- accepting by heme group within ; the e- are then given to cytochrome c ; 2 H+ also pumped

cytochrome c transfer the e- to complex IV ; e- transferred to oxygen to form water ; 8 protons pumped across

111
Q

Describe the ETC

A

Found on inner mitochondrial membrane

4 protein complexes :

3 proton pumps(complexes I,III and IV) and 1 linking to the TCA cycle (complex II)

2 small components:

CoQ and cytochrome C - they are free to move inbetween membranes

H+ return to matrix via ATP synthase; coupled with ATP synthesis

NADH makes 3 ATP

FADH2 makes 2 ATP

112
Q

Name 3 examples of ETC inhibitors

A

cyanide

azide

CO

(all these inhibit complex IV)

113
Q

Name 3 examples of ETC uncouplers

A

Dinitrophenol (synthetic)

thermogenin (natural)

114
Q

what would high lactate DH in blood indicate?

A

lots of anaerobic resp so there must be a lack of oxygen ; MI/ischaemia/necrotic bowel

Biochemistry year 1 (8 decks)

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