MCB Q’s
Explain the Cori Cycle?
During intense exercise, muscles respire anaerobically, producing lactate.
Lactate is transported to the liver, where it is converted back into glucose by gluconeogenesis.
Allows muscle to keep gaining ATP even when they run out of .
In the conversion of oxaloacetate to phosphoenolpyruvate, the phosphorus donor is?
GTP
Glucose 6 phosphatase transports?
Glucose-6-phosphate into the ER.
Glucose and phosphate outside.
The key regulatory enzyme for glycogen degradation is?
Glycogen phosphorylase, which exists in two forms: a more active form A and a less active form B.
The two forms differ in that a serine residue is phosphorylated.
State the steps when someone goes through starvation?
Glycogenolysis
Lipolysis
Protein Degradation
Gluconeogenesis
The body uses glucose by breaking down glycogen storage. When we run out of glycogen, other molecules such as fatty acids and proteins (lipolysis and proteolysis) are used for energy.
Fatty acids are converted into ketone bodies by the liver as an alternative source of energy.
Hyperthyroidism leads to increased production of glucose. Which two enzymes are required to form phosphoenolpyruvate from pyruvate?
Pyruvate Carboxylase
Phosphoenolpyruvate Carboxykinase
Name three ketone bodies and three organs which can utilize ketone bodies.
Ketone Bodies:
Acetoacetate
3-Hydroxybutyrate
Acetone
Organs that utilize:
Heart
Muscle
Brain
If diabetics were in starvation, what fuels would they use?
Ketone bodies
Describe the cellular actions of insulin in different tissues. Include the cell type.
Promotes glucose uptake in the liver, adipose, and skeletal muscles.
Promotes synthesis of glycogen (glycogenesis) in liver and skeletal muscle.
Inhibits breakdown of glycogen and also inhibits synthesis of glucose.
Increases TAG synthesis in all.
Decreases proteolysis in liver and skeletal muscle.
Reduces ketone formation in liver.
Cells enter futile substrate cycling during which increased intracellular glucose overwhelms the TCA cycle. As a result, non-oxidative glucose metabolism increases producing?
Lactate
What are the four steps of lipolysis?
Epinepherine and glucagon bind to 7TM receptors activating adenylate cyclase → activates protein kinase a
Activated PKA phosphorylates HS lipase and perilipen
phosphorylated perilipin restructors lipid droplets and releases coactivator CA which activates ATGL
Activated ATGL initiates lipolysis by converting TAG to DAG, then HS lipase converts DAG to MAG, then MAG lipase cleaves MAG to produce glycerol and fatty acids
Give a description of how hormone-sensitive lipase is controlled and its mechanism of action.
HS lipase is involves in metabolism of TAG, therefore it’s involved in TAG breakdown.
It regulates lipolysis; high amount of TAG and fatty acids inhibits HS lipase.
It is controlled by physiological and hormonal factors.
hormonal factors, which are associated with insulin and glucagon, inhibits it’s activity by insulin action, and activates it with glucagon.
physiological factors, which are associated with physical activity and stress.
This ensures proper lipid metabolism and energy homeostasis
Types of inhibitors and what happens?
Competitive:
Does not affect the maximum activity (Vmax) of an enzyme.
Increases the (Km) of an enzyme because higher substrate concentrations are required to achieve semi-maximal activity.
Non-competitive:
Vmax is lower than for the normal enzyme, but Km is the same.
The affinity of the enzyme for its substrate (Km) remains unchanged as the active site is not competed for by the inhibitor.
Uncompetitive:
Decreases Vmax and KM to the same extent.
Binds to and stabilizes the ES complex, it makes it more difficult for S to dissociate or be converted to product, increasing enzyme affinity.
How are ion channels regulated?
Ligand, etc.
What happens that causes Km to stay the same?
When Vmax decreases (noncompetitive).
What is attached to growing RNA in the ER?
Acetyl tRNA
What is a property of allosteric enzymes?
Binds to a different site than the active site.
What is a process that does not occur in muscles?
Gluconeogenesis
Which substance moves electrons from complex 1 to complex 3?
Ubiquinone
What can we conclude about an inhibitor if Km is the same with or without it?
It's non-competitive
Main glycogen degradation enzyme type and differences:
Glycogen phosphorylase
Two forms: a less active b form and a more active a form
The a form differs from the b form in that a serine residue is phosphorylated
Explain Diabetes with liver and how it affects glycogen:
Diabetes causes the absence of insulin or insulin resistance.
Glucose receptors in the liver are insulin independent, a minor amount is GLUT-4.
Although GLUT-2 is insulin-independent and can facilitate glucose transport into liver cells, insulin is crucial for regulating the balance between glycogen synthesis and breakdown in the liver.
Diabetes disrupts this balance by affecting insulin levels or its signaling pathways, ultimately impacting glycogen storage and leading to issues with blood glucose regulation.
No insulin results in the glycogen synthesis in the liver being impaired due to a lack of insulin signaling. This can lead to decreased glycogen storage and higher blood glucose levels because the liver continues to break down glycogen
Induced fit in an enzyme refers to:
Conformational change
Yeast cells convert pyruvate to lactate
False
All enzymes of the TCA cycle reside in the mitochondrial membrane:
False
Which of the following is untrue?
Protein folding is assisted by a protein molecule called chaperone
Proteins are present in cytoplasm and cell organelles of all cells
Transmembrane or organelle proteins contain a single peptide
Protein folding occurs in the Golgi bodies
In RNA Transcription, which is a part of TBP-associated factor (TAF)?
TFIID
In humans, glucose in the body is released by ..?
Liver
In cellular division, one cell gives rise to two daughter cells containing equal volume. However, such a case of regulation is observed in?
Oocytes
T-snares are present on the:
target compartment
The nucleosome is composed of how many histone proteins?
Eight
Which of the following enzyme present in the Rough ER removes the signal sequence from the?
Signal peptidase
An example of codominance is:
Human ABO blood group system
The segregation of alleles on one trait did not have any effect on the segregation of alleles on different trait
Mendel’s law of Independent Assortment
How many types of protein Kinases are there?
Five
A Cell’s reservoir of NADPH represents its:
Reducing power
If contraction is repeated, muscles regenerate NAD+ by converting pyruvate to:
Lactate
How many molecules of ATP are made per molecule of oxidation of glucose?
30-36
Allosteric enzymes are those with:
Multiple binding sites
Energy released by catabolic pathways is stored in how many forms?
2
A cell’s reservoir of NADPH represents it:
Reducing power
Q1) Which enzyme catalyzes the conversion of pyruvate to Acetyl CoA?
A) Acetyl CoA carboxylase
B) Pyruvate Kinase
C) Pyruvate dehydrogenase complex
D) None
Q2) Which is a negative regulator of PDC
A) ATP
B) NADH
C) ADP
D) Acetyl CoA
Q3) What is true about PDC Kinase
A) Activation of PDC Kinase stimulates PDC
B) Inhibition of PDC Kinase phosphorylates PDC
C) Activation of PDC Kinase phosphorylates PDC inactivating it
D) PDC is activated by dephosphorylation of PDC Kinase
Q4) Where does the Krebs cycle take place
A) Inner membrane of mitochondria
B) Cytosol
C) Outer membrane of mitochondria
D) Matrix of mitochondria
Q5) How many molecules of ATP are formed in one citric acid cycle
A) 2
B) 1
C) 3
D) 0
Q6) Where is the energy conserved in the Krebs cycle
A) FADH
B) NADPH
C) NAD+ and FAD+
D) NADH and FADH₂
Q7) What inhibits Isocitrate dehydrogenase
A) ATP
B) ADP
C) NADH
D) AMP
Q8) What inhibits a-Ketoglutarate dehydrogenase
A) ATP
B) Succinyl CoA
C) Acetyl CoA
D) NADH
Fill in the blanks
Q1) Formation of citrate from acetyl CoA + Oxaloacetate by citrate synthase
Q2) Isocitrate dehydrogenase is responsible for the oxidative decarboxylation and dehydrogenation of isocitrate to α-ketoglutarate and NAD+ is the reducing agent
Q3) Isomerization of citrate to isocitrate is by aconitase
Q4) α-Ketoglutarate dehydrogenase complex is responsible for conversion of α-ketoglutarate to succinyl CoA, while NAD+ is reduced
Q5) Succinyl CoA synthetase is responsible for conversion of succinyl CoA to succinate and uses GTP as an energy acceptor
Q6) Regeneration of oxaloacetate from succinate in step 1 oxidation to fumarate by succinate dehydrogenase reduces FAD to FADH₂
Q7) Fumarate is responsible for the hydration to malate
Q8) Malate dehydrogenase is responsible for oxidation of malate to oxaloacetate and reduces NAD+ to NADH
Q9) The NADH + FADH₂ formed in the citric cycle are oxidized by the electron transport chain
Q10) The enzymes for glycolysis are upregulated by insulin
MCQs
Q1) What is the major fuel store in the body
A) Carbohydrates
B) Triacylglycerol
C) Amino acids
D) Ketones
Q2) The first step of the Beta oxidation is catalyzed by which enzyme
A) Acetyl carboxylase 1
B) Acyl CoA synthetase
C) Carnitine palmitoyltransferase 1
D) Acyl CoA dehydrogenase
Q3) Where are fatty acids oxidized
A) Mitochondrion
B) Cytosol
C) Cytoplasm
D) Inner Membrane of the mitochondria
Q4) The enzyme that transfers Acyl back to CoA is
A) Carnitine palmitoyltransferase 1
B) Carnitine carrier protein
C) Carnitine palmitoyltransferase 2
D) None of the above
Q5) What primary organs/tissues are affected by deficiency of carnitine
A) Muscle
B) Liver
C)
D) Heart
E) Brain
Q6) How many ATP is generated per Acetyl CoA
A) 4
B) 7
C) 10
D) 8
E) 106
Q7) Fatty acid synthesis takes place in the
A) Mitochondrion
B) Cytoplasm
C) Cytoplasm of mitochondria
D) None of the above
Q8) The first step in the fatty acid synthesis is catalyzed by which enzyme
A) Acetyl CoA carboxylase 1
B) Acyl CoA carboxylase 1
C) Acetyl CoA carboxylase 2
D) Propionyl carboxylase
Q9) What is the carrier protein in Fatty acid degradation
A) ACP
B) CoA
C) Acyl
D) None of the above
Q10) What is the enzyme responsible for formation of Acetyl ACP
A) Transacetylase
B) Dehydrogenase
C) Reductase
D) Synthetase
Q11) What is the reducing agent in biosynthesis of fatty acid
A) NAD+
B) FADH
C) NADH
D) NADPH
Q12) What is a negative regulator of Carnitine palmitoyl transferase
A) Acyl CoA
B) ATP
C) Malonyl CoA
D) Acetyl CoA
Q13) Which is a positive regulator of Acetyl CoA carboxylase
A) Citrate
C) Insulin dependent dephosphorylation
Q14) Which is a negative regulator of Acetyl CoA carboxylase
A) AMP Dependent phosphorylation
B) cAMP dependent phosphorylation
C) Glucagon
D) Epinephrine
E) Palmitate
Fill in the blanks
Q1) Glucagon & epinephrine trigger the 7™ receptor that activates adenylate cyclase leading to stimulation of PKA and this phosphorylates perilipin + HSL which restructures lipid droplets and releases TAG for ATGL which initiates hydrolysis of TAG to DAG, followed by MAG by HSL, then to fatty acid and glycerol by MAG lipase
Q2) The enzyme(s) that are needed when we have polyunsaturated triglycerides are isomerase and reductase
Q3) Methylmalonyl CoA is converted to Succinyl CoA by methylmalonyl CoA mutase, and it's a Vitamin B12 requiring enzyme
Q4) Acetyl CoA cannot enter the citric acid cycle when oxaloacetate is depleted. Instead, acetyl CoA is converted to ketone bodies, which are acetoacetate and β-hydroxybutyrate
Q5) The three cells that can metabolize ketone are cardiac muscle, skeletal muscle, and brain
Q6) Diabetes mellitus is a condition which is characterized by the absence or resistance to insulin, and as a consequence glucose cannot enter the cell and all energy must be derived from fat, leading to production of acetyl CoA.
Q7) Excess production of Ketone which are acidic leads to ketoacidosis
True / False (with statements)
Q1) True – Acetyl CoA cannot be converted back to pyruvate in animals.
Q2) False – Fatty acid synthesis occurs in the cytoplasm, not the mitochondria.
Q3) False – Carnitine palmitoyltransferase 1 is inhibited, not activated, by malonyl CoA.
Q4) True – Glucagon and epinephrine activate lipolysis via phosphorylation of HSL and perilipin.
Q1) Which is a negative regulator of Pyruvate kinase?
A) ATP
B) AMP
C) Fatty acids
D) Acetyl CoA
Q2) Pyruvate Carboxylase requires which prosthetic group?
A) Vitamin B2
B) Ca+2
C) Vitamin B12
D) Vitamin B7
Q3) How many NTPs are needed for gluconeogenesis?
A) 4
B) 6
C) 2
D) 5
Q4) Which is a negative regulator of glycolysis?
A) ATP
B) Citrate
C) Alanine
D) ADP
Q5) Which is a positive regulator of gluconeogenesis?
A) Acetyl CoA
B) ADP
C) ATP
D) Citrate
Q6) Which is a positive regulator of PFK?
A) F-2,6-BP
B) AMP
C) Citrate
D) F-1,6-BP
E) ADP
Q7) Which is a negative regulator of Hexokinase?
A) Glucose
B) Glucose 6-phosphate
C) ATP
D) Fatty acids
E) ADP
Q8) Glucose can be formed from?
A) Glycerol
B) Amino acid
C) Lactate
D) All of the above
Q9) Which is a negative regulator of Gluconeogenesis?
A) ADP
B) F-2,6-BP
C) Acetyl CoA
D) AMP
True/False:
Q1) False
Q2) False
Q3) False
Q4) True
Fill in the Blank:
Q1) Conversion of pyruvate to phosphoenolpyruvate requires two enzymes which are
Pyruvate carboxylase
PEP carboxykinase
Q2) In the conversion of glucose 6 phosphate to glucose, glucose 6-phosphatase transports
glucose 6-phosphate into the lumen of ER and glucose to the cytoplasm.
Q3) F-2,6-BP is made by PFK-2 and hydrolysed by FBPase-2