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Biochem Exam 4
Terms in this set (209)
What is the tissue and sub-cellular location for fatty acid synthesis?
Liver (can occur in adipose tissue)
What does fatty acid synthesis use?
What is the carrier that moves acetyl CoA from the mitochondrion to the cytosol?
What is the enzyme catalyzing the regeneration of acetyl CoA in the cytoplasm?
What is the ATP requirement for the regeneration of of acetyl CoA in the cytoplasm?
What are the 3 malate dehydrogenase and where are they located?
cytosolic NAD+ dependent malate dehydrogenase (cytosol)
NADP+ dependent malate dehydrogenase- "Malic enzyme" (cytosol)
Mitocondrial malate dehydrogenase (mitochondria)
What malate dehydrogenase converts oxaloacetate to malate?
What reducing power does it use?
What reducing power does it produce?
Cytosolic NAD+ dependent malate dehydrogenase
What malate dehydrogenase converts Malate to oxaloacetate?
What reducing power does it use?
What reducing power does it produce?
Mitochondrial malate dehydrogenase
What malate dehydrogenase converts malate to pyruvate?
What reducing power does it use?
What reducing power does it produce?
NADP+ dependent malate dehydrogenase- "Malic enzyme"
Insulin increases what 5 enzymes to help induce FA synthesis?
1. G6P dehydrogenase
2. malic enzyme
4. FA synthase
What is the rate limiting enzyme of FA synthesis?
Acetyl CoA Carboxylase (ACC)
What reaction does the rate limiting enzyme of FA synthesis catalysis?
Acetyl CoA ---> Malonyl CoA
What is the energy requirement of the reaction from acetyl CoA to Malonyl CoA?
What is the immediate donor of the two-carbon units for FA synthesis?
Name the 5 mechanisms of ACC regulation.
1. Citrate allosterically activates ACC (feedforward)
2. Palmitoyl CoA Inhibits ACC (feedback)
3. AMP inhibits ACC through AMP-PK
4.Increase insulin induces ACC
5. Insulin activates the phosphatase that dephosphorylates and activates ACC
What is the sub-cellular location of FA Synthase complex?
What is the structual organization of FA Synthase complex?
consists of 7 catalytic activities and an acyl carrier protein in a continuous peptide chain
What is the role of phosphopantetheinyl? what does its sulfhydryl group react with?
linked to the serine residue of the ACP, help elongate & malonyl CoA
What is the role of Cysteinyl sulfhydryl group?
Each cycle of FA synthesis uses ___ NADPH.
Acetyl CoA first binds with the ___ group to begin FA synthesis?
Malonyl CoA donates ___ carbons that react with the ___ group?
What are the two key players in the counter-regulation of fatty acid synthesis and beta-oxidation in the liver?
malonyl CoA (inhibits CTP1) & CTP1 (takes FA into the mitochondria)
fatty acid synthesis and beta-oxidation ____ each other.
What is the key difference in TG synthesis between the liver and the adipose tissue?
Only the liver can synthesis glycerol 3-phosphate from glycerol. The adipose tissue relies on glycolysis for TG synthesis.
What is the enzyme responsible for the key difference in TG synthesis between the liver and the adipose tissue?
What is another (less significant) difference in TG synthesis between the liver and the adipose tissue?
TG made in the liver is packaged in blood VLD.
TG made in the adipose tissue is packaged in adipose stores.
What is the key difference between TG synthesis and its re-synthesis in intestinal epithelial cells?
In the intestinal epithelial cells TG synthesis starts with 2-monoacylglycerol. In the liver and adipose tissue TG synthesis starts with glycerol 3-phosphate.
What is the origin of VLDL?
What is the composition of VLDL?
TG, apoproteins, cholesterol, cholesterol esters, and phospholipids.
What is the major apoprotein for new VLDL?
VLDL enters the ___ and matures by acquiring ___and ___ from HDL.
VLDL apoprotein ___ is longer than CM apoprotein ___ BUT is transcribed from the same ___.
VLDL is mainly made up of what?
WHat are the 3 things needed for FA synthesis?
LPL cleaves ___ from both VLDL and CM yielding ___ and ___.
ApoCII activates ___.
In adipose tissue, the ___ are derived from VLDL TGs and are activated to form ___, which is combined with ___ to form ___.
Glycerol 3- Phosphate
Where is ATP needed in TG synthesis?
to convert FA to Fatty acylCoA
What are the 4 ways insulin stimulates TG synthesis in adipose tissue?
makes and releases more LPL
increase the amount of GLUT4 on surface of cell to increase glucose uptake
Allosterically activates PFK-1 (enhancing glucose)
Creating energy for FA Activation, glycolysis, and Glycerol 3-phosphate
What are the two key switches between anabolism and catabolism?
F2,6-BP allosterically activates ___ and inhibits ___.
What is glucokinase?
What is the impact of insulin and glucagon on the expression of glucokinase?
It is induced by insulin
it is repressed by glucagon
Glycogen synthase is regulated by inulin and glucagon through ___.
Covalent modification (phosphorylation).
Glucagon ___ glycogen synthase by activating protein kinase A.
Insulin ___ glycogen synthase though phosphorylation.
What are the 3 roles of glycolysis in TG synthesis in adipose tissue?
1. provide glycerol 3-phosphate
2. provide fatty acids
What is the TCA cycle intermediate that plays a pivotal role in integrating energy production with fatty acid synthesis?
increase ___&___ --->increase export of citrate--->increase ___ synthesis.
What are the 3 key players in the regulation of acetyl CoA carboxylase?
2. low AMP levels
What balances energy production and FA synthesis?
ACC is allosterically ___ by citrate.
low AMP levels ___ the AMP-PK, reducing the phosphorylation of ACC (leaving it active).
Insulin ___ a phosphatase, promoting the dephosphorylation and activation of ACC.
What is the enzyme responsible for glucagon-induced lipolysis?
HSL (hormone sensitive lipase)
What are the 4 mechanisms by which blood glucose levels are maintained during fasting?
4. FA & Keytone bodies
What is the citric acid cycle intermediate whose high abundance plays a critical role in diverting pyruvate to gluconeogenesis during fasting?
High mitochondrial acetyl CoA levels divert pyruvate to gluconeogenesis during fasting by inhibiting ___.
By inhibiting this ___ is not being made into ___.
ABCG5 & ABCG8 transports excess cholesterol out of the ___ in to the ___ to be excreted.
NPC1L1 absorbs cholesterol and transports it into the ___ from the ___.
rare genetic disorder that is caused by the functional defect in ABCG5 or ABCG8. leads to increase blood cholesterol.
treated by Ezetimibe
Ezetimibe targets the cholesterol transporter known as ___ causing blood cholesterol to ___.
Precursor of cholesterol de novo synthesis
reducing power of cholesterol de novo synthesis
Two energy sources of cholesterol de novo synthesis
Location of cholesterol de novo synthesis
Cytosol of: liver, intestines, adrenal glands, & reproductive organs.
Rate limiting enzyme of cholesterol de novo synthesis
In the rate limiting step of cholesterol de novo synthesis, 2 ___ are used and terminal CA is ___ to ___.
Step 1 of cholesterol de novo synthesis is the most important step and changes ___ to ___. This step also involves the ___.
Rate limiting enzyme
Mevalonate has ___ carbons.
The second step of cholesterol de novo synthesis turns ___ mevalonate to distinct activated isoprenes. These isoprenes have ___ carbons. This step cost ___ ATP.
Step three is used ___ times in order to get ___ c squalene.
Step four turns squalene into ___, which has ___ c, and then to ___, which has ___c.
What are the four key regulators or cholesterol synthesis?
What are the three mechanisms of regulation of HMG-CoA?
1. transcription control
2. proteolytic control
3. covalent modification
In transcriptional control when cholesterol is ___ DNA binding domain is ___. This activates ___ transcription to make ___ cholesterol.
HMG CoA reductase
Regulatory DNA sequence upstream of many genes involved in lipid metabolism.
membrane bound transcription factors of the ER/nuclear envelope
ER membrane protein that serves as a cholesterol sensor
If there is ___ cholesterol concentration in the cell, the enzyme will be ___. This is what type of regulation of HMG CoA reductase?
Glucagon and sterols ___ HMG CoA.
AMP ___ HMG CoA.
Insulin ___ HMG CoA.
What are the two enzymes responsible for the conversion of cholesterol to cholesterol ester?
Where is ACAT located?
Where is LCAT located?
ACAT transfers an acyl group from___.
fatty acyl CoA
LCAT transfers an acyl group from ___.
What is the substrate for bile acid synthesis?
What is the rate limiting enzyme for bile acid synthesis?
7-alpha-hydroxylase is regulated by ___. This is ___ regulation.
Where does the conversion of cholesterol to bile salts occur?
What is forward cholesterol transport?
Transporting cholesterol from the liver to the peripheral tissues.
What are the plasma lipoproteins involved in forward cholesterol transport?
What is the only apoprotein of LDL?
What is reverse cholesterol transport?
Transport of cholesterol from the peripheral tissues to the liver.
What is the major player in reverse cholesterol transport?
What are the three forms of HDL used in reverse cholesterol transport?
Pre-beta HDL gets free cholesterol from the cells by interacting with ___ through ___. This process is facilitated by ___.
___ occurs when defective ABCA1 reduces HDL and accumulates cholesterol in the liver and peripheral tissues.
___ is used to in reverse cholesterol transport to make cholesterol esters.
___ transfer cholesterol esters from HDL2 to ___ in exchange for ___.
Hepatic Lipase (HL) hydrolyes ___.
___ activates HL, promoting the conversion to less mature HDL. this accounts for lower HDL levels in men.
What is the ligand for LDLR?
What is the ligand for LRP?
Familial hypercholesterolemia is caused by a mutation in ___.
The two critical regulators of LDLR cell surface expression are ___&___. ___ induces LDLR expression and ___ facilitates degradation of LDLR.
low free cholesterol in cells
low free cholesterol in cells
inhibit cholesterol de novo synthesis and increase cholesterol uptake from the blood by increasing LDLR.
inhibit cholesterol absorption from the gut.
promote the intraheptic conversion of cholesterol into bile acids. (stays in guy to be excreted)
Bile acid sequestering resins
mAbs against PCSK9. inhibit LDLR degradation.
in FH, mutations in ___ allele of ___ can cause defecting uptake of LDL.
in FH, mutation in ___ allele of ___ Can cause this apoprotein to not be able to serve as a ligand.
in FH, mutation in ___ allele of ___ can cause its activity to increase degrading the function of LDLR.
what is the apoprotein responsible for autosomal recessive hypercholesterolemia and how many alleles are affected?
What is autosomal recessive hypercholesterolemia's response to PCSK9 inhibitor?
nothing will happen because no cholesterol can be taken up regardless the amount of receptors.
LDLRAP is directly involved in the ___ of ___ into the ___.
if the patient has a PCKS9 mutation (reduction of function), the the use of a statin will initially ___ cholesterol but PCSK9 will be ___ by statins through SREBP. Some people will be ___ to statins because of this so a ___ treatment must be added.
What are the two fates of carbon in amino acid catabolism?
What are the two fates of nitrogen in amino acid catabolism?
NH3/NH4 & Urea
Describe the reaction of Glutamate oxidative deamination.
used for nitrogen fixation
What is the enzyme for glutamate oxidative deamination?
glutamate dehydrogenase (GDH)
What are the coenzymes for glutamate oxidative deamination?
What is the sub-cellular location of glutamate oxidative deamination?
What are the roles for glutamate oxidative deamination?
To remove nitrogen from glutamate so it can be transferred to the liver to be converted to urea.
What is the role of alanine in the transport of amino acid nitrogen? how many does it carry at a time?
to transport from the muscle to the liver.
What is the role of glutamine in the transport of amino acid nitrogen? how many does it carry at a time?
to transport from the muscle & peripheral tissue tp the liver.
Is alanine or glutamine the better transporter of amino acid nitrogen?
what is the purpose of the urea cycle?
to remove NH3/NH4 from the cell because it is toxic in the body.
What are the primary substrates of the urea cycle?
The outcome of the urea cycle is ___.
What is the energy expenditure of the urea cycle?
What are the 5 key enzymes in the urea cycle?
What are the critical intermediates of the urea cycle?
What is the primary organ of the urea cycle?
What is the sub-cellular location of the urea cycle?
The major mechanism of regulation of the urea cycle is ___.
a ___ induces the urea cycle.
high protein diet
name the three enzymes responsible for the fixation of free ammonia into organic molecules.
carbamoyl phosphate synthase 1
What is the cause of urea cycle disorders? It can also be caused by ___ deficiency.
___ being deficient will cause the intermediate buildup in the urea cycle.
The most common urea cycle disorder is ___.
Clinical symptoms of urea cycle disorder include ___ nervous system activity.
Urea cycle disorders can lead to high levels of ___ and low ___.
What amino acids are involved in the biosynthesis of purine nucleotides?
The purine de novo synthesis pathway begins with ___.
Phosphoribosyl pyrophosphate (PRPP)
The first committed step in the biosynthesis of purines involves the enzyme ___ which catalyzes the reaction of ___ donating its amino group on to PRPP and at the same time generating ___.
___ is used as energy in the first pathway in the biosynthesis of purines. ___ is used in the second part.
In the first part of the biosynthesis of purines ___ is produced. in the second part ___ is used to create ___ and ___.
THF (folate) comes into play in biosynthesis of purines with what enzymes?
___ & ___ are added to the purine pathway at the same time.
PRPP amido-transferase is under ___ feedback control by the products of the pathway ___ & ___. IMP dehydrogenase is under ___ feedback from the product ___. Adenylosuccinate synthase is under ___ feedback from the product ___.
In part two fo the purine pathway, ___ adds ___ as an oxidizing agent and is the oxidation step.
In part two fo the purine pathway, ___ uses GTP to add ___to IMP.
there must be ___ between the biosynthesis pathway, salvage pathway, and catabolism pathway.
if the salvage path way or the de novo (biosynthesis) pathway are over active, the catabolism pathway will kick in and hypoxanthine or guanine can be converted to xanthine which can be oxidized into ___, a buildup of which in the joints can cause___.
Which pathway is over active if the patient has gout?
The first step of the pyrimidine pathway is catalyzed by ___, which adds a___ onto___. There is a positive feedback on this enzyme by ___ and a negative feedback control by high levels of pyrimidine ___.
Hypoxanthine guanine phosphoribosyl transferase (HGPRT) takes ___ and coverts it ___ to ___ using ___.
PRPP converts ___ to ___ in the salvage pathway.
Adenine phosohoribosyl transferase (APRT) does what to adenine?
brings it back to AMP
Allopurinol Uloric inhibits ___ to decrease ___.
The ring contributors of a pyrimidine is ___,___&___.
Majority of the pyrimidine is made up of what?
In the pyrimidine pathway, folate comes into play with the enzyme ___. The folate is put in the pathway in the form of ___ and makes ___.
In the pyrimidine pathway, ___ adds the amino acid group ___. This is a control point for the pathway. It is ___ affected by CTP and ___ affected by GTP.
In the pyrimidine pathway ___ is the oxidizing agent.
What does the pyrimidine pathway start with?
5FDUMP is what kind of inhibitor?
irreversible suicide inhibitor
ribose is incorporated into the pyrimidine pathway ___ as opposed to the purine pathway. This is done by___.
orotate phosphoribosyl transferase
In the pyrimidine pathway,___ catalyses the reaction from dUMP to TMP.
what do pyrimidine nucleotide salvage enzymes do?
convert back from monophosphate form.
___ inhibits the viral thymidine kinase.
DNA cannot be formed without what enzyme?
The ___ are on the regulatory domain of the Ribonucleotide reductase enzyme. They are for ___ and control ___.
what is made
The ___ are on the regulatory domain of a Ribonucleotide reductase enzyme. They are for___ and control ___.
The activity sites on Ribonucleotide reductase enzymes are ___ by high ATP levels and___ high dATP levels.
a___ is a drug that structurally resembles a metabolite and interferes with the function of that metabolite.
sulfamethoxazole is a ___ that blocks ___ in bacteria so that ___ is not made.
folate biotransformation involves ___. (the addition of ___ residues)
methotrexate is ___. the main thing it does is inhibit ___. It is an extremely ___ binding inhibitor but is still reversible.
dihydrofolate reductase (DHFR)
for cancer dosing, methotrexate blocks___ &___. for immunosuppressive dosing ___ is blocked.
6-mercaptopurine (azothiopine) mimics ___. this adds incorrect bases to the product.
using the medication azothiopine (6-mercaptopurine), ___ is incorporated into mRNA and rRNA and impairs translation. The main cytotoxic event is its incorporation into DNA which causes ___ and eventually cell___.
base pair mismatches
the main folate in cells is___.
A ___ hormone is a hormone that opposes the action of another hormone; specifically, hormones that oppose ___ by raising ___.
The counterregulatory hormones work through ___,___,&___.
In the pyrimidine pathway, PPRP (ribose) is added ___ by ___.
orotate phosphoribosyl trasferase
What are the 6 counter regulatory hormones?
4. epinephrine/ norepinephrine
5. glucocorticoid (cortisol)
6. thyroid hormone
What are the four hormones whose secretion is inhibited by somatostatin?
4. thyroid hormone
GH is a peptide hormone released during sleep. it stimulates the liver to make and release ___. Unlike insulin, GH is a ___ growth hormone.
insulin growth like factors (IGF)
GH is ___ (enhances lipolysis). it reduces the oxidation of ___ and ___. GH activates ___ leading to lipolysis.
hormone sensitive lipase (HSL)
The three metabolic pathways elevated by GH in the liver are ___, ___, &___.
In the muscle, GH ___ glucose uptake. GH increases the transport of ___ into muscle cells for ___.
Epinephrine ___ the secretion of insulin and ___ the secretion of glucagon.
What is the kinase activated by epinephrine or glucagon that promotes glycogen breakdown, gluconeogenesis, and lipolysis?
What is the enzyme responsible for the lipolysis?
The key difference between epinephrine and cortisol on glycogen metabolism in the liver is that cortisol causes glycogen ___ whereas, epinephrine causes glycogen ___. Epinephrine is secreted in response to ___ stress whereas, cortisol is secreted in response to ___ stress.
When cortisol is elevated, glucose use is ___ in the muscle.
Thyroid hormone _1__ lipolysis in adipose tissue, _2__ glycolysis in the liver, _3__ glycogenolysis in the liver, _4__ gluconeogenesis in the liver, _5__ glycolysis in the muscle, _6__ glycogenolysis in the muscle, _7__ protein synthesis in the muscle, & _8__ thermogenesis.
The three key characteristics of thyroid hormone are:
1. pro burning (both glucose and fat)
2. pro stress (gluconeogenesis)
3. pro anabolism
The two endogenous incretins are ___ and ___.
Incretins are gastrointestinal hormones that ___ insulin secretion and beta-cell ___. Increasing incretins is beneficial to ___.
type II diabetics
Both incretins have a ___ half life giving them ___ in vivo stability.
The protease responsible for incretin degradation is___.
dipeptidyl protease 4 (DPP-4)
GLP-1 receptor agonist include ___ & ___. ___ is more resistant to DDP-4 cleavage giving it a ___. ___ is an acylated human GLP-1 that protects it from DDP-4 cleavage giving it more ___.
DPP-4 inhibitors ,___ , inhibit DPP-4 and ___ steady state levels of both endogenous ___ & ___
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