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x M1 Biochem Quiz 2 > Lectures 13-19 > Flashcards

Lectures 13-19 Flashcards

1
Q

in Initially in starvation, what will we be using for energy? what will we switch to?

A

Initially use carbs, then after a few days switch to Fatty Acids.

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2
Q

Once you stop taking in glucose, where could it come from in the body? (3 places)

A
  1. glycogen (stored glucose)
  2. Proteins/amino acids
  3. fatty acids/triglycerides
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3
Q

what are the problems with using glycogen and proteins for energy during starvation?

A

glycogen: limited quantities
proteins: not a great idea to draw down on these

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4
Q

what are the 2 sources for fatty acids?

A
  1. direct ingestion

2. creation from ingested glucose and stored.

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5
Q

how are lipids defined?

A

substances that are not soluble in water, ie hydrophobic. only extractable with organic solvents

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6
Q

what is the structure of a fatty acid?

A

carboxyl group (COOH) with long hydrophobic hydrocarbon chain (HC)

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7
Q

what is the difference between saturated and unsat fatty acids?

A

sat: no double bonds
unsat: has double bonds. may be mono-unsat or poly-unsat

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8
Q

what are the essential fatty acids? why are they essential?

A

linoleate and linolenate. double bonds are less than 9 Cs from end/omega carbon. we cannot synthesize that structure.

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9
Q

what is the difference between cis and trans fatty acids?

A

cis: has a kink
trans: straight, despite double bond.

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10
Q

what does a trans fatty acid behave like?

A

a fully saturated fatty acid, ie it packs in tightly and has a high melting point.

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11
Q

what does commercial hydrogenation of a FA do to its melting point?

A

raises it despite fat content.

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12
Q

what is the problem with trans-unsaturated FAs in the body?

A

they are incorporated into cell membranes, and make them less flexible. more prone to atherosclerosis. (hence thrombi, infarction)

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13
Q

what are arachidonic and eicospentenoic acid?

A

long chain unsaturated FAs made from the 2 essential FAs

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14
Q

what is a triglyceride?

A

storage form of FA. 3 fatty acids attached to a glycerol backbone

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15
Q

where do most of adult fuel stores reside?

A

adipose tissue, as triglyceride.

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16
Q

where do we synthesize FAs?

A

in liver, lactating mammary. NOT in adipose tissue. we have to transport it to adipose.

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17
Q

where does beta-oxidation take place?

A

muscle, liver. in mitochondria, requires oxygen

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18
Q

where does ketogenesis take place?

A

liver only

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19
Q

what are the 4 enzymes that are critical to FA synthesis?

A
  1. ATP CItrate Lyase (ACL)
  2. Acetyl-CoA Carboxylase (ACC)
  3. Fatty Acid Synthase (FAS)
  4. Malic Enzyme
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20
Q

when are FAs synthesized? what needs to happen?

A

synthesized when there is enough glucose going through glycolysis that the TCA is running a lot. requires some citrate to be exported from mitochondria to yield a cytoplasmic pool of citrate. Then with ACL, creates a cytoplasmic pool of Acetyl-CoA

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21
Q

what is the ACL reaction? what does it require to get FA synthesis started?

A

Reaction: citrate + ATP + CoA + H2O -> Acetyl-CoA + ADP + Pi + oxaloacetate. Need to invest some ATP in order to create the FAs.

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22
Q

What does Acetyl-CoA Carboxylase do?

A 
rate limiting, highly regulated step in FA synthesis. Uses Acetyl-CoA, ATP, and HCO3 to create Malonyl-CoA, ADP. 
Contains Biotin (as do all carboxylase enzymes - remember pyruvate carboxylase).
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23
Q

what are the 2 isozymes of ACC?

A

ACC-alpha: cytosolic. high in liver, mammary glands, used for FA synthesis.
ACC-beta: mitochondrial. not impt for FA synthesis but provides Malonyl CoA for regulation which is impt later on.

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24
Q

Biotin is a vitamin: which one?

A

Vitamin B7

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25
Q

How many catalytic sites are there on the FAS enzyme? which one do we use for this particular pathway?

A

8 catalytic sites overall. We use the ACP Domain with Pantothenic Acid to synthesize FAs.

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26
Q

where does Pantothenic Acid attach to the FAS?

A

at the ACP domain

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27
Q

what’s at the end of Pantothenic Acid?

A

a thiol group (SH)

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28
Q

How does FAS make fatty acids? what is the process?

A

Dimeric enzyme. One Pantothenic Acid holds a Malonyl CoA, the other holds an Acetyl CoA. Carbons are transferred 2 at a time from Malonyl to Acetyl, up to 16. The role of Pantothenic Acid is basically to immobilize the reactants so they can react.

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29
Q

How many cycles of addition do the reactants go through to create a 16C Fatty Acid?

A

7 cycles. Start with 2C, add 14 more.

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30
Q

Fatty Acid synthesis: what are the 2 substrates, the enzyme, the cofactor, and the product?

A

2 substrates: Malonyl CoA and Acetyl CoA
Enzyme: Fatty Acid Synthase
Cofactor: NADPH
Product: Palmitic Acid

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31
Q

Why does FA synthesis require NADPH? how many moles are required?

A

it is a cofactor to reduce the double bonds created. Require 14 moles.

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32
Q

where is FAS expressed?

A

ONLY in lipogenic tissues (liver and lactating mammary)

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33
Q

What are the sources of NADPH cofactor for the FAS reaction?

A

2 places: 6 moles from the pentose phosphate pathway, 8 moles from citrate -> oxaloacetate -> malate -> pyruvate (which then diffuses back into the mito). Malate -> pyruvate releases CO2 and NADPH.

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34
Q

Malic enzyme: what does it do? what tissues is it expressed in?

A

Catalyzes rxn from malate -> pyruvate. expressed only in tissues that make FAs

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35
Q

Fate of newly synthesize or ingested FA?

A

synthesized: takes the VLDL taxicab from the liver to adipose tissue, where it is stored as triglyceride.
ingested: taxi = chylomicron

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36
Q

what enzyme allows fatty acids to enter adipose tissue cells?

A

lipoprotein lipase.

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37
Q

What is one way that glucose tempers its metabolism that fructose does not?

A

through producing ATP which then inhibits PFK-1, slowing the glycolysis pathway. Since fructose does not cause this, there is more cytoplasmic Acetyl-CoA created by fructose which leads to more FA synthesis.

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38
Q

What does fructose do to the creation of Fatty Acid Synthesis enzyme genes?

A

enhances their transcription, specifically FAS and ACC

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39
Q

What are the 3 lipases within the adipocyte that work to release 3 FAs per triglyceride molecule? What other protein is required for these to work?

A
  1. adipocyte triglyceride lipase (ATGL)
  2. hormone-sensitive lipase (HSL)
  3. monoglyceride lipase (MGL)
    Also: perilipin
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40
Q

What catalyzes lipolysis of circulating triglycerides (in VLDL and chylomicrons)? Where is it located?

A

lipoprotein lipase (LPL). Located extracellularly on the capillary endothelium of adipose tissue

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41
Q

What are Free Fatty Acids?

A

released to the blood stream during lipolysis, bound covalently to albumin. ‘Free’ because they are no longer attached to the glycerol backbone

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42
Q

what tissues can oxidize FFA? What is required for this oxidation?

A

nearly all tissues, except brain and RBCs. Process requires mitochondria and O2.

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43
Q

What is the regulated step in the oxidation of FFA? what 3 enzymes are required for this step?

A

Regulated step: updake of FFA into mitochondria. Requires carnitine, CAT-I and CAT-II

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44
Q

What is a inhibitor of CAT-1? What is the effect of this inhibition?

A

Allosterically inhibited by Malonyl-CoA (generated by ACC). Effect is to synchronize rates of FA synthesis and oxidation, and to regulate the rates of FA and glucose oxidation in muscle/heart.

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45
Q

Beta-oxidation of FAs generates how much ATP?

A

106 mol per mol of 18C FA

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46
Q

How does beta-oxidation of FAs generate ATP?

A

through the TCA and Electron Transport chain, using FADH2, NADH and Acetyl-CoA.

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47
Q

what is required to ensure the operation of the Krebs cycle?

A

oxaloacetate. created from pyruvate, via glucose metabolism. yields an ongoing requirement for glucose availability for FA oxidation.

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48
Q

Do FAs penetrate the blood-brain barrier?

A

very poorly, due to their hydrophobic nature.

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49
Q

how does the brain access the calories in FAs?

A

they are partially oxidized to ketone bodies (acetoacetate and beta-hydroxybutyrate) which can cross the barrier. once inside brain tissue, they are metabolized within mitochondria (again requiring glucose for ongoing TCA cycle intermediates).

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50
Q

Can humans synthesize glucose from FAs?

A

NO!!

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51
Q

What does adipose triglyceride lipase (ATGL) do?

A

major triglyceride lipase

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52
Q

What does hormone-sensitive lipase (HSL) do?

A

breaks down diglyceride

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53
Q

What does monoglyceride lipase (MGL) do?

A

breaks down monoglyceride

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54
Q

what does lipoprotein lipase do?

A

produced in adipocyte, secreted and lodged on extracellular surface of capillary endothelium, acts on VLDL and chylomicrons.

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55
Q

what does pancreatic lipase do?

A

enzyme responsible for hydrolysis of ingested triglycerides in the small intestine

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56
Q

Overall effect of ATGL, HSL, and MGL?

A

Adipose triglyceride –> glycerol + 3 FAs

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57
Q

Of the three enzymes that break down FAs, which are highly regulated?

A

ATGL and HSL

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58
Q

what happens to the products of lipolysis?

A

released from adipocyte to plasma.

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59
Q

What happens to the Free Fatty Acids that are circulating bound to albumin?

A

taken up as oxidative fuel, also available to liver for conversion to ketone bodies

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60
Q

what happens to the glycerol that is circulating in blood after lipolysis?

A

available as a gluconeogenic precursor in liver and kidney

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61
Q

what is the preferred fuel for oxidative metabolism in muscle that creates ATP?

A

Fatty acids.

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62
Q

where does FA oxidation take place?

A

in mitochondria

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63
Q

what happens when a FA enters a cell? where does this rxn take place?

A

a series of fatty-acyl-CoA synthases link FA to Coenzyme A. This rxn requires the investment of ATP. Takes place on the outer membrane of a mitochondrion.

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64
Q

what needs to happen for a FA to enter mito?

A

long chain FAs (>12C) cannot traverse the inner mito membrane. they are carried across by linking to carnitine. this rxn is catalyzed by the enzyme carnitine acyltransferase-1 (CAT-1).

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65
Q

What does CAT-I do? where is it located?

A

links FA to carnitine, so that the FA can traverse the inner mito membrane. Located on the outer surface of the inner mito membrane (ie, in the inter-membrane space)

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66
Q

What inhibits the addition of Carnitine to the FA by CAT-I?

A

Malonyl-CoA, which was produced by the ACC-beta enzyme. highly regulated reaction. yields an inverse and relationship between the rate of FA synthesis and the rate of FA oxidation in liver. swiching mechanism between utilization of glucose or using FA.

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67
Q

What will happen to malonyl-CoA levels when glucose is readily avail/glycolysis is high?

A

Malonyl-CoA will be abundant, FA will not be oxidized. When glucose is scarce, Malonyl-CoA levels will fall and FA oxidation will increase.

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68
Q

Once happens in the matrix once FA-carnitine has been transported across the inner membrane?

A

Fatty Acyl-CoA is reformed (carnitine removed) by CAT-II

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69
Q

What happens once the FA is inside the mito matrix?

A

FAs will be oxidized (at beta carbon first) and then a series of 2C fragments will be released. Thus each Palmitic Acid (16C) will undergo 7 oxid cycles, yielding 8 Acetyl-CoAs.

70
Q

What happens in the dehydrogenase reactions?

A

Formation of FADH2 and NADH. These are then avail for the ETC and production of ATP via ATP synthase.

71
Q

What will happen to the 8 Acetyl-CoAs?

A

available to the TCA cycle as long as sufficient oxaloacetate is present.

72
Q

About how many more times as much ATP generated from one mole FA as from one mole glucose?

A

about 3x. FA much more calorically dense

73
Q

What is ketogenesis? why is it important?

A

Conversion of FAs to ketone bodies. creates a water-soluble oxidative fuel out of FAs (which are only lipid soluble). ketone bodies can be used by muscle, but also are available to the brain.

74
Q

Where does ketogenesis occur?

A

LIVER ONLY

75
Q

What are the names of the ketone bodies (2)?

A
  1. acetoacetate

2. beta-hydroxybuturate

76
Q

When does ketogenesis occur?

A

when levels of oxolacetate are low – reflecting glucose unavailability. Acetyl-CoA will then be less converted to citrate, and has to be disposed of via ketogenesis.

77
Q

What is also formed during ketogenesis?

A

Acetone.

78
Q

What is ketoacidosis?

A

the accumulation of acetoacetate and beta-hydroxybutyrate (ketones) in plasma. They are organic acids so their accumulation leads to acidosis.

79
Q

Where does ketogenesis take place?

A

inside mitochondria

80
Q

Where does ketone oxidation take place?

A

mainly in brain and muscle

81
Q

what are required for ketone oxidation?

A

mitochondria, O2, oxaloacetate, succinyl-CoA (so glucose is required)

82
Q

What is the energy yield for ketones compared to glucose? do they require more or less oxygen?

A

higher energy yield, and less O2 required since they are already partially oxidized.

83
Q

During starvation, what is the preferred fuel for the brain?

A

ketones

84
Q

why can’t FAs be used to synthesize net glucose?

A
  1. the PDH reaction is irreversible, so pyruvate cannot be formed directly from Acetyl-CoA.
  2. (unsure, need to ask question)
85
Q

In the post-absorptive state, what pathways replenish our blood glucose?

A

hepatic glycogenolysis and gluconeogenesis (liver, kidney)

86
Q

what are the major gluconeogenic precursors? what tissues are they from?

A

amino acids (skel musc), glycerol (adipose), lactate (RBCs, musc)

87
Q

gluconeogenisis requires a lot of ATP: where does it derive from?

A

FA oxidation

88
Q

what is catabolism?

A

usage of stored energy/breakdown of storage products

89
Q

what is anabolism?

A

replenishment of energy stores

90
Q

what is the primary driver of the metabolic cycle (of catabolism/anabolism?)

A

insulin

91
Q

What does AMPK do? what does AMPK stand for?

A

stands for AMP-activated kinase.
part of regulation of enzymes in metabolic cycle. based on cell energy status. when ATP is low (and AMP rises), AMPK is activated and does 4 things: increases FA oxidation, increases cellular glucose uptake, decr FA synthesis, decr cell division.
when ATP is high, AMPK is inactivated.

92
Q

what controls the breakdown of cAMP?

A

phosphodiesterase

93
Q

glucagon and epinephrine work through what kind of receptors? what do they activate?

A

GPCRs. activate adenylate cyclase, which produces activated cAMP and PKA.

94
Q

in the fasted state, what initially provides energy? what does it switch to?

A

initially exogenous glucose, then glucogen stores, then gluconeogenesis from lipid calories. AAs, lactate, and glycerol provide precursors for gluconeogenesis and the necessary continued availability of glucose

95
Q

why is so little glycogen available to defend blood glucose levels?

A

because most glycogen is in muscles, which does not have glycogen-6P to export glucose.

96
Q

what energy sources can be used by RBCs?

A

only glucose. doesn’t have mitochondria for FA or ketone oxidation

97
Q

a rise in insulin is associated with anabolism or catabolism?

A

anabolism. because insulin brings glucose into cells from plasma, which follows a rise in blood glucose meaning that glucose should be stored

98
Q

one way to regulate enzyme activities during various nutrition states is for the substrates to regulate themselves. what does glucose do to self-regulate?

A

stimulates its own storage by enhancing net glycogen and FA synthesis

99
Q

one way to regulate enzyme activities during various nutrition states is for the substrates to regulate themselves. what do FAs do to self-regulate?

A

diminish rates of FA synthesis and increase FA oxidation (ie usage/breakdown)

100
Q

what acts as a metabolic sensor to read the availability of ATP and alter the rate of ATP generation or utilization?

A

AMPK.

101
Q

three hormones that are impt to controlling metabolism?

A

insulin, glucagon, epinephrine

102
Q

which hormones are the counter-regulatory hormones?

A

glucagon, epinephrine

103
Q

the secretion of insulin, glucacon, and epinephrine are all controlled by what?

A

glucose. glucose increases insulin levels, and decreases glucagon and epinephrine levels.

104
Q

what is generally the chemical-level change that occurs as a result of hormone activation of cell-surface receptors?

A

protein phosphorylation, based on activities of protein kinases and protein phosphorylases

105
Q

glucacon and epinephrine modulate what?

A

cAMP

106
Q

what are the downstream actions of glucagon and epinephrine (effects on glucose, FA and ketone metabolism)?

A
  1. activate net hepatic glycogen breakdown
  2. activate lipolysis in adipose tissue
  3. activate FA utilization (skel muscle)
  4. activate hepatic ketone synthesis
  5. activate hepatic gluconeogenesis
107
Q

what is insulin’s mechanism of action?

A

binds to extracellular domain of insulin receptor. results in receptor clustering, autophosphorylation of receptor and activation of intracellular domain (tyrosine kinase). eventually leads to activation of AKT.

108
Q

how does insulin impact cAMP phosphodiesterase? what is the impact on cAMP?

A

leads to phosphorylation of phosphodiesterase, which degrades cAMP and lowers intracellular cAMP.

109
Q

what does the destruction of cAMP (via insulin action) lead to?

A

glycogen storage, less gluconeogenesis and inhibition of lipolysis, inhibited ketogenesis.

110
Q

what does insulin do to GLUT-4?

A

stimulates insertion of GLUT-4 into membrane of skel muscle and adipose tissue. basically routes glucose to storage areas.

111
Q

when insulin decreases, where does glucose tend to go?

A

tends to go to insulin-independent tissues: RBC, brain.

112
Q

what controls the creation of glucose from glycogen?

A

activation of glycogen phosphorylase and inactivation of glycogen synthase

113
Q

what 2 things need to happen for gluconeogenesis to be activated?

A
  1. increased delivery of precursors to liver (AAs, glycerol, lactate)
  2. altered activity of enzymes in the gluconeogenic pathway (PFK2, Pyruvate kinase, PEP carboxykinase, Glucose-6-Phosphatase)
114
Q

what does PKA (cAMP dependent protein kinase) do to HSL and perilipin?

A

Phosphorylates them, causing them to be properly positioned and activated.

115
Q

what does phosphorylation via the cAMP/PKA pathway do to ACC-b activity?

A

decreases ACC-beta activity, lowering its product (malonyl-CoA), which no longer inhibits CAT-I, and thus allows more FA into mitochondria for increased use of FAs for energy.

116
Q

what state would be reached with uncontrolled diabetes: anabolic or catabolic?

A

catabolic or fasted state.

117
Q

what fuel source changes the most dramatically between 1-40 days of fasting?

A

ketones incr 1000x!

118
Q

what are 2 advantages to the ability of the brain to use ketones?

A
  1. mobility in face of scarce resources (adipose = light way to store energy, allows us to be mobile)
  2. maintenance of a larger brain relative to body size
119
Q

fall in glucose: intraprandial. what changes will take place?

A
  1. glycogen will be broken down by liver and used by brain.

2. lipolysis in adipose tissue, and FFAs used by muscle (b-oxidation) and liver (b-oxidation)

120
Q

fall in glucose: overnight. what changes will take place?

A
  1. glycogen breakdown by liver, fuels brain. but once run out of liver glycogen, initiate gluconeogenesis
  2. lipolysis in adipose tissue, FFAs used by muscle and liver (b-oxidation)
  3. FFAs going to liver, some will undergo ketogenesis –> muscle
  4. some muscle breakdown -> AAs, –> gluconeogenesis -> brain
121
Q

fall in glucose: prolonged fast. what changes will take place?

A
  1. no more glycogenolysis in liver (liver glycogen gone)
  2. lipolysis in adipose tissue, FFAs used by muscle and liver (b-oxidation)
  3. FFAs going to liver, some will undergo ketogenesis. no longer to go muscle, will go to brain
  4. some muscle breakdown -> AAs, –> gluconeogenesis -> brain
    cost: loss of adipose tissue and muscle
122
Q

what is autophagy?

A

process that involves the cell degrading its own content through lysosomal machinery.

123
Q

what is insulin’s normal effect on autophagy?

A

insulin normally restrains autophagy

124
Q

once the fed state is achieved, what does insulin do (generally)?

A
  1. causes changes in cAMP levels that reverse the protein kinase and protein phosphatase activities from the fasted state.
  2. stimulates FA, TG and protein synthesis
125
Q

when does autophagy occur?

A

at the outer limits of starvation, when there is no other fuel to use. eventually, we lose immune cells and that leads to death

126
Q

in uncontrolled diabetes, why does the blood glucose rise so dramatically? what is the origin of the glucose?

A

no insulin -> high hepatic gluconeogenesis

127
Q

in uncontrolled diabetes, what is responsible for the ketonemia/ketonuria, acidosis and fruity breath?

A

no insulin -> incr rate of lipolysis -> incr ketone synthesis in liver -> decr pH (acidosis) and acetone creation (fruity breath)

128
Q

in uncontrolled diabetes, how are the changes in blood glycerol and alanine related to the loss of adipose and skel muscle mass?

A

no insulin -> incr lipopytic rate -> glycerol release and loss of adipose tissue
also incr muscle breakdown -> AA release and loss of muscle mass

129
Q

What is the problem with high concentrations of fatty acids?

A

they are toxic; therefore have to be stored as triglycerides or attached to protein (albumin in blood)

130
Q

A phospholipid can be based on what two things?

A

can be based on glycerol or sphingosine.

131
Q

what is the initial acceptor of fatty acids during TAG/phospholipid synthesis?

A

glycerol phosphate

132
Q

how many pathways are there for glycerol phosphate production? where are these pathways located?

A

2 pathways. both located in liver, one located in adipose tissue.

133
Q

describe how glycerol phosphate can be made in liver. (precursors, enzymes, cofactors)

A
  1. from glucose, through glycolysis to DHAP. then NADH as cofactor with enzyme glycerol-P dehydrogenase –> glycerol phosphate.
  2. from glycerol (comes from lipolysis), using ATP, with enzyme glycerol kinase –> glycerol phosphate.
134
Q

describe how glycerol phosphate can be made in adipose tissue. (precursors, enzymes, cofactors)

A
  1. from glucose, through glycolysis to DHAP. then NADH as cofactor with enzyme glycerol-P dehydrogenase –> glycerol phosphate.
  2. no other pathway (no glycerol kinase pw in adipose tissue)
135
Q

what needs to happen to FAs for them to be metabolically active?

A

need to be activated by adding a CoA group

136
Q

what are the enzymes that activate FAs? what else is required to activate a FA?

A

group of enzymes called fatty acyl CoA synthases. also requires addition of CoA group and ATP.

137
Q

What enzymes are involved in going from glycerol phosphate to a triacylglycerol? how many steps are involved?

A

acyltransferase (x3) and a phosphatase. 4 steps.

138
Q

what is the fate of triglycerides in adipose tissue?

A

storage as a fat depot

139
Q

what is the fate of triglycerides in liver?

A

VLDL

140
Q

what is the fate of triglycerides in intestines?

A

chylomicrons

141
Q

what molecule is the precursor to both triglycerides and phospholipids?

A

phosphatidic acid

142
Q

how is phosphatidic acid formed?

A

starts with glycerol phosphate, and 2 fatty acyls are added via acyltransferase enzymes. (partly on the way to becoming a triacylglycerol). then can either go on to become triacylglycerol or become a glycerophospholipid (with addition of alcohol)

143
Q

what is the general structure of a phospholipid?

A

2 fatty acids, glycerol backbone, polar head group

144
Q

what are the 6 most impt phospholipids?

A

PS, PE, PC, PI, PG, and cardiolipin

145
Q

what are the 2 most abundant phospholipids in mammalian cells?

A

phosphatidylcholine (PC) and phosphatidylethanolamine (PE)

146
Q

where are choline and ethanolamine obtained from?

A

either from the diet or from the turnover of the body’s phospholipids.

147
Q

if humans can synthesize choline de novo, why is it an essential nutrient?

A

we are unable to synthesize it in sufficient quantity.

148
Q

what activates the precursors (ie choline, ethanolamine, diacylglycerol) to become a phospholipid?

A

CTP (not ATP)

149
Q

where is cardiolipin found? why is this location impt?

A

found in the inner mito membrane. this is impt because it is antigenic, and would prompt an autoimmune rxn by the body if it were in outer cell membranes

150
Q

how is cardiolipin formed?

A

the condensation of 2 molecules of phosphatidylglycerol (PG, a phospholipid)

151
Q

what causes Hughes Syndrome (antiphospholipid syndrome/APS)?

A

autoimmune disease: people have antibodies to cardiolipin in their blood. these antibodies tend to promote blood clotting and can cause miscarriage/preterm delivery.

152
Q

where is cardiolipin also found (not human)?

A

in bacterial membranes, particularly treponema (causes syphilis)

153
Q

what is the deficiency is Infant Respiratory Distress Syndrome?

A

surfactant: which is composed of dipalmitoylphosphatidulcholine (DPPC).

154
Q

what does DPPC do?

A

surfactant: lowers surface tension in alveoli so that it is easier to open/stay open.

155
Q

Sphingomyelin, ceramide, and all glycolipids are based on what?

A

sphingosine backbone

156
Q

what is caused by abnormal accumulation of sphingolipids?

A

sphingolipidoses (diseases)

157
Q

sphingosine derives from what?

A

serine (amino acid)

158
Q

sphingosine + a FA –> what?

A

ceramide, a sphingomyelin precursor

159
Q

ceramide + a choline polar group –> what?

A

sphingomyelin

160
Q

what else can happen to ceramine, if it does not get joined with a choline to form sphingomyelin?

A

it can be joined by a glucose or galactose and form a glycolipid.

161
Q

what enzyme degrades sphingomyelin?

A

sphingomyelinase

162
Q

what enzymes degrade phospholipids?

A

there are 4: phospholipases A1, A2, C, and D

163
Q

where is phospholipase A2 found? what inhibits it?

A

found in many mammalian tissues and also in bee/snake venom. causes membrane damage –> inflammation. inhibited by cortisol.

164
Q

where is phospholipase C found? what does cleavage by phospholipase C cause?

A

found in liver and in some bacilli (like Clostridia). degradation of phospholipids by phospholipid C produces second messengers and therefore signal transduction.

165
Q

what is Niemann-Pick disease?

A

sphingomyelinase deficiency. causes buildup of sphingolipids -> enlarged liver/spleen, neurodegeneration and mental retardation

166
Q

what population is Niemann-Pick disease prevalent in?

A

ashkenazi jewish

167
Q

what is the difference between Niemann-Pick disease types A and B?

A

severity: A is more severe. with Type B, individuals can survive into early adulthood. less CNS involvement.

168
Q

the phosphorycholine moiety of sphingomyelin comes from where?

A

phosphatidylcholine (PC) - a phospholipid.

169
Q

all glycolipids contain a ceramide and what?

A

sugar residues. since they have a ceramide, they are sphingosine-based.

170
Q

do we need ATP to synthesize triacylglycerol? what else do we need?

A

yes. also need glycerol phosphate and Fatty acyl-CoA.

x M1 Biochem Quiz 2 (2 decks)

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