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Biology - Year 2 > Biochemsitry - Metabolism in Health and Disease part 2 > Flashcards

Biochemsitry - Metabolism in Health and Disease part 2 Flashcards

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1
Q

What is the starting point of cholesterol synthesis?

What molecules have a positive regulatory effect on cholesterol synthesis?
What molecules have an inhibitory effect?

A

Acetyl CoA

Insulin - up regulates HMG-coA reductase

Glucagon - down regulates HMG-coA reductase

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2
Q

What is the substrate for the only control point in cholesterol synthesis?

What is this substrate converted to?

What enzyme catalyses this reaction?

A

Beta-Hydroxy-beta-methyl-glutaryl-coA

Mevalonate

HMG-coA-reductase

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3
Q

What other processes does cholestrol regulate?

What type of feedback process are these?

A

Stimulates the proteolysis of the controlling enzyme HMG-coA reductase

Decreases uptake of LDL particles by endocytosis

Negative

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4
Q

What happens to cholesterol to make it a cholestrol ester?

What effect does this have on cholestrol?

A

Fatty acid is esterfied at position 3

Makes cholestrol more hydrophobic

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5
Q

Why is de novo fatty acid synthesis important?

A

Conversion and storage of excess glucose - inefficient and abnormal fatty acid storage causes insulin resistance and diabetes

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6
Q

What is the initial substrate of de novo fatty acid synthesis?

What is the starting point for fatty acid synthesis?

Where does fatty acid synthesis occur?

A

Pyruvate

Acetyl coA

The cytosol

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7
Q

What are three ways in which pyruvate can be produced?

Which is the main pathway?

A

Glycolysis, alanine synthesis and lactic acid synthesis

Glycolysis

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8
Q

What is the control step in fatty acid synthesis?

What compounds have positive and inhibitory effects on the enzyme that controls this step?

A

Carboxylation of acetyl coA to malonyl coA, catalysed by acetyl coA carboxylase

Citrate - positive regulation
Long-chain fatty acyl coA

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9
Q

What effects do insulin, glucagon and adrenaline have on fatty acid synthesis? Why?

A

Insulin - feeding hormone wants to get rid of glucose so enhances fatty acid synthesis

Glucagon - fasting response, under fasting conditions metabolise to produce energy, fatty acid synthesis requires lots of energy so is inhibited

Adrenaline - fight/ flight response, need to generate ATP to help with this response - break down fatty acids not synthesise them so FA synthesis inhibited

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10
Q

Is acetyl coA carboxylase active or inactive when phosphorylated?

A

Active when not phosphorylated

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11
Q

What are the two essential fatty acids?

What type of double bond do they have?

A

Linolenic acid - three double bonds first is omega 3 double bond

Linoleic acid - two double bonds, first is am omega 6 double bond

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12
Q

Where does LDL deliver cholesterol?

What does HDL do with cholestrol?

A

Extrahepatic - non-liver tissues

Takes cholestrol from the cells

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13
Q

What are the two ways a cell can obtain cholestrol?

A

It can synthesise cholesterol

Or obtain cholesterol via LDL

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14
Q

Describe the process by which a cell takes up LDL?

A

Uses special LDL receptors

LDL particles bind to LDL receptor, several endosomes aggregate (endocytosis)

LDL particles are internalised and form endosome vesicles

In endosome LDL particle separates from receptor, receptor recycles back to plasma membrane

Part of the endosome containing LDL particle fuses with an intracellular lysosome

Lysosome hyrdrolyses lipids and proteins releasing cholesterol, fatty acids and amino acids to be used as needed

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15
Q

What is the lipoprotein(s) in the exogenous lipoprotein pathway?

What is the lipoprotein(s) in the endogenous lipoprotein pathway?

A

Chylomicrons

VLDL/ IDL, LDL and HDL

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16
Q

Why do acetyl coA and oxyaloacetate combine to form citrate at the start of fatty acid synthesis?

A

Acetyl coA is the starting point of fatty acid synthesis but there is no mitochondrial membrane transporter for acetyl coA but there is one for citrate.

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17
Q

How to insulin, glucagon and adrenaline affect the activity of acetyl coA carboxylase (ACC)?

A 
High glucagon and adrenaline bind to receptors and increase levels of cyclic AMP
cAMP activates a class of protein kinases which phosphorylate ACC and deactivate it.

Under feeding conditions insulin binds to receptors and through signal transduction mechanisms activates phosphatases which remove phosphates activating ACC and allowing acetyl coA to be converted to malonyl coA

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18
Q

What is the name of the enzyme that breaks fatty acids into their key components?

A

Hormone sensitive lipase

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19
Q

Describe these genetic disorders:

  • Refsum disease
  • X-linked adrenoleukodystrophy
  • MACD deficiency
  • Zellweger syndrome
A

Inability to breakdown phytanic acid, caused by lack alpha-hydroxylase enxyme, causes neurological damage

Defect in peroisomal activation of VLCFA, causes progressive brain damage

Most common deficiency in fatty acid oxidation, can oxidise FA up to about 14C long, causes severe hypoglycaemia

Peroxisome synthesis defect, causes enlarged liver

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20
Q

What are flippases, floppases and scramblases?

A

Flippases - used to flip PL from outer to inner bilayer

From inner to outer bilayer

Bidirectional, flip PL both ways, flip two at the same time

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21
Q

What is the only phospholipid with four fatty acids?

A

Cardiolipin

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22
Q

What do these terms mean:

  • endocrine
  • paracrine
  • autocrine
A

Hormones released from gland into bloodstream, travels through circulation

Adjacent cells, on cell secretory the other has specific receptors for secretory molecules

Same cell acts as secretory and target cell

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23
Q

What type of molecule can pass through the phospholipid bilayer, hydrophobic or hydrophilic?

A

Hydrophobic

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24
Q

What are the three amino acids that are targets for post translational modifications?

A

Serine, threonine and tyrosine

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25
Q

What are ways of terminating the signal transduction pathway?

A

Removal of extracellular signal

Receptor sequestration

Receptor down regulation

Inactivation of receptor protein

Inactivation of signalling protein

Production of a inhibitory protein

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26
Q

What are the three components to a G protein coupled receptor?

A

Receptor, trimeric G-protein, effector protein

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27
Q

What happens when a hormone binds to a G protein coupled receptor?

A

Hormone binding induces conformational change in receptor

Activated receptor binds to G-alpha subunit

Receptor causes conformation change in G-alpha triggering dissociation of GDP

Binding of GTP to G-alpha triggers dissociation of G-alpha from receptor and G-beta-gamma

Hormone dissociates from receptor, G-alpha binds to effector activating it

Hydrolysis of GTP to GDP causes G-alpha to dissociate from effector and re associate with G-beta-gamma

28
Q

What is the function of adenylate cyclase?

A

To hydrolyse ATP in a cell into cAMP

29
Q

Which lipoproteins are rich in triacylglycerols?

A

VLDL and chylomicrons

30
Q

What are membrane rafts contain high levels of?

A

Sphingolipids and cholesterol

31
Q

What are the substrates for gluconeogenesis?

A

Glycerol

Acetyl coA

Lactate

Amino acids

32
Q

Which lipoprotein enters the cells by endocytosis?

A

LDL

33
Q

What are the characteristics of the enzyme ATPase?

A

It regenerates ATP from ADP and Pi or it hydrolyses ATP to generate energy for the active transport of protons (H+) across membranes

34
Q

What do statins do?

A

Inhibit HMG coA reductase

35
Q

What is the main source of carbons for fatty acid synthesis?

A

Malonyl coA

36
Q

Why is de novo fatty acid synthesis important?

A

The reduction of blood glucose levels

37
Q

In fatty acid synthesis reducing equivalents are provided by?

A

NADPH

38
Q

Gluconeogenesis starts how long after a meal?

A

4 hours

39
Q

In the process of fatty acid beta-oxidation the enzyme carnitine pamlitoyl transferase 1 plays an important role, what is it?

A

The conversion of fatty acetyl coA to fatty acetyl carnitine

40
Q

What is the point of having pyruvate kinase as the final control point in gluconeogenesis?

A

Prevents a futile metabolic cycle that converts pyruvate > oxaloacetate > phosphenolpyruvate (PEP) > pyruvate

41
Q

What is the co factor required for fatty acid synthesis?

A

NADPH

42
Q

What are protein kinases, what do they do?

What are protein phosphatases?

A

A class of enzymes that use ATP to phosphorylate proteins within the cell by transferring a phosphate from ATP to a serine, threonine or tyrosine hydroxyl group in a protein

A group of enzymes that catalyse the removal of the phosphate by hydrolysis

43
Q

Give examples of serine/ threonine kinases?

Give examples of tyrosine kinases?

A

PKA, PCK, MAPK, CaMK2

Receptor tyrosine kinase which targets PI3

44
Q

Give examples of serine/ threonine protein phosphates.

Give examples of tyrosine phosphatases.

A

Ca2+ independent PP1 and PP2A

Protein tyrosine phosphatase (PTP)

45
Q

What are the three main families of Ga proteins?

A

G-alpha-s: activates adenylyl cyclase

G-alpha-i: inhibits adenylyl cyclase

G-alpha-q: phospholipase C-beta

46
Q

What factors modulate cAMP levels in the cells?

A

Activation of G-alpha-s and G-alpha-i (which is regulated by the ligand and GPCR activated pathways

Phosphodiesterase enzymes break down cAMP into inactive (5’-AMP)

Forskolin activates AC directly independent of GPCR pathway

47
Q

What are the downstream targets of cAMP?

A

EPAC (exchange protein activated by cAMP)

Cyclic nucleotide-gated ion channels (involved in olfactory and visual signals)

cAMP dependent protein kinase aka protein kinase A (PKA)

48
Q

What are some of the physiological processes regulated by cAMP?

A

Metabolism including glycogenolysis and lipolysis

Cardiac and smooth muscle contraction

Secretory processes

Ion channel conductance

Memory and cognitive functions

Cell growth differentiation and apoptosis

Inflammatory and immunological responses

49
Q

What does EPAC do?

A

Mediates integrin-mediated cellular adhesion

E.g. Epac moderates vascular endothelial cell barrier - initiates a rigorous program of protective anti-inflammatory responses in vascular endothelial cells

50
Q

What does PKA do in the cell?

A

Role in glycogenolysis - adrenaline mediates the breakdown of glycogen, cascade of events starts with hormone binding leading to activation of AC and then PKA which:

  • Increases production of glucose-1-p from glycogen by activating phosphorylase kinase which activates glycogen phosphorylase
  • Inhibits glycogenesis by directly phosphorylating and inhibiting glycogen synthase
  • Net increase in glucose-1-P levels

Cell function

  • in cardiac muscle activates contraction
  • in smooth muscle activates relaxation

Activates CREB - control of gene expression (transcription)

  • PKA translocates from cytoplasm to nucleus (where CREB resides), phosphorylate and activates CREB
  • CREB is a transcription factor that regulates cellular responses
51
Q

How many classes of PLC enzymes exist?

What are they all dependent on?

A

PLC-beta: activated by GPCR via G-alpha-q subunits

PLC-gamma: activated via tyrosine kinase receptors

Ca2+

52
Q

How does the GPCR/PLC pathway work?

A

PLC hydrolyses phosphatidyl inositol 4, 5- bisphosphate (PIP2) and generates two second messengers diacylglycerol (DAG) and inositol 1, 4, 5-triphosphate IP3

DAG activates protein kinase C (PKC) which phosphorylates a target protein causing cellular effects

IP3 causes opening of IP3 gated Ca2+ channels and Ca2+ release from the ER/SR
The increase in intracellular Ca2+ concentration activates protein kinase C

53
Q

What is the resting level of calcium in the cell?

What is the resting level of calcium outside the cell?

How much calcium is stored in the cell?

A

100nm

1.3 - 1.8mM

1mM in the ER/SR

54
Q

What are the two pathways that increase intracellular Ca2+ increase?

How does calcium exit the cell?

A

Calcium channels - entry of small amount of calcium into cell leads to huge release if calcium (caused by calcium binding to RyR receptors

Initiation of release of IP3, released by phospholipase C - IP3 binds to calcium gated channels causing calcium release

Pumped out by calcium sodium exchange

55
Q

When are store operated calcium channels (SOC/ CRAC) opened?

What is Orai1?

What happens when ER Ca2+ stores are depleted?

A

When ER/SR content is depleted

A protein calcium sensor that communicates with the store operated channel

STIM1 binds to Orai1 leading to channel opening, binding only occurs when calcium in store not bound to STIM1

56
Q

What activates calmodulin?

What does calmodulin do?

What are the targets of calmodulin?

A

Calcium

Has roles in many Ca2+ regulated processes! relays to protein kinases and protein phosphatases

CaM dependent protein kinase (CaMK2) and CaM dependent protein phosphatase (calcineurin) (CaN)

57
Q

What does CaM do?

What does CaN do?

A

Acts as a memory device

Is a major target for immunosuppressants, one of its main targets is the NFAT

58
Q

What are the six families of enzyme linked receptors?

A

Receptors tyrosine kinases

Tyrosine-kinase associated receptors

Receptor serine/ threonine kinases

Receptor guanylyl cyclases

Death receptors

59
Q

What are the three essential components of receptor tyrosine kinases?

A

Extracellular domain containing ligand-binding site

Single hydrophilic transmembrane alpha helix

Cytosolic domain that include a region with PTK

60
Q

What are the three factors that interact with receptor tyrosine kinases?

A

Phospholipase C gamma

Phosphotidylinositol (PI-3-K)

GTPase activating protein - activates MAPK

61
Q

What does PLC gamma do?

A

Cleaves PIP2 into DAG and IP3

DAG activates PKC

IP3 leads to activation of intracellular Ca2+

62
Q

Describe the receptor tyrosine kinase PI3 kinase signalling pathway?

A
  1. Growth factor binds to RTK and activates it
  2. Activated PI3 kinase phosphorylates PIP2 into PIP3
  3. PDK1 and AKt (PKB) dock to PIP3 in the membrane
  4. PDK1 phosphorylates AKt and activates it
  5. Activated AKt dissociates from PIP3 in the membrane and initiates several cell responses
63
Q

What is the ligand for receptor linker guanylyl cyclase?

What is the ligand for soluble guanylyl cyclase?

A

Natriuretic peptide

Nitric oxide gas

64
Q

What are natriuretic peptides?

What are the types?

Where are they expressed?

A

A family of peptide hormones

ANP and BNP

ANP is mainly expressed in the atria of the heart
BNP is synthesised in the the ventricular myocardium

65
Q

What are some of the functions of soluble guanylyl cyclase?

A

Relaxation of vascular

Regulation of synaptic signal transmission

Inhibition of platelet aggregation

Immunonmodulatory effects

66
Q

What are the common structural features of nuclear receptors?

A

Unique N-terminal region that acts as a transcription activation domain

Central DNA-binding domain (DBD)

C-terminal hormone (ligand) binding domain

Biology - Year 2 (9 decks)

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