Category: Quiz

Different types of Fatty Oxidation

Different types of fatty acid oxidation

Q. 1

Oxidation of odd-chain fatty acids result in the production of which of the following?

 A

Acetyl CoA

 B

Succinyl CoA

 C

Propionyl CoA

 D

Malonyl CoA

Q. 1

Oxidation of odd-chain fatty acids result in the production of which of the following?

 A

Acetyl CoA

 B

Succinyl CoA

 C

Propionyl CoA

 D

Malonyl CoA

Ans. C

Explanation:

Odd chain fatty acids are also oxidised exactly as even chain fatty acids. However, after successive removal of 2-carbon units, at the end, one 3 carbon unit, propionyl CoA is produced. The propionyl CoA is further metabolised to Succinyl CoA which enters the TCA cycle.
 
Ref: Vasudevan Biochemistry, 3rd Edition, Page 124

 


Q. 2

Fatty acid with even number of carbon atoms on oxidation produces:

 A

Acetyl CoA

 B

Succinyl CoA

 C

Propionyl CoA

 D

All of the above

Q. 2

Fatty acid with even number of carbon atoms on oxidation produces:

 A

Acetyl CoA

 B

Succinyl CoA

 C

Propionyl CoA

 D

All of the above

Ans. A

Explanation:

Fatty acids with an odd number of carbon atoms are oxidized by the pathway of β-oxidation, producing acetyl-CoA, until a three-carbon (propionyl-CoA) residue remains. This compound is converted to succinyl-CoA, a constituent of the citric acid cycle. Hence, the propionyl residue from an odd-chain fatty acid is the only part of a fatty acid that is glucogenic
         
Ref: Harper 28th edition, chapter 22.

Q. 3

Very long chain fatty acid is oxidised in:

 A

Mitochondria

 B

Cytoplasm

 C

Peroxisome

 D

All of the above

Q. 3

Very long chain fatty acid is oxidised in:

 A

Mitochondria

 B

Cytoplasm

 C

Peroxisome

 D

All of the above

Ans. C

Explanation:

A modified form of oxidation is found in peroxisomes and leads to the formation of acetyl-CoA and H2O2 (from the flavoprotein-linked dehydrogenase step), which is broken down by catalase.
Thus, this dehydrogenation in peroxisomes is not linked directly to phosphorylation and the generation of ATP. The system facilitates the oxidation of very long chain fatty acids (eg, C20, C22).
These enzymes are induced by high-fat diets and in some species by hypo-lipidemic drugs such as clofibrate.
Ref: Harper 28th edition, chapter 22.

Q. 4

Beta-oxidation of odd-chain fatty acids produces:

 A

Acetyl CoA

 B

Malonyl CoA

 C

Succinyl CoA

 D

Propionyl CoA

Q. 4

Beta-oxidation of odd-chain fatty acids produces:

 A

Acetyl CoA

 B

Malonyl CoA

 C

Succinyl CoA

 D

Propionyl CoA

Ans. D

Explanation:

Odd chain fatty acids are oxidized in the similar manner as of even chain fatty acid, beta-oxidation.

However, unlike even chain fatty acids which yields only acetyl CoA, odd chain fatty acids will yield Acetyl-CoA and one three carbon acid, Propionyl-CoA.

Propionyl CoA is further converted into succinyl CoA.                                                                                                                                                      
Fatty acids are an important source of energy. ?Oxidation is the process where energy is produced by degradation of fatty acids.

 

Beta Oxidation of fatty acids: The pathway for catabolism of fatty acids is referred to  as the b-oxidation pathway, because oxidation occurs at the b-carbon (C-3).
?The beta oxidation of fatty acids involve three stages:
1. Activation of fatty acids in the cytosol
2. Transport of activated fatty acids into mitochondria (carnitine shuttle)
3. Beta oxidation proper in the mitochondrial matrix.
 
1. Activation of Fatty Acid:
 
This proceeds by Fatty Acid  thiokinase (acyl COA synthetase) present in cytosol. Thiokinase requires ATP, COA SH, Mg++. The product of this reaction is Fatty Acid  acyl COA and water.
2. Transport of fatty acyl CoA from cytosol into mitochondria: (rate-limiting step) ?Long chain acyl CoA traverses the inner mitochondria membrane with a special transport mechanism called Carnitine shuttle.
  • Acyl groups from acyl COA is transferred to carnitine to form acyl carnitine catalyzed by carnitine acyltransferase I, in the outer mitochondrial membrane.
  • Acylcarnitine is then shuttled across the inner mitochondrial membrane by a translocase enzyme.
  • The acyl group is transferred back to CoA in matrix by carnitine acyl transferase II.
  • Finally, carnitine is returned to the cytosolic side by translocase, in exchange for an incoming acyl carnitine.
3. Proper of β – oxidation in the mitochondrial matrix:
There are 4 steps in β – oxidation
  • Step I – Oxidation by FAD linked dehydrogenase: oxidation of acyl CoA by an acyl CoA dehydrogenase to give α-β unsaturated acyl CoA (enoyl CoA). 
  • Step II – Hydration by Hydratase: hydration of the double bond to β-hydroxyacyl CoA (p-hydroxyacyl CoA).
  • Step III – Oxidation by NAD linked dehydrogenase: oxidation of β-hydroxyacyl CoA to produce β-Ketoacyl CoA a NAD-dependent reaction.
  • Step IV – Thiolytic clevage Thiolase:? cleavage of the two carbon fragment by splitting the bond between α and β carbons, by thiolase enzyme.
Beta oxidation of odd chain fatty acids:
Fatty acids that enter beta-oxidation with an even number of carbons are converted entirely to acetyl-CoA. The beta-oxidation of odd chain fatty acid results in a acetyl-CoA and the 3-carbon chain propionyl-CoA. Propionyl Coa is further converted to succinyl CoA.
Ref: Harper’s, Illustrated Biochemistry, 26th edition, Page 182

Quiz In Between


Q. 5

β-oxidation of odd-chain fatty acids produces:

 A

Succinyl CoA

 B

Propionyl CoA

 C

Acetyl CoA

 D

Malonyl CoA

Q. 5

β-oxidation of odd-chain fatty acids produces:

 A

Succinyl CoA

 B

Propionyl CoA

 C

Acetyl CoA

 D

Malonyl CoA

Ans. B

Explanation:

B i.e. Propionyl CoA

13- oxidation of odd chain fatty acid produces acetyl CoA plus a molecule of propionyl –CoAQ. But propionyl CoA is formed only in odd chain fatty acid oxidation (not in even fatty acids)


Q. 6

Short chain fatty acid produced by bacteria are maximally absorbed in :

 A

Duodenum

 B

Colon

 C

Ileum

 D

Jejunum

Q. 6

Short chain fatty acid produced by bacteria are maximally absorbed in :

 A

Duodenum

 B

Colon

 C

Ileum

 D

Jejunum

Ans. B

Explanation:

B i.e. Colon

  • Major fat absorption takes place in upper small intestine except (mainly jejunum & duodenum) short chain fatty acids which is absorbed in colon0.
  • Normal fecal fat excretion is less than 6gm/day, more than 6gm/day indicates malabsorptionQ.
  • Steatorrhea is defined as stool fat > 7gm/dayQ.
  • Daily fecal fat averages 15-25gm/d with small intestinal disease & exceeds 40gm /d with pancreatic exocrine insufficiency
  • Evaluation of fat malabsorption:

Q. 7

Oxidation of very long chain fatty acids takes place in ‑

 A

Cytosol

 B

Mitochondria

 C

Ribosomes

 D

Peroxisomes

Q. 7

Oxidation of very long chain fatty acids takes place in ‑

 A

Cytosol

 B

Mitochondria

 C

Ribosomes

 D

Peroxisomes

Ans. D

Explanation:

Quiz In Between



Rapoport- Leubering Cycle

Rapoport Leubering cycle

Q. 1

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

 A

Tyndall effect

 B

Warburg effect

 C

Hawthorne effect

 D

None of the above

Q. 1

The phenomenon of cancer cells switching to glycolysis even in the presence of adequate oxygen for oxidative phosphorylation is known as:

 A

Tyndall effect

 B

Warburg effect

 C

Hawthorne effect

 D

None of the above

Ans. B

Explanation:

Even in the presence of ample oxygen, cancer cells shift their glucose metabolism away from the oxygen hungry, but efficient, mitochondria to glycolysis.
This phenomenon, called the Warburg effect and also known as aerobic glycolysis, has been recognized for many years (indeed, Otto Warburg received the Nobel Prize for discovery of the effect that bears his name in 1931), but was largely neglected until recently.

This metabolic alteration is so common to tumors that some would call it the eighth hallmark of cancer.
             
Ref:
Robbins 8th edition Chapter 2.

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Q. 2

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all glycolytic enzymes from band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Ans. C

Explanation:

During Hypoxia, the glycolytic enzymes that bind in the same region of band 3 of Hb are released from the membrane resulting in an increased rate of glycolysis. Increased glycolysis increases ATP production and the hypoxic release of ATP.
 
Ref: Oxygen Transport to Tissue, Xxxiii, edited by Martin Wolf, David K Harrison, 2012, Page 188.

Q. 3

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia Stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all Glycolytic enzymes from Band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Q. 3

Within the RBC, hypoxia stimulates glycolysis by which of the following regulating pathways?

 A

Hypoxia Stimulates pyruvate dehydrogenase by increased 2,3 DPG

 B

Hypoxia inhibits hexokinase

 C

Hypoxia stimulates release of all Glycolytic enzymes from Band 3 on RBC membrane

 D

Activation of the regulatory enzymes by high PH

Ans. C

Explanation:

C i.e. Hypoxia stimulates release of all glycolytic enzymes from Band 3 on RBC membrane

RBC membrane cytoskeletal protein spectrin is anchored to transmembrane anion exchanger protein Band 3 by protein ankyrin & protein 4.2. Another cytoskeletal protein actin is attached to transmembrane glycophorin C by protein 4.1. Tropomyosin, tropomodulin, adducin and 4.9 are other proteins.

  • Band 3, is a multifunction RBC transmembrane protein, which is important for its cytoskeletal structure, cell shape, anion exchange activity and glycolysisQ. Band 3 is responsible for chloride shift in RBCQ. Hypoxic deoxygenation of hemoglobin causes Band 3 tyrosine phosphorylation and thereby stimulates glycolysis by releasing glycolytic enzymes from band 3 on RBC membraneQ.
  • In kidney, I cells contain Band 3, an anion exchange protein in their basolateral cell membrane, which may function as a

Cl- – HCO3 exchanger for the transport of HCO3 to interstitial fluid.

  • In animal cells, principal regulators of intracellular pH are HCO3 transporters such as Band 3 CI – Hog; exchanger, 3Na+ – Hcq cotransporters and a le – HCO3 cotransporter.

Q. 4

Number of ATP produced by RBC when Glycolysis occurs through Rapoport Leubering pathway

 A

1

 B

2

 C

3

 D

4

Q. 4

Number of ATP produced by RBC when Glycolysis occurs through Rapoport Leubering pathway

 A

1

 B

2

 C

3

 D

4

Ans. A

Explanation:

 

Usually 2 ATP molecules are formed in glycolysis by substrate level phosphorylation.

Quiz In Between



Metabolism of Chylomicron

Metabolism of Chylomicron

Q. 1 In chylomicrons, the Principle Apo-protein is:
 A Apo A-I
 B Apo A-II
 C Apo B-100
 D Apo B-48
Q. 1 In chylomicrons, the Principle Apo-protein is:
 A Apo A-I
 B Apo A-II
 C Apo B-100
 D Apo B-48
Ans. D

Explanation:

Apo B-48


Q. 2

Which of the following are incorporated into the core of nascent chylomicrons?

 A

Triglyceride

 B

Triglyceride and Cholesterol

 C

Triglyceride, Cholesterol and Phospholipids

 D

Free fatty acids

Q. 2

Which of the following are incorporated into the core of nascent chylomicrons?

 A

Triglyceride

 B

Triglyceride and Cholesterol

 C

Triglyceride, Cholesterol and Phospholipids

 D

Free fatty acids

Ans. B

Explanation:

After ingestion of a meal, dietary fat (triglyceride) and cholesterol are absorbed into the cells of the small intestine and are incorporated into the core of nascent chylomicrons.


Q. 3

The chyle from intestine is rich with chylomicrons. Which of the following form the protein core of chylomicrons?

 A

Triglyceride only

 B

Triglyceride + cholesterol

 C

Triglyceride + cholesterol + phospholipid

 D

Only cholesterol

Q. 3

The chyle from intestine is rich with chylomicrons. Which of the following form the protein core of chylomicrons?

 A

Triglyceride only

 B

Triglyceride + cholesterol

 C

Triglyceride + cholesterol + phospholipid

 D

Only cholesterol

Ans. C

Explanation:

The triacylglycerol, cholesterol ester and phospholipid molecules along with apoproteins B48, and apo-A are incorporated into chylomicrons.
 

Four major groups of lipoproteins:

  • Chylomicrons, derived from intestinal absorption of triacylglycerol and other lipids.
  • Very low density lipoproteins (VLDL, or pre–lipoproteins), derived from the liver for the export of triacylglycerol.
  • Low-density lipoproteins (LDL, or -lipoproteins), representing a final stage in the catabolism of VLDL.
  • High-density lipoproteins (HDL, or -lipoproteins), involved in cholesterol transport and also in VLDL and chylomicron metabolism.

Triacylglycerol is the predominant lipid in chylomicrons and VLDL, whereas cholesterol and phospholipid are the predominant lipids in LDL and HDL, respectively.

Ref: Botham K.M., Mayes P.A. (2011). Chapter 25. Lipid Transport & Storage. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

Quiz In Between


Q. 4

A human subject takes part in a nutritional research study. After ingesting a very fatty meal, serum samples are taken for research studies at 1 hour and 3 hours. These studies measure the average diameter of the chylomicrons, showing an average chylomicron diameter of 500 nm at 1 hour, which drops to an average diameter of 150 nm at 3 hours. Where is the enzyme responsible for this change located?

 A

Adipocytes

 B

Endothelial cells

 C

Enterocytes

 D

Hepatocytes

Q. 4

A human subject takes part in a nutritional research study. After ingesting a very fatty meal, serum samples are taken for research studies at 1 hour and 3 hours. These studies measure the average diameter of the chylomicrons, showing an average chylomicron diameter of 500 nm at 1 hour, which drops to an average diameter of 150 nm at 3 hours. Where is the enzyme responsible for this change located?

 A

Adipocytes

 B

Endothelial cells

 C

Enterocytes

 D

Hepatocytes

Ans. B

Explanation:

Chylomicrons are produced by enterocytes (intestinal epithelial cells), using gut luminal triglycerides for the source of the lipid. The chylomicrons are secreted into the gut lymphatic system, and from there drain eventually into the systemic venous system from the thoracic duct, and hence into the serum portion of the blood. They are initially large and have a very high triglyceride content. With time, lipoprotein lipase releases triglycerides from the chylomicron core by hydrolyzing them to more easily absorbed fatty acids. The enzyme is located on the external surface of the vascular endothelium of tissues with triglyceride needs such as skeletal muscle, cardiac muscle tissue, and lactating breast. The result of lipoprotein lipase activity is that the chylomicrons shrink in size.

While adipose tissue can utilize chylomicrons, lipoprotein lipase is located on the endothelial cells rather than adipocytes. Adipocytes have an adipose tissue lipase, which is an intracellular enzyme that can cleave triglycerides to glycerol and fatty acids, allowing them to be released into the circulation when chylomicrons are low.
 
Enterocytes have the ability to pick up mixed micelles from the gut lumen for repackaging in the smooth endoplasmic reticulum as chylomicrons.
Hepatocytes pick up the chylomicron remnants after the lipoprotein lipase shrinks them.
Ref: Barrett K.E., Barman S.M., Boitano S., Brooks H.L. (2012). Chapter 26. Digestion, Absorption, & Nutritional Principles. In K.E. Barrett, S.M. Barman, S. Boitano, H.L. Brooks (Eds), Ganong’s Review of Medical Physiology, 24e.

Q. 5

Which helps in the transport of chylomicrons from intestine to liver :

 A

Apoprotein B

 B

Apoprotein A

 C

Apoprotein C

 D

Apoprotein E

Q. 5

Which helps in the transport of chylomicrons from intestine to liver :

 A

Apoprotein B

 B

Apoprotein A

 C

Apoprotein C

 D

Apoprotein E

Ans. A

Explanation:

A i.e. Apoprotein B


Q. 6

Major apolipoprotein of chylomicrons

 A

B-100

 B

D

 C

B-48

 D

None

Q. 6

Major apolipoprotein of chylomicrons

 A

B-100

 B

D

 C

B-48

 D

None

Ans. C

Explanation:

Ans. is ‘c’ i.e., B-48 

Quiz In Between



Cholesterol Synthesis

Cholesterol synthesis

Q. 1

The major step of regulation of cholesterol synthesis is:

 A

Cyclization of squalene to lanosterol

 B

3-hydroxy-3-methylglutaryl-CoA synthase

 C

3-hydroxy-3-methylglutaryl-CoA lyase

 D

3-hydroxy-3-methylglutaryl-CoA reductase

Q. 1

The major step of regulation of cholesterol synthesis is:

 A

Cyclization of squalene to lanosterol

 B

3-hydroxy-3-methylglutaryl-CoA synthase

 C

3-hydroxy-3-methylglutaryl-CoA lyase

 D

3-hydroxy-3-methylglutaryl-CoA reductase

Ans. D

Explanation:

Cholesterol is obtained from the diet as well as by de novo synthesis.

Although many cells can synthesize cholesterol, the liver is the major site of its production.

The rate of cholesterol production is highly responsive to feedback inhibition from both dietary cholesterol and synthesized cholesterol.

Feedback regulation is mediated by changes in the activity of 3-hydroxy-3-methylglutaryl-CoA reductase.  

This enzyme is the first committed step in the production of cholesterol from acetyl-CoA.

3-Hydroxy-3-methylflutaryl-CoA, the substrate of the reductase, also can be synthesized into the ketone by acetoacetate by the action of 3-hydroxy-3-methylglutaryl-CoA lyase

Ref: Essentials of Medical Biochemistry; With Clinical Cases, 1st Ed, page 215


Q. 2

The first step in synthesis of steroids is derived from the cleavage of cholesterol. What is the enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone?

 A

Delta 5-3 beta-hydroxysteroid dehydrogenase (3B – HSD)

 B

HMG-CoA reductase

 C

Aromatase

 D

17 alpha-hydroxylase

Q. 2

The first step in synthesis of steroids is derived from the cleavage of cholesterol. What is the enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone?

 A

Delta 5-3 beta-hydroxysteroid dehydrogenase (3B – HSD)

 B

HMG-CoA reductase

 C

Aromatase

 D

17 alpha-hydroxylase

Ans. A

Explanation:

The enzyme responsible for the cleavage of 20,22-dehydrocholesterol to pregnenolone is termed Delta 5-3 beta-hydroxysteroid dehydrogenase ( 3B HSD). Pregnenolone is a precursor to progesterone. Conversion to progesterone is necessary for eventual synthesis of testosterone and estrogen. Although there are different enzymes for their production, progesterone converted from cholesterol is of primary importance.
 
Ref: Weil P. (2011). Chapter 41. The Diversity of the Endocrine System. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.
 

Q. 3

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

 A

HMG -Co-A Reductase

 B

HMG-Co-A Lyase

 C

HMG-Co-A Synthase

 D

Thiokinase

Q. 3

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

 A

HMG -Co-A Reductase

 B

HMG-Co-A Lyase

 C

HMG-Co-A Synthase

 D

Thiokinase

Ans. C

Explanation:

C i.e. HMG-Co-A Synthase

Quiz In Between


Q. 4

Which of the following blocks DNA replication with getting incorporated in DNA strand:

 A

Cytarabine

 B

Nalidixic acid

 C

Ciprofloxacin

 D

Paclitaxel

Q. 4

Which of the following blocks DNA replication with getting incorporated in DNA strand:

 A

Cytarabine

 B

Nalidixic acid

 C

Ciprofloxacin

 D

Paclitaxel

Ans. A

Explanation:

A i.e. Cytarabine


Q. 5

Cholesterol is synthesized from:

 A

Acetyl CoA

 B

Alpha-ketoglutarate

 C

Glutaric acid

 D

Oxalate

Q. 5

Cholesterol is synthesized from:

 A

Acetyl CoA

 B

Alpha-ketoglutarate

 C

Glutaric acid

 D

Oxalate

Ans. A

Explanation:

Q. 6

Cholesterol is:        

 

 A

Tocopherol

 B

Lipoprotein

 C

Steroid

 D

Lipopolysacchride

Q. 6

Cholesterol is:        

 

 A

Tocopherol

 B

Lipoprotein

 C

Steroid

 D

Lipopolysacchride

Ans. C

Explanation:

 

Cholesterol is an amphipathic lipid and is an important structural component of membranes and of the outer layer of plasma lipoproteins.

It is mainly synthesized in many tissues from Acetyl-CoA and is the precursor of all other steroids in the body, including corticosteroids, sex hormones, bile acids, and vitamin D.

Quiz In Between


Q. 7

Cholesterol is not a precursor of:

 A

Bile acid

 B

Bile pigment

 C

Vitamin D

 D

Sex hormones

Q. 7

Cholesterol is not a precursor of:

 A

Bile acid

 B

Bile pigment

 C

Vitamin D

 D

Sex hormones

Ans. B

Explanation:

 

Cholesterol is the precursor of bile acids [Bile contains bile salts (conjugated bile acids), which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, A, D, E, and K].

 


Q. 8

Mineral required for cholesterol biosynthesis ‑

 A

Fe

 B

Mn

 C

Mg

 D

Cu

Q. 8

Mineral required for cholesterol biosynthesis ‑

 A

Fe

 B

Mn

 C

Mg

 D

Cu

Ans. C

Explanation:

 

Mg is required in stage 2 of cholesterol synthesis.

Biosynthesis (De Novo Synthesis) of cholesterol

  • The liver is the major site for cholesterol biosynthesis. Some cholesterol is also synthesized in intestine adre‑nal cortex, gonads and skin. The microsomal (smooth endoplasmic reticulum) and cytosol fraction of cell is responsible fir cholesterol synthesis; However most of the reactions in synthesis occurs in cytosol.
  • Cholesterol is a C-27 compound. All 27-carbon atoms of cholesterol are derived from a single precursor, i.e. acetyl-CoA (activated acetate).
  • First two molecules of acetyl-CoA condense to form acetoacetyl-CoA. Next, a third molecule of acetyl- CoA condenses with acetoacetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). Then HMG-CoA is converted to mevalonate by HMG-CoA reductase, the key regulatory enzyme of cholesterol synthesis.

Q. 9

Rate limiting step in cholesterol synthesis –

 A

HMG CoA reductase 

 B

HMG CoA synthase 

 C

Mevalonate kinase

 D

Squalene synthetase

Q. 9

Rate limiting step in cholesterol synthesis –

 A

HMG CoA reductase 

 B

HMG CoA synthase 

 C

Mevalonate kinase

 D

Squalene synthetase

Ans. A

Explanation:

Ans. is ‘a’ i.e., HMG Co A reductase

Reactions Rate limiting enzymes 
Glycolysis Phosphofructokinase 
Glycogen synthesis  Glycogen synthetase 

Glycogenolysis

Glycogen phosphorylase 

TCA cycle

Isocitrate dehydrogenase 
Fatty acid synthesis  Acetyl CoA carboxylase 
Cholesterol synthesis  HMG CoA reductase HMG 
Ketone body synthesis CoA synthase 
Bile acid synthesis  7-a-hydroxylase
Catecholamine synthesis  Tyrosine hydroxylase 
Urea synthesis

Carbamoyl transferase

Quiz In Between



Metabolism of HDL

Metabolism of HDL

Q. 1

Which of the following statements about High Density Lipoprotein (HDL) is false:

 A

HDL increases oxidation of LDL

 B

HDL reduces foam cell production by LDL

 C

HDL is the best predictor of CAD

 D

HDL helps to clear lipids from atheromas

Q. 1

Which of the following statements about High Density Lipoprotein (HDL) is false:

 A

HDL increases oxidation of LDL

 B

HDL reduces foam cell production by LDL

 C

HDL is the best predictor of CAD

 D

HDL helps to clear lipids from atheromas

Ans. A

Explanation:

HDL prevent oxidation of LDL in complex in vitro models as a result HDL function as a naturally acting antioxidant which protect vessel wall from oxidative damage and resulting atherogenesis.

Ref: Current Pharmaceutical Design, Page 6.


Q. 2

Good cholesterol found in:

 A

HDL

 B

LDL

 C

VLDL

 D

IDL

Q. 2

Good cholesterol found in:

 A

HDL

 B

LDL

 C

VLDL

 D

IDL

Ans. A

Explanation:

A i.e. HDL

  • HDL contains good cholesterolQ. So there is an inverse relation between HDL (HDL2) concentrations and coronoary heart disease. This is consistent with the function of HDL in reverse cholesterol transport.
  • Diseases (eg. diabetes mellitus, lipid nephrosis, hypothyroidism and other considtions of hyperlipedimea) in which prolonged elevations of VLDL, IDL, LCD or chulomicron remnants in blood are often accompanied by premature or severe atherosclerosis. This makes LDL : HDL cholesterol ratio a good predective parameter for atherosclerosis & coronary heart disease.

Q. 3

Reverse cholesterol transport is mediated by

 A

HDL

 B

VLDL

 C

LDL

 D

IDL

Q. 3

Reverse cholesterol transport is mediated by

 A

HDL

 B

VLDL

 C

LDL

 D

IDL

Ans. A

Explanation:

Ans. is ‘a’ i.e., HDL

Reverse cholesterol transport

  • All nucleated cells in different tissues synthesize cholesterol, but the excretion of cholesterol is mainly by liver in the bile or by enterocytes in gut lumen.
  • So, cholesterol must be transported from peripheral tissue to liver for excretion.

o This is facilitated by HDL and is called reverse cholesterol transport because it transports the cholesterol in reverse direction to that is transported from liver to peripheral tissues through VLDL                        LDL cycle. Process

o HDL is synthesized in liver and small intestine.

o Nascent HDL contain phospholipids and unesterified cholesterol and Apo-A, C, E.

  • This nascent HDL is secreted into circulation where it acquires additional unesterified cholesterol from peripheral tissues.

o Within the HDL particle, the cholesterol is esterified by lecithin – cholesterol acetyltransferase (LCAT) to form cholesteryl ester and additional lipid are transported to HDL from VLDL and chylomicrons.

o There are two pathway by which this cholesterol is transported to liver.


Q. 4

All are bad cholesterol except:    

 A

HDL

 B

LDL

 C

VLDL

 D

IDL

Q. 4

All are bad cholesterol except:    

 A

HDL

 B

LDL

 C

VLDL

 D

IDL

Ans. A

Explanation:

 

HDL can remove cholesterol from atheroma within arteries and transport it back to the liver for excretion or re-utilization, which is the main reason why HDL-bound cholesterol is sometimes called “good cholesterol”, or HDL-C. A high level of HDL-C seems to protect against cardiovascular diseases, and low HDL cholesterol levels (less than 40 mg/ dL or about 1mmol/L) increase the risk for heart disease.

Cholesterol contained in HDL particles is considered beneficial for the cardiovascular health, in contrast to “bad” LDL cholesterol.

Quiz In Between


Q. 5

Lipoprotein involved in reverse cholesterol transport‑

 A

LDL

 B

VLDL

 C

IDL

 D

HDL

Q. 5

Lipoprotein involved in reverse cholesterol transport‑

 A

LDL

 B

VLDL

 C

IDL

 D

HDL

Ans. D

Explanation:

 

The HDL particles are referred to as scavengers because their primary role is to remove free (unesterified) cholesterol from the extrahepatic tissues.

HDL particles transport cholesterol from extrahepatic tissues to liver (i.e. reverse cholesterol transport) which is then excreted through bile.

Reverse cholesterol transport

All nucleated cells in different tissues synthesize cholesterol, but the excretion of cholesterol is mainly by liver in the bile or by enterocytes in gut lumen. So, cholesterol must be transported from peripheral tissue to liver for excretion. This is facilitated by HDL and is called reverse cholesterol transport because it transports the cholesterol in reverse direction to that is transported from liver to peripheral tissues through VLDL → LDL cycle.

Process

HDL is synthesized in liver and small intestine. Nascent HDL contain phospholipids and unesterified cholesterol and Apo-A, C, E. This nascent HDL is secreted into circulation where it acquires additional unesterified cholesterol from peripheral tissues. Within the HDL particle, the cholesterol is esterified by lecithin – cholesterol acetyltransferase (LCAT) to form cholesteryl ester and additional lipid are transported to HDL from VLDL and chylomicrons. Apo-A1 activates LCAT.


Q. 6

Lipoprotein associated with carrying cholesterol from peripheral tissues to liver is ‑

 A

 HDL

 B

LDL

 C

VLDL

 D

IDL

Q. 6

Lipoprotein associated with carrying cholesterol from peripheral tissues to liver is ‑

 A

 HDL

 B

LDL

 C

VLDL

 D

IDL

Ans. A

Explanation:

 

HDL particles transport cholesterol from extrahepatic tissues to liver (i.e. reverse cholesterol transport) which is then excreted through bile.


Q. 7

Cholesteryl ester transfer protein transport cholesterol from HDL to ‑

 A

VLDL

 B

IDL

 C

LDL

 D

Chylomicrons

Q. 7

Cholesteryl ester transfer protein transport cholesterol from HDL to ‑

 A

VLDL

 B

IDL

 C

LDL

 D

Chylomicrons

Ans. A

Explanation:

 

Cholesteryl ester is tranfered from HDL to VLDL and chylomicrons in exchange with triglyceride by the cholesteryl ester transfer protein (CETP).


Q. 8

Lipoprotein associated with carrying cholesterol from periphery tissues to liver is ‑

 A

HDL

 B

LDL

 C

VLDL

 D

1DL

Q. 8

Lipoprotein associated with carrying cholesterol from periphery tissues to liver is ‑

 A

HDL

 B

LDL

 C

VLDL

 D

1DL

Ans. A

Explanation:

Ans. is ‘a’ i.e., HDL 

Quiz In Between



Vitamin B3- metabolism

Vitamin B3- metabolism

Q. 1

Niacin is required for growth of – Oxidase

 A

M. tuberculosis

 B

M. kansasii

 C

M. Scrofuloderma

 D

M. Avium

Q. 1

Niacin is required for growth of – Oxidase

 A

M. tuberculosis

 B

M. kansasii

 C

M. Scrofuloderma

 D

M. Avium

Ans. A

Explanation:

Ans. is ‘a’ i.e., M. tuberculosis 


Q. 2

One mg. of Niacin is produced by…………………….. mg. of Tryptophan-

 A

22

 B

37

 C

55

 D

60

Q. 2

One mg. of Niacin is produced by…………………….. mg. of Tryptophan-

 A

22

 B

37

 C

55

 D

60

Ans. D

Explanation:

Ans. is ‘d’ i.e., 60 

About 60 mg of tryptophan is required to result in I mg of niacin.


Q. 3

Niacin is synthesized from ‑

 A

Arginine

 B

Histidine

 C

Tryptophan

 D

Tyrosine

Q. 3

Niacin is synthesized from ‑

 A

Arginine

 B

Histidine

 C

Tryptophan

 D

Tyrosine

Ans. C

Explanation:

Q. 4

Niacin is derived from which amino acid?

 A

Tyrosine

 B

Phenylalanine

 C

Tryptophan

 D

Methionine

Q. 4

Niacin is derived from which amino acid?

 A

Tyrosine

 B

Phenylalanine

 C

Tryptophan

 D

Methionine

Ans. C

Explanation:

Quiz In Between



Vitamin B3 Deficiency

Vitamin B3 & Deficiency

Q. 1

Nicotinamide is preferred over Niacin because?

 A Flushing is seen with niacin
 B

Abdominal pain is seen with niacin

 C Breathlessness is seen with niacin
 D

Less bioavailability

Q. 1

Nicotinamide is preferred over Niacin because?

 A Flushing is seen with niacin
 B

Abdominal pain is seen with niacin

 C Breathlessness is seen with niacin
 D

Less bioavailability

Ans. A

Explanation:

Flushing is seen with niacin REF: Nutrition Almanac by John D. Kirschmann, Nutrition Search, Inc page 31

Niacin causes sudden release of histamine which produces certain s/e which are not seen with nicotinamide

  • Intense flushing
  • Tingling
  • Numbness
  • Throbbing headache due to cerebral vasodilation.

Q. 2

A 54-year-old man has a total cholesterol of 272 and LDL level of 210. His therapy is initiated with dietary modification and an exercise regimen, but he is unresponsive and so is prescribed nicotinic acid (Niacin). Which of the following symptoms will this patient likely experience from this drug?

 A

Bradycardia

 B

Facial flushing

 C

Hypoalbuminemia

 D

Hypoglycemia

Q. 2

A 54-year-old man has a total cholesterol of 272 and LDL level of 210. His therapy is initiated with dietary modification and an exercise regimen, but he is unresponsive and so is prescribed nicotinic acid (Niacin). Which of the following symptoms will this patient likely experience from this drug?

 A

Bradycardia

 B

Facial flushing

 C

Hypoalbuminemia

 D

Hypoglycemia

Ans. B

Explanation:

Niacin, or vitamin B3, is an agent that results in the following physiologic changes: LDL reductions tend to occur in 5-7 days with the maximal effect seen in 3-5 weeks; triglycerides and VLDL are reduced by 20% to 40% in 1-4 days; and HDL levels can increase by 20%.

This agent is indicated as adjunctive therapy in patients with elevated cholesterol and triglycerides when diet and other nondrug therapies are inadequate. 

The most common adverse effect of this agent is generalized flushing with a sensation of warmth, especially in the facial area.

This reaction may be so severe in some patients that they discontinue therapy.

Other common adverse effects include hepatotoxicity, tachycardia, hypoalbuminemia, hyperglycemia, nausea, vomiting, hyperuricemia, glucose intolerance, pruritus, peptic ulcer disease, and dry skin.


Q. 3

Maize contains the vitamin niacin. Pellagra is a disease that results from niacin deficiency.

Assertion: Consumption of maize may aggravate Pellagra.

Reason: Some strains of maize contains excess of Leucine which interferes in the conversion of Tryptophan into Niacin.

 A

Both Assertion and Reason are true, and Reason is the correct explanation for Assertion

 B

Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion

 C

Assertion is true, but Reason is false

 D

Assertion is false, but Reason is true

Q. 3

Maize contains the vitamin niacin. Pellagra is a disease that results from niacin deficiency.

Assertion: Consumption of maize may aggravate Pellagra.

Reason: Some strains of maize contains excess of Leucine which interferes in the conversion of Tryptophan into Niacin.

 A

Both Assertion and Reason are true, and Reason is the correct explanation for Assertion

 B

Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion

 C

Assertion is true, but Reason is false

 D

Assertion is false, but Reason is true

Ans. A

Explanation:

Pellagra is caused by Niacin deficiency and anything that interferes in the absorption or production of Niacin will aggravate the condition.

Ref: Park’s Textbook of Preventive Medicine, 17th Edition, Page 427.

Quiz In Between


Q. 4

A 10 year old child is suspected of having pellagra because of chronic symptoms including diarrhea, a red scaly rash, and mild cerebellar ataxia. However, his diet is not deficient in protein and he appears to be ingesting adequate amounts of niacin. A sister has a similar problem. Chemical analysis of his urine demonstrates large amounts of free amino acids. Which of the following is the most likely diagnosis?

 A

Alkaptonuria

 B

Carcinoid syndrome

 C

Ehlers-Danlos syndrome

 D

Hartnup’s disease

Q. 4

A 10 year old child is suspected of having pellagra because of chronic symptoms including diarrhea, a red scaly rash, and mild cerebellar ataxia. However, his diet is not deficient in protein and he appears to be ingesting adequate amounts of niacin. A sister has a similar problem. Chemical analysis of his urine demonstrates large amounts of free amino acids. Which of the following is the most likely diagnosis?

 A

Alkaptonuria

 B

Carcinoid syndrome

 C

Ehlers-Danlos syndrome

 D

Hartnup’s disease

Ans. D

Explanation:

The child has Hartnup’s disease.
This condition clinically resembles pellagra (“diarrhea, dementia, and dermatitis”), and may be misdiagnosed as this nutritional (niacin) deficiency. In fact, niacin therapy may actually be helpful in controlling the symptoms.
The underlying problem is a defect in the epithelial transport of neutral amino acids, including tryptophan, which can act as a precursor of niacin. The defective amino acid transport leads to poor absorption of dietary amino acids as well as excess amino acid secretion in the urine.
Alkaptonuria  is characterized by urine that turns black upon standing and a debilitating arthritis.
 
Carcinoid syndrome is seen in patients with carcinoid tumor. It is characterized by episodes of flushing, diarrhea, hypertension, and bronchoconstriction.
 
Ehlers-Danlos syndrome is a disease characterized by abnormal collagen formation leading to very elastic skin, joint problems, and fragility of some blood vessels and the intestines.
 
Ref: Bender D.A. (2011). Chapter 44. Micronutrients: Vitamins & Minerals. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds),Harper’s Illustrated Biochemistry, 29e.

Q. 5

In Niacin deficiency, all of the following are seen except:

 A

Deafness

 B

Diarrhea

 C

Dementia

 D

Dermatitis

Q. 5

In Niacin deficiency, all of the following are seen except:

 A

Deafness

 B

Diarrhea

 C

Dementia

 D

Dermatitis

Ans. A

Explanation:

Ans. is ‘a’ i.e., Deafness 

o Niacin deficiency results in ‘Pellagra’

Pellagra is identified by the presence of three ‘D’s —> Diarrhea, Dementia, Dermatitis


Q. 6

Niacin deficiency causes all except –

 A

Diarrhea

 B

Dyspepsia

 C

Dementia

 D

Dermatitis

Q. 6

Niacin deficiency causes all except –

 A

Diarrhea

 B

Dyspepsia

 C

Dementia

 D

Dermatitis

Ans. B

Explanation:

Ans. is ‘b’ i.e., Dyspepsia 

Quiz In Between


Q. 7

Niacin deficiency cause –

 A

Pellagra

 B

Scurvy

 C

Rickets

 D

Lathyrism

Q. 7

Niacin deficiency cause –

 A

Pellagra

 B

Scurvy

 C

Rickets

 D

Lathyrism

Ans. A

Explanation:

Ans. is ‘a’ i.e., Pellagra 


Q. 8

Niacin deficiency in a maize-eating population is due to-

 A

High Tryptophan 

 B

High lsoleucine

 C

High leucine

 D

High Phenylalanine

Q. 8

Niacin deficiency in a maize-eating population is due to-

 A

High Tryptophan 

 B

High lsoleucine

 C

High leucine

 D

High Phenylalanine

Ans. C

Explanation:

Ans. is ‘c’ i.e., High Leucine 

Excess of Leucine interferes in conversion of Tryptophan into Niacin, and aggravates the pallagrogenic action of inake.


Q. 9

Niacin deficiency causes ‑

 A

Pigmentation

 B

Diarrhea

 C

Rash

 D

Lactic acidosis

Q. 9

Niacin deficiency causes ‑

 A

Pigmentation

 B

Diarrhea

 C

Rash

 D

Lactic acidosis

Ans. B

Explanation:

Ans. is ‘b’ i.e., Diarrhea 

  • Deficiency of niacin (and tryptophan) causes pellagra which is characterized by 3 Ds, i.e. dermatitis, diarrhea and dementia.
  • Pellagra is common in people consuming maize and sorghum (jowar) as their staple foods.
  • These two are poor in niacin and tryptophan, and rich in leucin.
  • Excess of leucine inhibits the conversion of tryptophan into niacin.

Quiz In Between



Lipoprotein Structure

Lipoprotein- structure

Q. 1 The major lipid of the lipoproteins is:
 A Oleic acid
 B Palmitic acid
 C Linoleic acid
 D Arachidonic acid
Q. 1 The major lipid of the lipoproteins is:
 A Oleic acid
 B Palmitic acid
 C Linoleic acid
 D Arachidonic acid
Ans. D

Explanation:

Arachidonic acid


Q. 2

Human plasma lipoprotein containing the highest percentage of triacylglycerol by weight is:

 A

VLDL

 B

Chylomicrons

 C

HDL

 D

LDL

Q. 2

Human plasma lipoprotein containing the highest percentage of triacylglycerol by weight is:

 A

VLDL

 B

Chylomicrons

 C

HDL

 D

LDL

Ans. B

Explanation:

Triacylglycerol or triglyceride is an ester that is derived from glycerol and three fatty acids. Chylomicrons are lipoproteins that are lowest in density and largest in size which contains the highest percentage of triacylglycerol and the smallest percentage of protein.

Besides containing 80 to 95 percent triglyceride, chylomicrons contain 2 to 7 percent cholesterol, 3 to 6 percent phospholipid, and 1-2 percent protein.
 
Ref: Lippincott’s Illustrated Reviews: Biochemistry, 3rd Edition, Page 225; Fitness and Health By Brian J. Sharkey, Steven E. Gaskill, 2007, Page 274.

Q. 3

. The human plasma lipoprotein containing the highest percentage of triacylglycerol by weight is:

 A

VLDL

 B

Chylomicrons

 C

HDL

 D

LDL

Q. 3

. The human plasma lipoprotein containing the highest percentage of triacylglycerol by weight is:

 A

VLDL

 B

Chylomicrons

 C

HDL

 D

LDL

Ans. B

Explanation:

B i.e. Chylomicrins

Lipoproteins may be differentiated on the basis of their lipid & protein compositions. The lipoproteins containing the largest percentage of triacylglycerol are Chylomicrons (90%).

Lipoprotein Structure



Glycolipids

Glycolipids

Q. 1 Glycerol  is  the  backbone  of  all  of  the following phospholipids EXCEPT
 A Phosphatidylethanolamine
 B Cardiolipin
 C Phosphatidylcholine
 D Sphingomyelin
Q. 1 Glycerol  is  the  backbone  of  all  of  the following phospholipids EXCEPT
 A Phosphatidylethanolamine
 B Cardiolipin
 C Phosphatidylcholine
 D Sphingomyelin
Ans. D

Explanation:

Sphingomyelin   = phosphorylcholine + ceramide

Ceramide            = fatty acid + sphingosine

Sphingosine        = condensing palmitic acid with a decarboxylated   serine   and   then   reducing   the product

Glycerol  never  is  involved  in  the  structure  of sphingomyelin. Phosphatidylethanolamine, cardiolipin, phosphatidylcholine, and phosphatidylinositol are synthesized using phosphatidic acid as the basic building block  Phosphatic acid  is  diacylglycerol with a phosphate  ester on carbon three; therefore, glycerol is the backbone of all of these compounds. FAQ Sphingomyelin :-

–  Membranous myelin sheath that surrounds nerve cell axons.

–    It is the only sphingolipid NOT derived from Glycerol.

–       Associated  with  increased  accumulation  in Niemann-Pick  Disease.


Q. 2

Which of the following occurs in the lipidosis known as Tay-Sachs disease?

 A

Synthesis of a specific ganglioside is excessive

 B

Xanthomas due to cholesterol deposition are observed

 C

Phosphoglycerides accumulate in the brain

 D

Ganglioside GM2 is not catabolized by lysosomal enzymes

Q. 2

Which of the following occurs in the lipidosis known as Tay-Sachs disease?

 A

Synthesis of a specific ganglioside is excessive

 B

Xanthomas due to cholesterol deposition are observed

 C

Phosphoglycerides accumulate in the brain

 D

Ganglioside GM2 is not catabolized by lysosomal enzymes

Ans. D

Explanation:

In the genetic disorder known as Tay-Sachs disease, ganglioside GM2 is not catabolized. As a consequence, the ganglioside concentration is elevated many times higher than normal. The functionally absent lysosomal enzyme is β-N- acetylhexosaminidase.

The elevated GM2 results in irreversible brain damage to infants, who usually die before the age of 3 years. Under normal conditions, this enzyme cleaves N- acetylgalactosamine from the oligosaccharide chain of this complex sphingolipid, allowing further catabolism to occur.

The cause of most lipidoses (lipid storage diseases) is similar.

That is, a defect in catabolism of gangliosides causes abnormal accumulation.

None of the other choices result in lipidotic disorders. 

Ref: Hopkin R., Grabowski G.A. (2012). Chapter 361. Lysosomal Storage Diseases. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison’s Principles of Internal Medicine, 18e.

 


Q. 3

Glycosphingolipidis made up of:

 A

Glucose

 B

Fatty acids

 C

Sphingosine

 D

All Correct

Q. 3

Glycosphingolipidis made up of:

 A

Glucose

 B

Fatty acids

 C

Sphingosine

 D

All Correct

Ans. D

Explanation:

A, B, C i.e. Glucose, Sphingosine, Fatty acids

Glycosphingolipid = Ceramide (Sphingosine / amino alcohol + Fatty acid) + Mono/oligo saccharide like glucose, galactose. Ganglioside (acidic glycosphingolipid) = Ceramide + Oligosaccharide + NANA (N-acetylneuraminic acid or sialic acid)

 

–  Glyco-sphingolipid is made up of ceramide (which is a long chain fatty acid attached to amino group of sphingosine through an amide linkage i.e. = sphingosine/ amino alcohol + Fatty acid) attached directly to mono /oligo saccharide

(polar head) by an 0-glycosidic bond. Glycosphingolipids differ from sphingomyelin (phospho- sphingolipid) in that they do not contain phosphate (polar group); and differ from glycerophospholipids (phosphoglycerides) that they do not contain glycerol.

Ganglioside (acidic, negatively charged glyco-sphingolipid) contain sphingosine alcohol (4 sphingenine) 1 molecule, long chan fatty acid (1 mol), Oligosaccharide polar head and 1 or more residues of N- acetylneurminic acid (Neu 5 Ac), a sialic acid (often simply called sialic acid) giving it a negative charge, at termini. Ganglioside do not contain glycerol and phosphateQ.

Ceramide containing sphingosine amino alcohol is present in all sphingolipids (ie. phospho & glyco- sphingolipids)Q.



Q. 4

Which of the following is not a glycerosphingolipid?

 A

Lecithin

 B

Cardiolipin

 C

Plasmalogens

 D

Sphingomyelin

Q. 4

Which of the following is not a glycerosphingolipid?

 A

Lecithin

 B

Cardiolipin

 C

Plasmalogens

 D

Sphingomyelin

Ans. D

Explanation:

 

Phospholipids are :

  1. Glycerophospholipids (glycerol containing) :- Phosphatidylcholine (lecithin), phosphatidylethanolamine (cephaline), phosphatidylserine, phosphatidylinositol, plasmalogens, lysophospholipids, cardiolipin.
  2. Sphingophospholipids (sphingosine containing) :- Sphingomyeline

Quiz In Between



Isoenzymes

ISOENZYMES

Q. 1

True about isoenzymes is:

 A

Same quaternary structure

 B

Same distribution in different organs

 C

Same enzyme classification with same umbers

 D

Catalyze the same reaction

Q. 1

True about isoenzymes is:

 A

Same quaternary structure

 B

Same distribution in different organs

 C

Same enzyme classification with same umbers

 D

Catalyze the same reaction

Ans. D

Explanation:

    • Isoenzymes are the multiple forms of the same enzyme in a single species that catalyze the same chemical reaction or reactions, but differ from each other structurally, electrophoretically and immunologically.
    • Though the same chemical reaction is catalyzed, the different isoenzymes may catalyze the same reaction at different rates.
    • Isoenzymes have different pH optimes, Km and V max values.
    • Isoenzymes may differ in their amino acid sequence and their quarternary structures.
    • The isoenzymes may have different properties also for e.g. LDH-4 and LDH-5 are easily destroyed by heat, whereas LDH-1 and LDH-2 are not, if heated upto 60°C. (Heat resistant).
    • Individual isoenzymes (isozymes) are distinguished and numbered on the basis of electrophoretic mobility, with the number 1 being assigned to that form having the highest mobility toward the anode, for e.g. LDH-1 has the highest mobility towards the anode and LDH-5 is the slowest.
    • Isoenzymes have different tissue distributions. Therefore the pattern of isoenzymes found in the plasma may serve as a means of identifying the site of tissue damage. Example of the diagnostic use of isoenzymes are the study of Lactate Dehydrogenase and Creatine Kinase.

Q. 2

True about isoenzymes is/are:

 A

Different km value

 B

Act on different substrate

 C

Same electrophoretic mobility

 D

All

Q. 2

True about isoenzymes is/are:

 A

Different km value

 B

Act on different substrate

 C

Same electrophoretic mobility

 D

All

Ans. A

Explanation:

  • Isozymes are the physically distinct forms of the same enzymes that catalyze the same reaction, and differ from each other structurally, electrophoretically and immunologically.
  • They differ in their physical properties because of genetically determined difference in amino acid sequence.
  • They are separated by electrophoresis as they have different electrophoretic mobility.
  • They have different Km value.
  • Isoenzyme of an oligomeric enzyme process differ in combination of its peptide protomer.

Q. 3

Which isoenzyme of LDH is seen in heart

 A

LDH 1

 B

LDH 2

 C

LDH 3

 D

LDH 4

Q. 3

Which isoenzyme of LDH is seen in heart

 A

LDH 1

 B

LDH 2

 C

LDH 3

 D

LDH 4

Ans. A

Explanation:

Ans. is ‘a’ i.e., LDH1

Quiz In Between


Q. 4

First enzyme to be raised in MI is ‑

 A

CPK-MB

 B

LDH

 C

Myoglobin

 D

Troponin-I

Q. 4

First enzyme to be raised in MI is ‑

 A

CPK-MB

 B

LDH

 C

Myoglobin

 D

Troponin-I

Ans. C

Explanation:

Ans. is ‘c’ i.e., Myoglobin 


Q. 5

Enzyme specificity is given by ‑

 A

Km

 B

Vrm„

 C

Both

 D

None

Q. 5

Enzyme specificity is given by ‑

 A

Km

 B

Vrm„

 C

Both

 D

None

Ans. A

Explanation:

Ans. is ‘a’ i.e., K. 

  • The Km of an enzyme is the concentration of the substrate that enables the enzyme to function at half maximum activity and is therefore a measure of the specificity of a substrate.for the enzyme” Clinical biochemistry
  • Actually enzyme specificity is not measured by Km alone.
  • It is measured by the ratio Kcat/Km which is a second order rate constant for the reaction between substrate and free enzyme.
  • This ratio is important, for it provides a direct measure of enzyme efficiency and specificity.
  • Note : Kcat is turnover number and measures the rate of the catalytic process.

Q. 6

Q10 in enzyme matches with ‑

 A

2

 B

4

 C

8

 D

10

Q. 6

Q10 in enzyme matches with ‑

 A

2

 B

4

 C

8

 D

10

Ans. A

Explanation:

Ans. is ‘a’ i.e., 2

  • Most enzyme show a 50-300% (average 200%) increase in reaction rate when the temperature is increased by 10°, and the ratio of rate constant at two temperatures 10° apart is usually between 1.5 to 4 (average 2) for most enzymes.
  • This value is termed as Q10.
  • “The rate of enzymatic reaction doubles with every 10° rise in temperature. “

Q. 7

Fastest acting enzyme ‑

 A

LDH

 B

Trypsin

 C

Catalase

 D

None

Q. 7

Fastest acting enzyme ‑

 A

LDH

 B

Trypsin

 C

Catalase

 D

None

Ans. C

Explanation:

Ans. is ‘c’ i.e., Catalase 

Measurement of enzyme activity

  • The activity of enzyme is measured in terms of the following :
  • Unit of enzyme activity : – By international agreement, one unit enzyme activity is defined as the amount causing transformation of 1.0 micro mole of substrate per minute at 25° C. It is usually expressed as mole of substrate disappeared or mole of product formed per minute.
  • Specific activity : – It refers to the number of enzyme units per milligram of protein. It is a measure of enzyme purity; higher the enzyme purity, more is the specific activity.
  • Turn over number : – This refers to the number of substrate molecules transformed per unit time by a single enzyme molecule (or by a single catalytic site), when the enzyme concentration alone is rate-limiting factor. Catalase has the highest turnover number and hence is the fastest active enzyme. Carbonic anydrase has the 2″ fastest turnover number; therefore, it is 2nd fastest active enzyme (after catalase). Lysozyme has the lowest turnover number and therefore is slowest acting.

Quiz In Between



Malcare WordPress Security