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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
• List the repetitive steps in fatty acid synthesis
condense reduce dehydrate reduce
26
• Describe the activation of free fatty acids in hepatocytes
d
27
• Describe the activation of free fatty acids in hepatocytes
activation with CoA ester
28
• Discuss the purpose and regulatory steps of the carnitine shuttle
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
29
• Explain the role of FAD and NAD+ in β-oxidation.
FAD for first dehydrogenation | NAD for second dehydrogenation
30
• List the repetitive steps in β-oxidation
dehydrogenation, hydration dehydrogenation thiolysiis
31
• Understand the link between β-oxidation and gluconeogenesis
beta oxidation makes NADh and atp for gluconeogenesis
32
• Describe the steps of ketogenesis.
in mitochondria of liver with a lyase
33
• Discuss how cells can use ketone bodies as metabolic fuel
gives Acetyl CoA to the TCA for ATP
34
d• Compare and contrast the initial steps of cholesterol biosynthesis and ketogenesis.
both have 2 acety CoAs condensed to form acetoacetyl CoA and then a thrind added to form HMG-CoA
34
initial steps of cholesterol biosyn vs ketogenesis
both have 2 acetyl coAs condensed to form acetoacetyl CoA which have a 3rd acetyl coa added to form HMG - coa
35
• Explain and discuss in detail the regulation and importance of HMG CoA reductase.
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
36
regulation and importance of HMG coA reductasse
RLS is HMG coA to mevalonate by HMG CoA reducase
37
• Compare and contrast the roles of chylomicrons and VLDL particles.
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
38
Describe the role of LDL particles and be able to explain how cholesterol is delivered and stored in cells.
brings cholesterol to cells not really sure | supply cholesterol to tissue by binding to receptors which can be blocked by drugs
39
• Discuss HDL-mediated reverse cholesterol transport (cholesterol efflux).
``` 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 ```
40
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)
loss of dolichol or anything else downstream like ubiquinone could happen
41
What will happen to the levels of HMG CoA Reductase in the presence of high intracellular concentrations of sterols? Why?
high sterols mean high insigs mean ubiquitin ligating enzymes and degredation of HMG CoA
42
What is the role of ‘insig’ in the regulation of HMG CoA Reductase?
it associates to a ubiquitin so it degreades HMG CoA
43
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?
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
5. What is the difference in the roles of chylomicrons and VLDL particles?
Chylomicrons are for exogenous
45
6. Why is LDL considered to be bad cholesterol, while HDL is considered to be good?
LDL delivers cholesterol while HDL removes it from tissue
46
• Describe the relationship between cholesterol and the steroid hormones
cholesterol is the building block of all steroid hormones and it converted to the pregnenalone precursor by Cytochrome P450
47
• Outline the function and general features of the cytochrome P450 enzymes
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
Define the pathway leading to the synthesis of steroid hormones in the adrenal cortex
pregnenolone to progesterone before aldosterone or cortisol | regulated by hormone receptor interactions
49
Discuss the synthesis of pregnenolone and its relationship with the other steroid hormones
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
Describe the general function of aldosterone, glucocorticoids, androgens and estrogens
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
Define how steroid hormones activate their receptors and exert their biological response
hydrophobic so slip through membrane | bind to receptor causeing dissascoiation of HSP and exposing NLS of TF which goes to effect DNA
52
Define nuclear receptors
transcription factors that get activated by steoirids
53
• Compare general transcription factors with specific transcription factors
general - throughout all Transcription specific regulate levels nuclear receptors do this,
54
• Contrast transcriptional activation with transcriptional repression
activation by methylation to open up chromatin and repression to close chromatin
55
• Define the general structure of nuclear receptors
trans activation domain DNA binding domain hinge domain ligand binding domain
56
• Describe the metabolic effects and immune effects of cortisol
fight or flight so gluconeogenesis up, aa catabolism up, glucose to muscles, fat breakdown up reduces inflammation
57
Compare the general differences between type 1 and type 2 nuclear receptors and provide examples of each
``` 1 steroid glucocorticoid receptor 2 non steroidal for growht and develeopment PPARs heterodimers ```
58
essential aa
from diet | Phe, Val, Thr, Trp, Ile, Met, His, Leu, and Lys
59
ketogenic
only degrade to ketone bodies | leucine and lysine
60
keto-glucogenic
phenylalanine isoleucine tryptophan tyrosine
61
transamination
``` 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
oxidative deamination
removes amino gropu from glutamate making ammonia and alpha KG uses NAD and NADP
63
ammonia transport and detoxification
found in blood in Gln and Aln Glu + ammonia to Gln liver takes ammonia from Gln and Aln for urea cycle
64
Urea cycle
ammonia to non toxic urea to platelets to kidneys and out uses 4 ATP 5 rxns 2 mito 3 cyto
65
RL enzyme of urea
CPSI enzyme involved in formation of carbamoyl phosphate requires allosteric activator NAG UC regulation by substarte concentratin, NAG activator changes in enzyme concentration
66
UC diseases
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
BCAAs and primary site of metabolisim
leucine, valine, isoleucine. | skeletal muscle
68
2 aa from BCAA
ala from transamination of pyruvate | gln
69
glucose alanine intertissue cycle
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
coenzyme from tryptophan | and diseases
NAD and NADP deficiency causes pellagra 4 Ds
71
tyroseine
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
alkaptonuria
deficiency in homogentisate oxidase first inborn error disease identified dark pigment one from oxidation cant degrade tyrosene
73
low homocystein levels? 2 pathways
high leves are associated with vascular disease 1 hcy remeth to met requires vit b12 2) Hcy + ser = cystathionine
74
folate trap
deficient vit b12 makes THF trapped in one useable form so hcyy levels increase
75
SAM
s-adenosylmethionine Met condesnes with ATP to form this cone carbon carrier of methyl group cosubstrate
76
THF
cosubstrate one carbon carrier for methylene, methenyl, formyl also methyl for hcy tomet
77
biotin
prosthetic group one carbon carrier for CO2 a couple biotin dependent carboxylations
78
PLP
coenzyme for aminotransferases derivative of Vit B6 covalently linked to lysine
79
THB(BH4)
coenzyme synthesized from GTP | used in hydrozylation
80
Generation of SAM
met condesnse w/ ATP hydrolysis of all three P gropus activating methyl group
81
2 aa from BCAA
d
82
first three steps of BCAA catabolims, enzymes, reducing equivalents producets, and specifice metabolic ends of each BCAA
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
pathology from BC alpha ketoacid dehydrogenase deficiency and treatment
maple syrup urine disease because of accumulation of BCA and keto acids dietary modification and BCAA free formula and essential aa supplements
84
tyroseine
d
85
alkaptonuria
d
86
low homocystein levels?
d
87
liver
``` maintains fasting blood glucose G-6-ptase ketogenesis selflessly uses fa and aa UC FA oxidation and TAGs in VLDL ```
88
SAM
d
89
THF
d
90
biotin
d
91
PLP
d
92
THB(BH4)
D
93
Generation of SAM
d
94
glucogenic
other 14 aa become pyruvate or a TCA intermediate
95
first three steps of BCAA catabolims, enzymes, reducing equivalents producets, and specifice metabolic ends of each BCAA
d
96
glycogen
``` short term reserve liver and kidney systemic muscle local (no phosphotase) ```
97
fat
long term energy reserve (amount=time) in adipose as TAG glycerol no fa for gluconeogenesis
98
protein
long term stored as muscle as last resort glucogenic aa for glucose
99
liver
``` maintains fasting blood glucose G-6-ptase ketogenesis selflessly uses fa and aa UC FA oxidation and TAGs in VLDL ```
100
muscle
local store only pyruvate to lactate sent to blood then used in liver for gluconeogenesis transaminase BCAA insulin depended glucose uptake
101
adipose
stores FA as TAG from VLDL sends fa to liver and muscle sends glycerol to liver and kindey
102
brain
requires glucose can use ketone bodies when starving never fatty acids
103
enzymes of storage vs retreival
storage are dephosphoryalted to activate

Core II (11 decks)

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