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Core II > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

different ways phospholipids can be made

A

2 FA to glycerol 3 phosphate makes phosphatidic acid
diacylglycerol reacts with an alcohol
either diacylglycerol or alcohol is activated first

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2
Q

sphingolipids special?

A

sphingosine backbone instead of glycerol

key component of myelin sheath

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3
Q

lipid diversity

A

big diversity within and btwn species

immune system can target bacterial glycolipids

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4
Q

lipases

A

hydorlize ester bonds within lipids
Pancreatic turn diety triglycerols into FA and monacylglycerol to get absorped
hormone sensitive lipase in adipose to break down to free fatty acids to share
lipoportein breaks down triglycerols os they can enter cells

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5
Q

phopholipases

A

hydrolyze phospholipids
to release energy or for cell signalling
can release arachidoinc acids

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6
Q

eiconosoids

A

local hormones from arachidonic aiid

can cause inflamation and platetlet aggregation among other things

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7
Q

arachidonic acid

A

released from phospholipids by phopholipases

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8
Q

PGHS

A

catalyzes RLS in two step prostanoid biosynthiesis (arachidoninc acid to protaglandin) and target for NSAIDs to inhibit as antiinflammatory

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9
Q

5-lipoxygenase

A

catalyesses committed step in leukotriene biosynthesis

related to asthma

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10
Q

effects of protaiglandins

A

prostacyclin-vasodilation and reduce platele aggregation thromboxane - vasoconstriction, increased platelet aggregation, bronchospasms

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11
Q

effect of leukotrienes

A

mediate symptoms of asthma

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12
Q

why do lipids require dedicated solubilization and transport mechanism

A

not water soluble on their own
solubalized by bile salts (detergents) in digestive tract
apolipoproteins form complexes to make solubalized ones travel

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13
Q

three lipoprotein pathways for lipid transport

A

chilomicrons - make exogenous lipids available trhought body, triacylglycerol +apolipoproteins
VLDL - triglyercols in ER of liver cells combined in ER lumen with apolipoproteinsthen sent out as VLDL particls
HDL - cholesterol transport
VLDL and HDL are endogenous
all three are broken up by lipoprotein lipase to enter target cells

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14
Q

COX1 vs COX2

A

COX1 - constitutively housekeeping

COX2 - regulated and pro inflammatory (makes prostanoids)

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15
Q

cis unsaturated fatty acid vs tans unsaturated fatty aid

A

cis is more common and causes kink

trans dont pack well and make membrane too rigid

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16
Q

regulatory mechanism that prevents beta oxidation of fatty acids while you are trying to synthesis palmitate

A

i think malonyl coA upregualtes faty acid synthesisi but down regulates beta oxidationpal

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17
Q

why need shuttle to transpoert acetyl COA in mito to cyto

A

CoA cannot crosss the innermito membrane

so turn acetate into citrate and then back

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18
Q

relationship btwn beta oxidation and gluconeogeneisis

A

beta oxidation makes NADH and ATP used in gluconeogensis

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19
Q

epinephrines effect on adipocytes

A

d

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20
Q

how are KB an important fuel source

A

can be used by brain during a starving state

can be made in but not used by the liver

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21
Q

Differentiate between saturated and unsaturated fatty acids.

A

saturated means no doublle bonds

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22
Q

Describe how the acetyl-CoA is delivered to the cytosol.

A

turn acetyl coa into citrate with citrate synthase, move it accrose then citrate lyase makes acetyl coa in cytosol

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23
Q

Discuss the steps and regulatory mechanisms of acetyl CoA carboxylase

A

acetyl CoA +CO2 +ATP to malonyl CoA
committed and ratelimint of FA biosynthesis
irreversible

allosteric: citrate up malonyl CoA down
covalent regulation: deph up phosh down
Biotin (vit B7) prosthetic group needed

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24
Q

Describe the fatty acid synthase enzyme

A

1 protein w/ 6 active sites
4 repeating steps: condesnation reduction dehydration reduction to keep adding 2 C from acetyl coa a
starts with 2 C from malonyl coA
thiolyase cuts it off at palmitic acid with 16 C
long term transcriptional control and only active as dimer

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25
Q

• List the repetitive steps in fatty acid synthesis

A

condense
reduce
dehydrate
reduce

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26
Q

• Describe the activation of free fatty acids in hepatocytes

A

d

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27
Q

• Describe the activation of free fatty acids in hepatocytes

A

activation with CoA ester

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28
Q

• Discuss the purpose and regulatory steps of the carnitine shuttle

A

CoA derivatives cant cross the inner mitochondrial membrane
so Fatty Acyl Coa gets through outter membrane then CPT I trades CoA for carnitine so fatty acylcarnitine can use a translocase to get to matrixe where CoA is swapped back for carnitine
CPT 1 is rate limiting and regulated by malonyl CoA which inhibits it

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29
Q

• Explain the role of FAD and NAD+ in β-oxidation.

A

FAD for first dehydrogenation

NAD for second dehydrogenation

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30
Q

• List the repetitive steps in β-oxidation

A

dehydrogenation, hydration
dehydrogenation
thiolysiis

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31
Q

• Understand the link between β-oxidation and gluconeogenesis

A

beta oxidation makes NADh and atp for gluconeogenesis

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32
Q

• Describe the steps of ketogenesis.

A

in mitochondria of liver with a lyase

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33
Q

• Discuss how cells can use ketone bodies as metabolic fuel

A

gives Acetyl CoA to the TCA for ATP

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34
Q

d• Compare and contrast the initial steps of cholesterol biosynthesis and ketogenesis.

A

both have 2 acety CoAs condensed to form acetoacetyl CoA and then a thrind added to form HMG-CoA

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34
Q

initial steps of cholesterol biosyn vs ketogenesis

A

both have 2 acetyl coAs condensed to form acetoacetyl CoA which have a 3rd acetyl coa added to form HMG - coa

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35
Q

• Explain and discuss in detail the regulation and importance of HMG CoA reductase.

A

RLS of HMG COa to mevalonate by HMG coa reductaase
major control point for entire cholesterol biosyn pathway
statins synthetic and natural can inhibit this

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36
Q

regulation and importance of HMG coA reductasse

A

RLS is HMG coA to mevalonate by HMG CoA reducase

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37
Q

• Compare and contrast the roles of chylomicrons and VLDL particles.

A

Chylomicrons are for dietary lipids
VLDL are fore endogenous ilipids
both delevir lipids to muscle and adipoose
CHylomicron remnats bring cholesterol to liver
VLDL become LDL when they are mostly cholesterol

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38
Q

Describe the role of LDL particles and be able to explain how cholesterol is delivered
and stored in cells.

A

brings cholesterol to cells not really sure

supply cholesterol to tissue by binding to receptors which can be blocked by drugs

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39
Q

• Discuss HDL-mediated reverse cholesterol transport (cholesterol efflux).

A 
brings cholesterol out of the body 
smallest and densest 
takes to liver  mostly 
takes liipids from VLDL but those get degraded 
idk how much detail
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40
Q

If a patient were taking statins to reduce their cholesterol levels, what other side effects
might you anticipate? (consider the importance of the isoprenoid pathway)

A

loss of dolichol or anything else downstream like ubiquinone could happen

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41
Q

What will happen to the levels of HMG CoA Reductase in the presence of high
intracellular concentrations of sterols? Why?

A

high sterols mean high insigs mean ubiquitin ligating enzymes and degredation of HMG CoA

42
Q

What is the role of ‘insig’ in the regulation of HMG CoA Reductase?

A

it associates to a ubiquitin so it degreades HMG CoA

43
Q

f a patient had a mutation in apoC-II that led to a dysfunctional protein, what should
build-up in the blood? Will it matter if the patient has been fasting or as just eaten a big
meal?

A

Lipoprotein lipase is activated by presensce of apoC-II so without it Chylomicrons and VLDL would both build up in the blood,
I dont think it would matter as far as relative amounts in regardss to the fed/fasting state cuz it should be higher than normal in either

44
Q
  1. What is the difference in the roles of chylomicrons and VLDL particles?
A

Chylomicrons are for exogenous

45
Q
  1. Why is LDL considered to be bad cholesterol, while HDL is considered to be good?
A

LDL delivers cholesterol while HDL removes it from tissue

46
Q

• Describe the relationship between cholesterol and the steroid hormones

A

cholesterol is the building block of all steroid hormones and it converted to the pregnenalone precursor by Cytochrome P450

47
Q

• Outline the function and general features of the cytochrome P450 enzymes

A

inserts oxygen into substrate and reduces other oxygen to water
step 1 lipid substrate and CYP ferric ion tae e from NADH
step 2 give e to O2
step 3 oxidize substrate
gets cholesterol into inner membrane
makes pregenalone by cleaving side chain of cholesterol

48
Q

Define the pathway leading to the synthesis of steroid hormones in the adrenal
cortex

A

pregnenolone to progesterone before aldosterone or cortisol

regulated by hormone receptor interactions

49
Q

Discuss the synthesis of pregnenolone and its relationship with the other steroid
hormones

A

is is the fist step after cholesterol and is the prohoromone precursor of all other hormones
cleavage of side chain of cholesterol by cytochrome p450 does this

50
Q

Describe the general function of aldosterone, glucocorticoids, androgens and
estrogens

A

aldosterone - raoses BP and FL and Na uptake
glucocorticoids - like cortisol effects stress, BP and immune system
androgens - like testosterone for male sex characterisitics
estrogen - estradiol female sex characterisitics

51
Q

Define how steroid hormones activate their receptors and exert their biological
response

A

hydrophobic so slip through membrane

bind to receptor causeing dissascoiation of HSP and exposing NLS of TF which goes to effect DNA

52
Q

Define nuclear receptors

A

transcription factors that get activated by steoirids

53
Q

• Compare general transcription factors with specific transcription factors

A

general - throughout all Transcription
specific regulate levels
nuclear receptors do this,

54
Q

• Contrast transcriptional activation with transcriptional repression

A

activation by methylation to open up chromatin and repression to close chromatin

55
Q

• Define the general structure of nuclear receptors

A

trans activation domain
DNA binding domain
hinge domain
ligand binding domain

56
Q

• Describe the metabolic effects and immune effects of cortisol

A

fight or flight so gluconeogenesis up, aa catabolism up, glucose to muscles, fat breakdown up
reduces inflammation

57
Q

Compare the general differences between type 1 and type 2 nuclear receptors
and provide examples of each

A 
1 steroid 
glucocorticoid receptor
2 non steroidal for growht and develeopment
PPARs
heterodimers
58
Q

essential aa

A

from diet

Phe, Val, Thr, Trp, Ile, Met, His, Leu, and Lys

59
Q

ketogenic

A

only degrade to ketone bodies

leucine and lysine

60
Q

keto-glucogenic

A

phenylalanine
isoleucine
tryptophan
tyrosine

61
Q

transamination

A 
transfer of alpha amimno group from aa to alpha keto glutartate makinge alpha keto aid and glutamate
no net loss of nitrogen
reversible 
catalyzed by ubiquitous enzymes
aminotransferases
highly specific
coenzyme req: pyridoxal phosphat PLP
2 steps
alpha-NH2 transfer
second alpha NH2 transfer
62
Q

oxidative deamination

A

removes amino gropu from glutamate making ammonia and alpha KG
uses NAD and NADP

63
Q

ammonia transport and detoxification

A

found in blood in Gln and Aln
Glu + ammonia to Gln
liver takes ammonia from Gln and Aln for urea cycle

64
Q

Urea cycle

A

ammonia to non toxic urea to platelets to kidneys and out
uses 4 ATP
5 rxns 2 mito 3 cyto

65
Q

RL enzyme of urea

A

CPSI enzyme involved in formation of carbamoyl phosphate
requires allosteric activator NAG
UC regulation by substarte concentratin, NAG activator
changes in enzyme concentration

66
Q

UC diseases

A

x-linked OTC deficiencty leads to hyperammonemia
restric diet and add aa analogs without ammonia
n scavenging drugs
antibiotics reduce gut bacteria
try to prevent hyper, and promote development

67
Q

BCAAs and primary site of metabolisim

A

leucine, valine, isoleucine.

skeletal muscle

68
Q

2 aa from BCAA

A

ala from transamination of pyruvate

gln

69
Q

glucose alanine intertissue cycle

A

transfer between muscle and liver
ala goes to liver glutamate and pryvate reform
Glu is deaminated, NH3 enters UC
pyruvate is used for gluconeogenesis and sent to muscle

pyruvate from muscle or BCAA to ala to liver to pyruvate to glucose to blood to muscle

70
Q

coenzyme from tryptophan

and diseases

A

NAD and NADP
deficiency causes pellagra
4 Ds

71
Q

tyroseine

A

nonessential but made from essential Phe with PAH enzyme and coenzyme TBH/BH4
deficiency pf PAH makes PKU - minor pathways become major causing buildup and mousey odor
treatment is low Phe and tyr supplement

72
Q

alkaptonuria

A

deficiency in homogentisate oxidase
first inborn error disease identified
dark pigment one from oxidation
cant degrade tyrosene

73
Q

low homocystein levels? 2 pathways

A

high leves are associated with vascular disease
1 hcy remeth to met requires vit b12
2) Hcy + ser = cystathionine

74
Q

folate trap

A

deficient vit b12 makes THF trapped in one useable form so hcyy levels increase

75
Q

SAM

A

s-adenosylmethionine
Met condesnes with ATP to form this
cone carbon carrier of methyl group
cosubstrate

76
Q

THF

A

cosubstrate
one carbon carrier for methylene, methenyl, formyl
also methyl for hcy tomet

77
Q

biotin

A

prosthetic group
one carbon carrier for CO2
a couple biotin dependent carboxylations

78
Q

PLP

A

coenzyme for aminotransferases
derivative of Vit B6
covalently linked to lysine

79
Q

THB(BH4)

A

coenzyme synthesized from GTP

used in hydrozylation

80
Q

Generation of SAM

A

met condesnse w/ ATP
hydrolysis of all three P gropus
activating methyl group

81
Q

2 aa from BCAA

A

d

82
Q

first three steps of BCAA catabolims, enzymes, reducing equivalents producets, and specifice metabolic ends of each BCAA

A

transamination - BCAA aminotransferase: glu and some alpha stuff
oxidative decarboxylation - BC alpha keto acid dehydrogenase: CO2, NADH, iso iso alpha methyl
dehydrogenation: FADH2, acetoacetate and acety co a, propoinyl coa and succinyl coa

83
Q

pathology from BC alpha ketoacid dehydrogenase deficiency and treatment

A

maple syrup urine disease because of accumulation of BCA and keto acids
dietary modification and BCAA free formula and essential aa supplements

84
Q

tyroseine

A

d

85
Q

alkaptonuria

A

d

86
Q

low homocystein levels?

A

d

87
Q

liver

A 
maintains fasting blood glucose
G-6-ptase
ketogenesis selflessly
uses fa and aa
UC
FA oxidation and TAGs in VLDL
88
Q

SAM

A

d

89
Q

THF

A

d

90
Q

biotin

A

d

91
Q

PLP

A

d

92
Q

THB(BH4)

A

D

93
Q

Generation of SAM

A

d

94
Q

glucogenic

A

other 14 aa become pyruvate or a TCA intermediate

95
Q

first three steps of BCAA catabolims, enzymes, reducing equivalents producets, and specifice metabolic ends of each BCAA

A

d

96
Q

glycogen

A 
short term reserve
liver and kidney systemic
muscle local (no phosphotase)
97
Q

fat

A

long term energy reserve (amount=time)
in adipose as TAG
glycerol no fa for gluconeogenesis

98
Q

protein

A

long term
stored as muscle as last resort
glucogenic aa for glucose

99
Q

liver

A 
maintains fasting blood glucose
G-6-ptase
ketogenesis selflessly
uses fa and aa
UC
FA oxidation and TAGs in VLDL
100
Q

muscle

A

local store only
pyruvate to lactate sent to blood then used in liver for gluconeogenesis
transaminase BCAA
insulin depended glucose uptake

101
Q

adipose

A

stores FA as TAG from VLDL
sends fa to liver and muscle
sends glycerol to liver and kindey

102
Q

brain

A

requires glucose
can use ketone bodies when starving
never fatty acids

103
Q

enzymes of storage vs retreival

A

storage are dephosphoryalted to activate

Core II (11 decks)

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