Medical Biochemistry I-Exam 2

molecules transported simultaneously in opposite directions
molecules transported simultaneously in same direction
one molecule type is transported
primary active transport

driven directly by release of energy


ATP hydrolysis

secondary active transport

driven by large favorable gradient but the molecule described moves against a small unfavorable gradient


uses energy derived from pumping other ions to fuel its own movement

passive facilitated diffusion
driven by a favorable gradient and uses a transport protein to get across the membrane
simple diffusion
driven by a favorable gradient and does not require a transport protein to get through the membrane
Give an example of a hormone that is released in response to sensing a condition by the same tissue that synthesizes and secretes the hormone
insulin is released by the pancreas in response to low blood sugar
Some hormones involve a complicated stimulation, a cascade involving sensing of the stimulus, release of a factor from one tissue, the hormone stmulates release of another factor from another tissue. Name a hormone that is an example of this, the tissue the hormone is secreted from, and its stimulus.
cortisol is released by the adrenal cortex in response to stress

Two hormones that largely control blood glucose.


Which is released in response to high blood glucose?


Which is released in response to low blood glucose?

insulin and glucagon


insulin is released in response to high blood glucose and brings blood glucose levels down


glucagon is released in response to low blood glucose levels and brings blood glucose levels up

What is circulating form of carbs in animals?


Storage form of carbs in animals?


Aerobic pathway of carb degradation that produces energy?


Anaerobic pathway pathway of carb degradation that produces energy?


Pathway of glucose synthesis?





glycolysis accompanied to TCA cycle coupled with oxidative phosphorylation


glycolysis diverted to form lactic acid




Which of the following NOT directly required for synthesis of nucleotides?


A. carbohydrate

B. amino acid

C. fatty acid

C. fatty acid
Pathway that is involved in degrading carboxylic acid group on amino acids?
urea cycle
Chem process by which energy is obtained from biological fuels such as the carbon skeletons of carbs, fatty acids, or amino acids (or any fuel)?

Organ that is the “brain” of metabolism


Organ that has priority over all others for supply of fuel


Why other tissues called extrahepatic tissues with respect to metabolism?





b/c liver is so impt to metabolism

Organ that is king of metabolism

Fatblox is a drug that cannot be absorbed by cells in dig tract or cells lining blood vessels. Fatblox binds fats, thus preventing their absorption. When Fatblox is taken as a pill, you find that it prevents fats from being absorbed by the intestine, but the adipose tissues of those who take it shrink only a little. When Fatblox is given by IV into the circulation, adipose tissue shrinks drastically.


Explain and what are drawbacks to its use in IV form.

Other organs can interconvert molecules to make fats


Fatblox can inhibit the transport of lipid signaling molecules by binding to them, preventing them from reaching their targets, could cause problems

Why can’t brain use fatty acids as fuel for energy?
blood brain barrier blocks them
What organ is most responsible for uptake and disposal of glucose from circulation and uses most glucose?
skeletal muscle
What metabolic pathways used for energy skeletal muscles at rest and during contractile activity?

In order of work rate (from high to low):


free ATP


Creatine Pi




fatty acids



Where does glycolysis take place?
Where does TCA cycle take place?
Where does urea cycle take place?
cytosol and mitochondria
Where are many components of plasma membrane synthesized?

The Multi-Drug Resistance gene, which encodes a protein known as p-glycoprotein, is often turned on in cancer cells. P-glycoprotein is a transporter that has the capability of pumping certain cancer drugs such as doxorubicin, daunorubicin, vinblastine and vincristine is a process driven by hydrolysis of ATP. Thus, the cancer cell is able to evade being killed by the cancer drug, even when the drug concentation outise the cell are high. This process would best be described as


A. primary active transport

B. secondary active transport

C. passive facilitated diffusion

D. simple diffusion

E. cannot be determined from info given

A. primary active transport
What are difficulties in transducing a signal outside cell into cellular response inside cell?
cell must be able to respond to signal and molecules causing the signal generally need to be impermeable to the cell membrane
Two major classifications of signal transduction (due to two major places receptors are found)?

membrane receptors-cause intracellular stimulation


intracellular receptors-affect gene regulation

What is a ligand?
extracellular protein that is able to bind to a specific receptor
What is the property of ligands that accounts for two major classifications of signal transduction?
permeability of the ligand
Two differences between three histamine receptors in their response to histamine

H1 located in endothelium and smooth muscle and causes a vasodilation effect when acted upon by an antagonist (Claritin Allegra)

Acts on sinus and allergy


H2 receptor is located in the stomach and causes a decrease in gastric acid secretion when acted upon by an antagonist (Zantac)

Ciproxifan is a potent and specific histamine H3 receptor antagonist. Would it be expected that ciprofan would alleviate allergy symtoms or suppress gastric acidity?
It would not be expected to do either because the H3 receptor is located in the brain and neurons
2 major types of molecular switches for intracellular signaling and how is their action reversed?

cAMP formation and phosphorylation


cAMP turned on by cyclases

turned off by phosphodiesterases


phosphorylation by kinases

turned off by phosphatases

3 ways to make a cell less responsive to adenosine receptor action even when adenosine is present in adequate amounts

receptor inactivation by phosphorylation


receptor internalization


receptor degradation

Role of proto-oncogene ras in intracellular signal transduction
small GTPase, hydrolyzes GTP

How do cytokines alter gene expression?

bind to cytokine receptors which activate secondary messengers that activate gene expression
The effect of cholera toxin on signal tranduction
the toxin enters the cells by riding in on a ganglioside and enters by endocytosis and inducing ADP ribosylation of G-protein. This K/O the GTPase activity that would have shut off the cyclase. Results in increases secretion, diarrhea, and death.
Molecule that is precursor for lipid involved in signal mediation of inflammation, blood clotting, control of vascular tone, pain, and fever is released from membranes by a phospholipase?
arachidonic acid is cleaved which is a precursor for eicosanoids

Are all signal transduction pathways independent of each other?


What do they do or not do to account for this?

No, pathways are independent on each other


They inhibit one pathway and pick up slack on other pathway

Where does glycolysis take place?
Starting substrate for glycolysis
Ending products for glycolysis

aerobic – pyruvate


anaerobic – lactate

What must every cell that metabolizes glucose do first?


What enzymes do this?

phosphorylate glucose to glucose-6-phosphate


enzyme – hexokinase (in all tissues)




glucokinase (only in liver)

Enzyme Substrate and Product for Committed Step of glycolysis?


Is ATP generated or used in this reaction?

enzyme – phosphofructokinase-1


fructose-6-phosphate ;fructose-1,6-bisphosphate


ATP is not generated in this step, but is used to transfer Pi to fructose-6-phosphate

Control factors that affect glycolysis?

Phosphofructokinase-1 is committed step and heavily regulated by enzymes.




In muscle, phosphofructokinase-1 is inhibited by citrate and increased levels of ATP.


AMP, ADP, cAMP, and Pi reverse the inhibitory affects of ATP on PFK-1.


Another control is from the synthesis of pyruvate and ATP from PEP and ADP. In muscle, pyruvate kinase is feedback inhibited by ATP.




fructose-1,6-bisphosphatase will remove phosphate from f-1,6-bisphosphate, converting it backwards into fructose-6-phosphate. Phosphatase is also monitored.


Fructose-2,6-Phosphate (vasopressin and phenylephrine promote its synthesis) will inhibit this enzyme from removing the phsophate, thus activating PFK-1 when blood glucose is low. Fructose-2,6-Bisphosphate acts as a competitive inhibitor of fructose-1,6-bisphosphatase, inhibiting it from deposphorylating F-1,6-Bisphosphate and increasing the flux of F-6 Phosphate through PFK-1. Glucagon controls F-2,6-bisphosphate, stopping glycolysis and enhancing gluconeogenesis.


Another control is from the synthesis of pyruvate and ATP from PEP and ADP. In liver, pyruvate kinase feedback is inhibited by ATP and positively affected by fructose-1,6-bisphosphate.







In what steps are ATP generated?

2 steps:


1) 1,3-bisphoshoglycerate;3-phosphoglycerate

(phosphoglycerate kinase)


1 ATP produced.



2) PEP;pyruvate

(pyruvate kinase)


A total of 4 ATP (2 net ATP are produced) from glycolysis. 2 ATP are used up during the glycolysis process.

What steps of the glycolysis pathway cannot be reversed for use in gluconeogenesis?

3 steps:


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2 types of approaches that are used to get around barriers encountered in reversing glycolytic pathway

gluconeogenesis uses enzymes specific to glucose synthesis


Certain processes are localized to certain cellular compartments

Subcellular organelles involved in gluconeogenesis




Malate shuttle and where does it take place?

Mitochondrial matrix.



The malate shuttle is when oxaloacetate is changed to malate so it can be transferred across the mitochondrial membrane.

How does glucose-6-phosphate get converted into glucose?

conversion of glucose-6-phosphate occurs in the lumen of the ER.


There is a series of transporter proteins that play an integral role in the conversion of glucose.


1) T1 translocase pumps G-6-Phosphate into the lumen of the ER. The phosphatase for converting G-6-Phosphate lies in the lumen.


2) After dephosphorylation, the dissociated Pi is removed from the lumen into the cytosol by T2 translocase. T2 requires Ca to pump out Pi. A separate channel allows Ca to flow in the ER lumen.


3) glucose is pumped out of ER to cytosol by T3 translocase.


Enzyme used in gluconeogeneis both inside mitochondria and outside cytosol?
malate dehydrogenase
Tissues capable of carrying out ALL STEPS of gluconeogenesis?
liver and cortex of kidney

Is ATP or NADPH utilized or produced in the petose phosphate pathway?


What rxns produce/utilize ATP or NADPH?

PPP does not produce or utilize any ATP, but NADPH (reducing agent) is produced


NADPH produced in oxidative reactions of G6P and 6-phosphogluconate.

What are functions of the pentose phosphate pathway?

1) produce reducing agents, NADPH, for cytosolic rxns


2) produce ribulose-5-phosphate for nucleotide synthesis


3) provide alternative method for metabolizing glucose


4) allow for interconversion of pentoses and hexoses

Possible starting materials for pentose phosphate pathway?
Enzymes , substrate, and product for rate limiting step of pentose phosphate pathway?

Rate limiting step


glucose-6-phosphate converted to 6-phosphoglucono-δ-lactone by glucose-6-phosphate dehydrogenase.


Glucose-6-dehydrgoenase is inhibited by NADPH and activated by ↑ NADP+ (substrate availability)

How can glucose-6-phosphate dehydrogenase deficiency be related to hemolytic anemia?

Reduced glutathione in RBCs react with peroxides to form glutathionedimers. Glutathione can prevent oxidative damage to RBCs. NADPH is used to break up glutathione dimer in the cell and restore glutathione levels to react with other peroxides.


A deficiency in glucose-6-phosphate dehydrogenase can’t produce enough NADPH to restore glutathione levels.


This has 2 effects:


1) peroxides build up and damage RBC membranes


2) Heinz bodies (cross linkings of Hb) will reduce Hb flexibility, causing rupture of now fragile hemoglobin that is passed through small vesssels.


Weakened membranes and Heinz bodies will lead to acute hemolytic anemia, black urine, and increased urine flow (compensation to reduce renal damage from lysed RBCs)

In what kinds of tissues is this pathway most active?


In what part of the cell is it carried out?

Carried out in tissues with high amts of oxidation such as erythrocytes and leukocytes. Essential is nucleotide synthesis (gastric mucosa, bone marrow, and skin). Frequently occurs in tissues heavily involved in lipid and catecholamine synthesis (adipose, liver, lactating mammary, adrenal cortex, nervous system)


Takes place in the cytoplasm.

What tissues require ribose phosphate for high rates of nucleotide synthesis?

skin cells


bone marrow


gastric mucosa


generally tissues with a high rate of turnover of cells

What tissues require NADPH for lipid and catecholamine synthesis?



adrenal cortex


lactating mammary




nervous system

What tissues require NADPH for protection against oxidative damage?




What categories of rxns are utilized in the pentose phosphate pathway?

3 categories


1) oxidative rxns


2) isomerization or epimerization rxns


3) rxns that require C-C bonds to be cleaved or formed


Fatty acid synthesis occurs in what compartment of the cell?
A hormone that stimulates fatty acid synthesis is?
insulin stimulates fatty acid synthesis in the liver
Acetyl CoA carboxylase has a covalently bound prosthetic group called?
Substrates that are required by acetyl CoA carboxylase to form malonyl CoA





acetyl CoA

Describe how mitochondrial acetyl CoA is made available in the cytosol

acetyl CoA in mitochondrial matrix combined with OAA to form citrate


citrate is transported via a transporter from the mitochondria into the cytosl


citrate lyase using CoA cleaves citrate, into OAA and acetyl CoA



Redundant that is required for fatty acid synthesis
Substrate and products of malic enzyme
malate catalyzed by malic enzyme into pyruvate and CO2
vitamin derivative that is part of the ACP portion of the fatty acid synthesis complex?
Starting from acetyl CoA and malonyl CoA, describe the steps that are involved in the synthesis of palmitate

1) acetyl CoA + enzyme → acetyl-Enz by acetyl transferase


2) malonyl CoA + ACP → Malonyl-ACP by malonyl transferase


3) acetyl-enz+malonyl-ACP → acetoacetyl-ACP by keto synthase or condensing enzyme


4) acetocetyl-ACP → beta-hydroxybutyryl-ACP by beta-ketoacyl ruductase


5) beta-hydroxybutyryl-ACP → crotonyl-ACP by dehydratase


6) crotonyl-ACP → butyryl-ACP by enoyl reductase


7) butyryl-ACP → palmitoyl-ACP using 6 more malonyl coA in 6 rounds of steps 1-6


8) palmitoyl-ACP → palmitic acid by thioesterase

name enzyme domain that releases palmitate from the fatty acid synthase complex
thioesterase I domain
name the enzyme that is expressed during lactation in mammary glands that is relevant to fatty acid synthesis
thioesterase II
Name fatty acids that are released by thioesterase II

capric (C10)


lauric (C12)


myristic (C14)


easier to digest compared to palmitate for sucking infants

Name 2 essential fatty acids

linoleic (18:2)(9,12)


linolenic (18:3)(9,12,15)

All naturally occurring double bonds of fatty acids are of cis configuration?


true or false

false (I think)
Linoleic acid is the precursor for the biosynthesis of what?
arachidonic acid
Storage form of fatty acid
Triglycerides are stored in what tissue?
adipose tissue
Precursors for the synthesis of triglycerides

fatty acids are acylated by condensing with CoA to form Fatty acyl CoA


3 fatty acyl CoAs are then esterified to glycerol-3-phosphate to eventually form triglycerides (also called triacylglycerol)

backbone compound on which fatty acids are esterified to form triglycerides are
glycerol phosphate
Before beta-oxidation, activated fatty acids are esterified to THIS compound so that it can be transported from cytosol to mitochondria
fatty acyl carnitine
Name 3 energy related compounds that are produced upon beta-oxidation of fatty acids





acetyl CoA

Name enzyme in mitochondrial matrix that cleaves fatty acylc carnitine
carnitine acyltransferase II (CPT II)
Complete oxidation of stearic acid, myristic acid, and lauric acid, leads to the formation of how many moles of ATP
Name a methylated fatty acid that is derived from dairy products
phytanic acid
name an enzyme that uses vitamin B12 derivative as a coenzyme in the enzyme catalysis
methyl malonyl CoA mutase
Name a 3 carbon compound that is formed from the oxidation of odd chain fatty acid
propionyl CoA
Name 2 enzymes that convert propionyl CoA into succinyl CoA



methy malony CoA mutase

Name 2 carboxylases that require biotin as a coenzyme

propionyl CoA carboxylase


acetyl CoA carboxylase

Name a compound that is catabolized by alpha-oxidation
phytanic acid
Name an allosteric activator and an inhibitor of acetyl CoA carboxylase?

allosteric activator – citrate


inhibitor – fatty acyl CoA

Carnitine acyl-transferase is inhibited by what?
malonyl CoA
A hormone that triggers catabolism of fats

Phosphorylation of acetyl CoA carboxylase by protein kinase A inactivates the enzyme


True or False?


Phosphorylation of acetyl CoA carboxylase by hormone sensitive lipase activates the enzyme?


True or False?

Name the defect in Refsum’s disease
inability to properly degrade phytanic acid due to deficiency in the alpha hydroxylase enzyme
In Sudden Infant Death Syndrome the enzyme that is defective is?
medium chain fatty acyl CoA dehydrogenase deficiency
Name 2 conditions that would result in methylmalonic acedemia

methylmalonyl CoA mutase is missing


conversion of Vitamin B12 into coenzyme is missing

Definition of Obesity
BMI > 30
Name a natural and an artificial compound that inhibits fatty acid synthase

natural inhibitor compound – cerulenin


artificial inhibitor compound – C75

Malonyl CoA inhibits production of a neuropeptide compound called?

Neuropeptide Y signals the inhibition of feeding?


True or False?

Describe diabetic ketoacidosis?

blood concentrations of acetoacetic acid and beta-hydroxybutyric acid are as high as 20 mM.


These compounds are strong acids with a pKa of ~3.5, resulting in acidosis


In biochemical terms, the events are very similar to starvation mediated ketosis:


a) increased glucagon/insulin ratio results in elevation of liver cAMP


b) Elevated liver cAMP leads to decreased malonyl CoA


c) decreased malonyl CoA leads to de-inhibition of CPT I


d) de-inhibition of CPT I results in activation of fatty acid oxidation (fatty acid degradation) and increased ketone body production



Name 2 enzymes that convert alcohol into acetate

alcohol dehydrogenase


aldehyde dehydrogenase

Name the reductant that is produced during the oxidation of alcohol
How many moles of ATP are produced upon complete oxidation of ethanol?
12 ATP
Name a few compounds that are metabolized by omega-oxidation pathway



adjacent methylene carbon of fatty acids


fatty acids 6-10 Cs long

Upon complete oxidation of capric acid, how many moles of net ATP are produced?

Capric acid = C10   4 NADH + 4 FADH2 + 5 Acetyl CoA = (4×3) + (4×2) + (5×12) = 80 ATP


What are advantages of having fatty acid synthase as a multi enzyme complex as seen in mammals as  opposed to individual polypeptides as seen in bacteria?
more control
Why is fat storage energetically better compared to glycogen?

Adipose storage of TAG’s initially uses less energy to produce TAG’s, plus, degradation via ß-oxidation provides

            more energy/ ATP than Glycogen storage


Explain how ketone bodies can serve as an energy source in brain during starvation?

ketone bodies are synthesized by liver during starvation to feed the brain


acetoacetate is converted to acetoacetyl CoA by thiophorase after cross blood brain barrier


acetoacetyl CoA can be converted to 2 acetyl CoA by thiokinase


2 acetyl CoA then undergo citric acid cycle to produce energy in the brain

Why can carnitine palmitoyltransferase I deficiency lead to hypoketosis?

defect in transporting fatty acid carnitine


don’t have free fatty acids to make acetyl CoA and subsequently don’t get ketone bodies


don’t make enough ketone bodies

Why are alcoholics hypoglycemic?
What compound is the source of all carbons in cholesterol?
acetyl CoA
Cholesterol is the precursor for what 4 major types of compounds?

bile salts


vitamin D




sex hormones

What are the 5 stages in cholesterol biosynthesis that we discussed and their products?

1.)  Mevalonate synthesis → Mevalonate


2.) Isoprenoid synthesis → Isoprenoid units


3.) Squalene synthesis → Squalene


4.)  Lansterol Synthesis → Lansterol

5.)  Synthesis of Cholesterol from Lanosterol → Cholesterol


What are substrate, enzyme, and product of the rate-limiting step of cholesterol synthesis?

rate limiting step


HMG-CoA + 2 NADPH + 2 H+ → Mevalonate + 2 NADP+ + CoASH

What are different means by which cholesterol synthesis is controlled naturally?

1.)  Bicyclic control system:

      As insulin ↑ ­, cholesterol ­↑

      As glucagon ↑ ­, cholesterol ↓


2.)  HMG-Reductase degradation:

As cholesterol ↑ ­HMG-Reducases downregulates.


3.)  Genetic controls:  Sterols and mevalonate metabolites inhibit HMG-Reductase RNA synthesis


What are the main dietary sources of cholesterol?






How does the body get rid of cholesterol?

The body metabolizes some cholesterol into bile salts and steroids.


Rest go to tissues for storage or excreted out of body in feces.

What are bile salts and their use?

modification of cholesterol by ring hydrozylations and side chain oxidation result is cholic acid


cholic acid reacts with amino acids to form amides known as bile salts


Fxn: released by gall bladder to help solubilize dietary fats

What is the route of circulation for the re-absorption of bile salts?

Liver  → Gall bladder storage Intestine (some to lymphatics)   Bloodstream Liver.

What are 2 ways in which pharmaceutical intervention is used to lower patient cholesterol levels?

1) inhibition of HMG-CoA reductase; Mevacor


2) in small intestine removal and excretion of bile salts; Colestipol or Cholestyramine

What types of compounds supply the precursors for the eicosanoids and where are they found?
glycerophospholipids in plasma membrane
What enzyme cleaves the fatty acid off of the starting material?
phospholipase A2
What kinds of compounds activate phospholipase A2?








What kinds of compounds inhibit phospholipase A2?
inhibited by anti-inflammatory corticosteroids through induction of protein inhibitor of phospholipase A2 → lipocortin
Where are the general types of eicosanoids and how their names arise?

Eicosanods: Latin for “20” (number of C atoms in the molecules)


Prostaglandins:  Thought to be from the prostate gland


Thromboxanes:  Isolated from platelets


Leukotrienes:  Isolated from leukocytes


What enzyme  paths are used for the synthesis of prostaglandins, thromboxanes, and leukotrienes?

glycerophospholipid → arachidonic acid


cyclooxygenase reaction of arachidonic acid → thromboxane or prostaglandin


lipoxygenase reaction of arachidonic acid → leukotriene

What compounds inhibit cyclooxygenases?



non-steroidal anti-inflammatory drugs (NSAIDS)

What are some of the effects that prostaglandins can have?



stimulate smooth muscle contraction


regulate steroid synthesis


inhibit gastric secretion


inhibit hormone sensitive lipases


inhibit platelet aggregation


regulate nerve transmissions


sensitive to pain


mediate inflammatory response

What effects do thromboxanes have?
platelet aggregation and vasoconstriction
Where are leukotrienes found?



mast cells


vascular tissue





What pathway is used to synthesize leukotrienes?
leukotrienes are synthesized from arachidonic acid or linolenic acid by the lipoxygenase path
What are the slow reacting substances of anaphylaxis?
What biological effects do leukotrienes have?

contraction of smooth muscle in pulmonary airway


alteration in permeability of microvasculature, resulting in fluids and proteins leaking into tissues

Is the NADH/NAD+ ratio high or low in alcoholics?
Why does high NADH production in alcoholics lead to lipid formation?

↑ NADH levels indicate excess energy; therefore, ß-oxidation of triacyglycerols doesn’t occur resulting in high lipid levels

What are ω-3 and ω-6 fatty acids?

ω-3 = Omega-3 Fatty acids = Fatty acids with a double bond 3 carbons away from the last (ω) carbon on the F.A. chain

                   Example = Linolenic acid 18:3 (9,12,15) 

         ω-6 = Omega-6 Fatty acids = Fatty acids with a double bond 6 carbons away from the last (ω) carbon on the F.A. chain

                   Example = Linoleic acid  18:2 (9,12)


Describe the citrate lyase catalyzed reaction
Can carbon skelton from C-17 fatty acid oxidation enter gluconeogenic pathway. If yes, explain how
Can a carbon skeleton from C-16 fatty acid oxidation enter the gluconeogenic pathway?
Excretion of higher methylmalonic acid through urine is a sign of what vitamin deficiency?
What are the biochemical reasons for the peripheral neuropathy in Vitamin B12 deficient individuals?
lack of vitamin B12 inhibits fat beta oxidation which further has negative effects on myelin synthesis and results in peripheral neuropathy?
Describe the pathway of ketogenesis

1) 2 molecules of acetyl CoA → acetoacetyl CoA (thiolase)


2) acetoacetyl CoA → HMG CoA

(HMG CoA synthase)


3) HMG CoA → Acetoacetate + Acetyl CoA

(HMG CoA lyase)


4a) Acetoacetate → Acetone





4b) Acetoacetate → Beta-Hydroxy Butyrate




Describe the pathway of ketogenolysis

Ketogenesis occurs before




1) Acetoacetate → Goes Through Blood to Tissue


2) Acetoacetate + succinyl CoA → Acetoacetyl CoA



3) Acetoacetyl CoA → 2 Acetyl CoA

(thiokinase + CoA)


4) 2 Acetyl CoA enter TCA cycle to produce energy



Can muscle use ketone bodies as energy source? If yes, explain how ketone bodies enter energy metabolism?

Yes, muscles can use ketone bodies as energy source


2) Acetoacetate + succinyl CoA → Acetoacetyl CoA



3) Acetoacetyl CoA → 2 Acetyl CoA

(thiokinase + CoA)


4) 2 Acetyl CoA enter TCA cycle to produce energy


Explain the hormonal bases of ketogenesis (in liver) and ketogenolysis (in extrahepatic tissues) in Type I diabetes?

Insulin production = [Glucagon]/[Insulin] ratio, hence, F.A.’s will be mobilized via Hormone sensitive Lipase. 


Due to  Insulin, there will be an increase in F.A. ß-oxidation producing an overabundance of Acetyl CoA, which is then converted into Ketone Bodies.  The [Ketone Body] , and because these compounds contain highly acidic protons (pKa = 3.5), the blood pH will become acidic = DKA.

High NADH/NAD+ in alcoholics results in the production of what?
3-hydroxybutyrate (beta-hydroxybutyrate)
A person with a deficiency of vitamin B12 is recommended to avoid what type of food?
fatty food ???
A person with biotin deficiency cannot metabolize what fatty acid?
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