Chp 14; Metabolism Of Lipids

Question 1

1. What is triacylglycerol/fatty acid cycle?
2. About _____% of these FFA converted back to TG & Sent back to adipose tissue?
3. What is wolman’s disease?
   Due to deficiency if which enzyme?
4. _______ is the stored fat in the adipose tissue?
5. Which hormone remove fatty acid from triacylglycerol? And from which carbons?
6. What is lipolysis?
7. About 95% of energy obtained from fats comes from the oxidation of?

Answer 1

1. The triacylglycerol/fatty acid cycle is the process by which the body stores, breaks down, uses, and then re-stores fat.
   Process of lipolysis of triglycerides and reesterification of FFA to TG

Storage: Fat is stored in fat cells as triglycerides.

Breakdown: When energy is needed, triglycerides (TG stored in adipose tissue) are broken down into free fatty acids and glycerol.

Utilization: Fatty acids are used by cells for energy.
(Skeletal muscle & cardiac muscle)

Re-storage: After use, fatty acids can be converted back into triglycerides and stored again.

2. 65%
3. 3. Genetic disease characterized by
      Accumulation of lipids (TG,
      Cholestryl esters etc ) in spleen, liver, intestine and adrenal gland
      Due to deficiency of
      Lysosomal acid lipase
4. Triacylglycerols
5. Hormone-sensitive triacylglycerol lipase
   From either
   C 1 or 3
6. Complete degradation of triacylglycerol to
   Glycerol &
   Fatty acids
7. Fatty acids

Question 2

1. Which cells have the limited ability to oxidize fatty acids?
2. Which cells can’t oxidize fatty acids?
3. Lipase is activated by?
4. Effect of Caffein on lipolysis?
5. Why glycerol produced by lipolysis can’t be phosphorylated?
6. Which hormone increase lipolysis? And why?
7. Which hormones decrease lipolysis?

Answer 2

1. Brain (astrocytes)
2. Erythrocytes
   Adrenal medulla
3. Protein kinase (cAMP dependent protein) that phosphorylates it to lipase a
4. Promotes lipolysis
   Inhibits phosphodiesterase activity (normally breaks down cAMP)
   So prevents cAMP breakdown—-protein kinase—-lipolysis
5. Bcz adipose tissue lack glycerol kinase
6. By increasing activity of adenylate cyclase;
   Epinephrine (most imp)
   Norepinephrine
   Glucagon
   Thyroxine
   ACTH
7. Insulin
   Decrease cAMP levels —–inactivates lipase

Question 3

1. Give 2 reasons why fats should be the fuel reserve of the body?
2. Why TG give more energy as compared to carbs & proteins?
3. 1g of glycogen combines with how many g of water for storage?
4. How much energy does 1 g fat stored in the body releases as compared to 1 g of hydrated glycogen?
5. What is arachidonic acid? Its imp?

Answer 3

1. Triacylglycerols yield 9 cal/g
   As compared to carbs & proteins yielding only 4 cal/g

• stored in pure form (without water**

2. Bcz fatty acids in TGs are found in reduced form
   (More H-atoms than C-atoms)
   So can be oxidized more—– more energy
3. 2g
4. Six times
5. An imp lipid
   -Unsaturated fatty acid
   - 4 double bonds
   - 20 carbon atoms
   - formed from linoleic acid
   - and it is used as a substrate for synthesis of eicosonoids;
   Thromboxane(platelet aggregation i.e, thromboxane A2 + vasoconstriction)
   Prostaglandins (inflammation + vasodilation + smooth muscle activity i.e, uterine contraction)
   Prostacyclin
   *Opposite effect of thromboxane**
   (Inhibit platelet aggregation + vasoconstriction + cytoprotection in GIT (dec. Acid secretion & Inc. mucos production))

Question 4

1. The COOH group has a pka around?
2. In which condition ketoacidosis occur?
   Treatment?
3. Name ketogenic & antiketogenic substances?
4. How ketogenesis is regulates by hormones?
5. The appearance of ketone bodies in urine indicate?
6. Conc of ketone body on severe diabetes?
7. Why TCA is impaired in starvation? And it leads to what?

Answer 4

1. 4
   (So will dissociate & give H+ if pH is higher than 4 i.e blood (7.35 - 7.45)
2. In diabetis mellitus
   (Due to insulin deficiency)
   Not in starvation
   - treat by insulin administration
3. Ketogenic
   Fatty acids
   Certain amino acids
   (Leucine
   Lysine
   Tyrosine)

AntiKetogenic
Glucose
Glycerol
Glucogenic amino acids
(Alanine
Glysine
Glutamate
Serine)

4. Glucagon— promotes
   Insulin —- inhibits
5. Active fat metabolism
6. 100mg/dl—–blood plasma
   500mg/day—–urinary excretion
7. Bcz if no glucose —
   Oxaloacetate is diverted for glucose synthesis

So no TCA cycle
So acetyl coA can’t be utilized
—-accumulates—-ketone bodies

Question 5

1. What is hypermesis? Leads to what?
2. Conc of ketone bodies in blood?
3. Ketones in urine are tested by which test?
4. What is ketonemia?
5. What is ketonuria?
6. What is ketosis?
7. Smell of _______ in breath is a common feature of ketosis?

Answer 5

1. Hyperemesis, more specifically known as hyperemesis gravidarum, is a condition characterized by severe and persistent nausea and vomiting during pregnancy. This can lead to dehydration, weight loss, and electrolyte imbalances. It is more extreme than typical morning sickness and often requires medical treatment to manage the symptoms and ensure the health of both the mother and the baby.

Leads to starvation——-ketosis

2. 1 mg/dl
3. Rothera’s test
4. More synthesis of ketones than utilization
5. Excretion of ketone bodies in urine
6. Ketosis is a metabolic state in which the body uses fat as its primary source of energy instead of carbohydrates. This occurs when carbohydrate intake is low, causing the liver to convert fatty acids into ketones, which are then used as an alternative fuel by the brain and other tissues. Ketosis can be induced by fasting, prolonged exercise, or following a ketogenic diet that is high in fat and low in carbohydrates. While ketosis is a normal physiological process, it differs from ketoacidosis, which is a dangerous and excessive accumulation of ketones, often associated with uncontrolled diabetes.
7. Acetone
   (Is volatile so not used by body instead excreted by lungs —breath
   & In urine

Question 6

1. In starvation the fuel source for brain? & Meet how much % of brain energy needs?
2. Which tissues can’t utilize ketone bodies?
3. Which amino acids can generate ketone bodies?
4. Which ketone body is most predominant, quantitatively?
5. Name ketone bodies?
6. Which are true ketone bodies & why?
7. Which is volatile & excreted by?

Answer 6

1. Ketone bodies (50-70% of brain’s energy needs)
2. Eryhthrocytes—- lack mitochondria
   Liver—lack thiophorase
3. Leucine
   Lysine
   Phenylalanine
4. B-hydroxybutyrate
5. Acetone
   Acetoacetate
   B-hydroxybutyrate
6. Only
   Acetone
   Acetoacetate
   Bcz B-hydroxybutyrate has no keto (C=O) group
7. Acetone
   (By lungs)

Question 7

1. Ketogenesis occurs in ?
2. Precursor of ketone bodies?
3. How acetoacetate can form acetone?
4. Mnemonic for ketogenesis?
5. How ketone bodies are utilized?
   Acetoacetate is activated to acetoacetyl coA by?
   And it is absent in?
   And this coA is donated by?
6. Acetoacetyl coA is cleaved into 2 acetyl coAs by?
7. Ketone bodies synthesis is regulated by which enzyme?

Answer 7

1. Liver (mitochondiral matrix)
2. Acetyl coA
   (From;
   Fatty acids oxidation
   Pyruvate
   Aminoacid)
3. By spontaneous decarboxylation

4.
A A A Humming bird ate Apple Bnana

5. Reversal of synthesis
   -Thiophorase
   -absent in liver
   -succinyl coA
6. Thiolase
7. HMG coA synthase
   (cholestrtol—-HMG coA reductase)

Question 8

1. Where does biosynthesis of fatty acids occur? Also called?
2. Where does it occur? Enzyme machinery located?
3. Building block of fatty acids?
4. Name the 3 stages of fatty acid synthesis?
5. Sources of acetyl coA?
6. Acetyl coA is only permeable thru mitochondria when?
7. In cytosol, oxaloacetate is converted to?
8. What is the main source of NADPH for biosynthesis of fatty acids? What’s the other?

Answer 8

1. In liver
   Kidney
   Adipose tissue
   Lactating mammary glands
   - de novo synthesis
2. Cytosol of cell
3. Acetyl coA
4. Production of Acetyl coA & NADPH
   Conversion of Acetyl coA to malonyl coA
   Reaction of fatty acid synthase complex
5. Produced in mitochondria by
   Fatty acids oxidation
   Pyruvate oxidation
   Certain amino acids degradation
   Ketone bodies
6. In form of citrate
   When binds with oxaloacetate to form citrate
7. Malate by malate dehydrogenase
   Malate—-pyruvate by
   Malic enzyme
8. HMP shunt (pentose phosphate pathway)
   - when malic enzyme converts malate to pyruvate

Question 9

1. How acetyl coA is converted to malonyl coA?
   By which enzyme?
   Requires?
2. Which enzyme regulates fatty acid synthesis?
3. Fatty acid synthase complex (FAS) structure?
4. ACP in FAS is bound to?
5. How FAS of prokaryotes differs from eukaryotes?
6. In FAS rxn each time, fatty acid chain is lengthened by a _____ carbon unit obtained from?
7. Which enzyme separates palmitate from fatty acid synthase?

Answer 9

1. Carboxylated
   -acetyl coA carboxylase
   - ATP, biotin, CO2
2. -acetyl coA carboxylase
3. A dimer
   - 7 different enzymes
   - Acyl carrier protein
   (Bound to 4’ - phosphopanthethien)
4. 4’ - phosphopanthethine
5. In prokaryotes ÀCP is not a part of FAS complex but is separate unlike Eukaryotes
6. 2 carbon unit
   From malonyl coA
7. Palmitoyl thioesterase

Question 10

1. Of 16 carbons of palmitate how many are from acetyl coA and malonyl coA?
2. In which forms, acetyl coA is activated and de activated?
3. Effect of citrate and succinyl coA & palmitoyl coA on fatty acid synthesis?
4. Which hormone promotes fatty acid synthesis?

5.Which hormone inhibits fatty acid synthesis?

Answer 10

1. Acetyl coA—–2
   Malonyl coA—–14
2. Activated
   Polymer (citrate)
   Dephosphorylated

Inctivated
Monomer (succinyl coA, palmitoyl coA)
phosphorylated

3.
Citrate—- promotes (bcz activates acetyl coA carboxylase)
Succinyl coA & palmitoyl coA—- inhibit (bcz deactivates acetyl coA carboxylase)

4. insulin
   Dephosphorylates & activates acetyl coA carboxylase
5. Glucagon, epinephrine, norepinephrine
   phosphorylates & deactivates acetyl coA carboxylase

Question 11

1. For desaturation kf fatty acid chains, which enzyme is used?
   Other involves?
2. Monounsaturated fatty acids,
   Are made;
   Oleic acid from?
   Palmitoleic acid from?
3. No of carbon atoms & double bonds in linoleic and linolenic acids and arachidonic acids?
4. What is the end product of rxns of fatty acid synthase in cytosol?
5. Difference between microsomal (ER) Chain elongation & mitochondrial?
6. Which chain elongation is almost reversal of B-oxidation of fatty acids?

Answer 11

1. Microsomal enzyme system
   Fatty acyl coA desaturase
   - flavin dependant cytochrome b5 reductase
   - NADH
   - Molecular O2
2. Oleic acid (9-10) —–stearic acid
   Palmitoleic acid —palmitate
3. Both have 18 carbons
   Linoleic
   2 double bonds (at 9 & 12)

Linolenic
3 double bonds (at 9, 12, 15)

Arachidonic
4 double bonds (at 5,8,11,14)

4. Palmitate
5. Difference in addition of coA;
   Mitochondrial—acetyl coA
   Microsomal—malonyl coA
6. Mitochondrial

Question 12

1. Almost all cells except ______ can synthesize phospholipids?
2. Synthesis of phospholpids occurs in?
3. What is ceramide?
4. Precursor of all phospholipids is? Simplest form?
5. Another name for;
   Lecithin
   Cephalin
6. Surfactant is composed of?
   If deficient leads to?
7. The only phospholipid responsible for antigenic properties?

Answer 12

1. RBC
2. Smooth endoplasmic reticulum
3. Sphingosine + fatty acid
4. Phosphatidic acid
5. Lecithin—-phosphatidylcholine
   Cephalin—-phosphatidylethanolamine
6. Dipalmitoyl lecithin
   Deficincy—-respiratory distress syndrome
7. Cardiolipin

Question 13

1. How plasmalogens differ from other phospholipids?
   Give an example
2. Sphingomyelin is produced when?
3. Which 2 specie unsergoe sequence of rxn to produce sphingosine
4. Type of linkage in sphinginyelins?
5. Cardiolipin is formed by combination of?

Answer 13

1. Ether linkage instead of ester
   E.g
   Platelet activating factor
   (1-alkenyl 2-acetyl glycerol 3-phodphocholine)
2. Ceramide + CDP-choline
3. palmitoyl coA + serine
4. Amide linkage
5. Phosphatidyl glycerol +
   Phosphatidyl glycerol

Question 14

1. Why phospholipid synthesis starting with choline & ethanol amine is regarded as salvage pathway?
2. Phosphatidyl enthanolamine can be converted to phosphatidyl choline on?
3. Phosphatidyl serine is produced by exchanging serine with?
   And what happens when it is decarboxylated?
4. Which phospholipid cpntains arachidonic acid and on which carbon?
5. Importance of phosphatidyl inositol?

Answer 14

1. Bcz both are mostly derived from prexisting phospholipids
2. Methylation
3. Ethanolamine of phosphatidyl ethanolamine
   - phosphatidyl serine on decarboxylation phosphatidylethanol amine
4. Phosphatidylinositol
   On carbon 2 of glycerol
5. Signal transmission across memebranes

Question 15

1. Phospholipids are degraded by? By breaking which bond?
2. Sources of phospholipase A2?
3. Which phospholipase cleaves and removes nitrogenous bases?
4. Role of phospholipase C?
   Found in?
5. Which phospholipase acts on phosphotidyl inositol to liberate archidonic acid?

Answer 15

1. Phospholipases
   -phosphodiester bond
2. Snake venom
   Bee venom
   Pancreatic juice
3. Phospholipase D
4. Cleaves phosphate & glycerol bond
   -lysosomes of hepatocytes
5. Phospholipase A2

Question 16

1. What is LCAT?
   Function
   Synthesized in?
   Its activity is associated with?
2. LCAT transfers acyl group from?
3. Which enzyme degrades sphingomyelins & to what?
4. What is Niemman-Pick disease?
   Due to deficiency of?
   Symptoms?
5. What is Farber’s disease?
   Due to deficiency of?
   Symptoms?

Answer 16

1. Lecithin cholesterol acyl transferase is a plasma enzyme
   - helps to remove cholesterol
   - esterifies cholesterol on HDL
   - in liver
   - with Apo 1 of HDL
2. 2nd position of lecithin to cholesterol
3. Sphingomyelinase
   -to ceramide & phophorylcholine
4. Accumulation of sphingomyelins in liver & spleen (enlarged)
   - deficiency of sphingomyelinase
   - symptoms;
   Mental retardation
   Enlarged liver & spleen
5. Ceramide accumulates
   - deficiency of ceramidase
   - skeletal deformation
   - subcutaneous nodules
   - dermatitis

Question 17

1. Glycolipids are also called?
   They are derivative of?
2. Simplest form of glycosphingolipids is?
3. What are the types of glycosphingolipids?
4. Cerebrosides has what 2 compounds?
5. Where is galactocerebroside found?
6. What is Gaucher’s disease?
   Due to defect in?
   What accumulates?
   Symptoms?

Answer 17

1. Glycosphingolipids
   - ceramide (fatty acid + sphingosine)
2. Cerebrosides
3. Cerebrosides
   -glucocerebroside
   -galactocerebroside
   Gangliosides
4. Ceramide bound to monosaccharide
5. In nervous tissue (high in myelin sheath
6. A metabolic disorder of cerebrosides
   Due to defect in B-glucosidase
   -glucocerebroside
   - symptoms;
   Glu—glucoscerebroside accumulates
   Has—-hepatospleenomegaly
   An—-Anemia
   Ost—-osteoporosis
   Pig—-pigmented skin
   Men—mental retardation

Question 18

1. What is krabbe’s disease
   Due to defect of?
   Accumulation of
   Main symptom?
2. Gangliosides are found in?
   Contain?
3. Defect in ganglioside degradation causes?
4. What is Tay-sach disease?
   Due to defect of?
   Accumulation of?
   Leads to
5. Defect in a-galactosidase causes?
   nd leads to accumulation of?

3.

Answer 18

1. Metabolic disorder of cerebrosides
   - B-galactosidase
   -galcatocerebroside
   -total absence of myelin in nervous tissue
2. Ganglion cells
   - N-acetylneuraminic acid (NANA) bound to ceramide + oligosaccharide
3. Tay-sach disease
4. Genetic disorder
   Sphingolipidoses (lipid storage disease)
   Due to lysosomal storage defect
   Affects nervous tissue
   - defect of hexosamine A
   - Ganglioside GM2
   -blindness, mental retardation
5. Fabry’s disease
   -Ceramide trihexoside

Question 19

1. Cholesterol is _____ in nature?
2. Used for synthesis of vitamin?
   And what other?
3. Formula?
4. Double bond betw?
5. -Oh attached to carbon?
6. Methyl attached to?
7. Hydrocarbon chain at?
8. Contains what ring?

Answer 19

1. Amphiphatic
2. Vitamin D
   Steroid hormones
   Bile acids
3. C27 H46 O
4. Carbon 5 & 6
5. 3
6. Carbon 10, & 13
7. At C 17
8. Cyclopentanoperhydrophenanthrene (CPPP) ring

Question 20

1. How much cholesterol synthesised per day by adults?
2. Contribution of organs in cholesterol synthesis?
3. Where are the enzyme of cholesterol synthesis found?
   Cholesterol synthesis occurs in which part of cell?
   & Ketone body synthesis in?
4. All carbons of cholesterol are provided by?
5. For 1 mole of cholesterol how much;
   Acetyl coA
   ATP
   NADPH

Answer 20

1. 1g
2. Liver (20%)
   Intestine (18%)
   Skin
   Adrenal cortex
   Reproductive tissue
3. Cytosol
   Microsomal fractions of cell
   -Cholesterol–cytosol
   -ketone body–mitochondria
4. Acetate of acetyl coA
5. Acetyl coA—18
   ATP—-36
   NADPH—-16

Question 21

1. Rate limiting enzyme in cholesterol synthesis?
   Found in?
2. How many isoenzymes of HMG CoA?
   How do they differ in Synthesis?
3. Name 2 isoprenoid units having 5 carbons in cholesterol syntheis?

4.
Name the 5 stages of cholesterol synthesis?

Answer 21

1. HMG coA reductase
   In ER
2. 2
   Cytosomal coA—-Cholesterol
   Mitochondrial coA—-ketone bodies
3. Isopentenyl pyrophosphate (IPP)
   Dimethylallyl pyrophosphate (DPP)
4. 1.Synthesis of HMG coA (6C)
5. Formation of mevalonate (6C)
6. Formation of isoprenoid units (5C)
7. Synthesis of squalene (30C)
8. Conversion of squalene to cholesterol (27C)

Question 22

1. In cholesterol synthesis, the penultimate product is______ which is converted to choleterol?
2. How many enzymatic rxn till lanosterol forms cholesteol?
   Name imp?
3. A 10C compound formed in cholesterol synthesis is?
4. A 15C compound formed in cholesterol synthesis is?
5. Functions of farnesyl pyrophosphate beside cholesterol synthesis?
6. A 30 C compound in cholesterol synthesis?

Answer 22

1. 7-dehydrocholesterol
2. 19
   Carbon atoms (30 to 27)
   Shifting = from C8 to C5
   Removing = btw C24 & C25
   Removing 2 -CH3 from C4 & C14
3. Geranyl pyrophosphate
4. Farnesyl pyrophosphate
5. 1.Formation of ubiquinone(coenzyme Q in ETC)
   Formation of dolichol
   (For glycosylation of proteins)
   Prenylation of proteins
   (Adding lipids such as farnesyl pyrophosphate to proteins to attach them to membranes)
6. Squalene

Question 23

1. Hormonal regulation of cholesterol synthesis?
2. During fasting cholesterol synthesis?
3. Name the drugs for cholesterol inhibition?
   What type of inhibitors?

Answer 23

1. Glucagon decreases synthesis
   (Phosphorylates HMG coA reductase (inactivates))
   Insulin & thyroxine increases synthesis
   (Dehosphorylates HMG coA reductase (activates))
2. Decreases bcz insulin low & glucagon high
3. Lovastatin (mevinolin)
   Comactin
   (Both fungal products)
   - competitive inhibitors of HMG coA reductase

Question 24

1. Bile acid has _____ carbon atoms?
2. How many hydroxyl groups?
3. Bile acid synthesis occurs in the?
4. Rate limiting step in bile acid synthesis?
5. Name primary bile acids? And on conjugation produce? Function as?
6. What are bile acids?
7. Where are the secondary bile acids formed?
   How?
   Name them?

Answer 24

1. 24
2. 2 or 3
3. Liver
4. 7-a-hydroxylase
5. Cholic acid &
   Chenodeoxycholic acid
   - with glycin — glycocholic acid
   - with taurine — taurocholic acid
   - surfactants
6. In bile, conjugated bile acids exist as sodium & potassium salts called bile salts
7. In intestine by bacteria
   Dehydroxylation & deconjugation
   -deoxycholic acid
   - lithocholic acid

Question 25

1. What is enterohepatic circulation? 2.Which vein returns bilesalts to liver? 3. How much bile salts secreted into intestine? 4. How much bile salts are synthesized in liver? How much is lost in feces? 5. What is the only way to remove cholesterol from the body? 6. What is cholelithiasis? Patient respond to which bile acid?

Answer 25

1. **Enterohepatic circulation** is the recycling process of bile salts. Here’s how it works: 1. **Release:** Bile salts are released from the liver into the small intestine to help digest fats. 2. **Reabsorption:** After their job is done, most of the bile salts are absorbed back into the blood from the intestine. 3. **Return to Liver:** They travel through the blood back to the liver, where they are reused to make new bile. In simple terms, enterohepatic circulation is like a **recycling system** that allows the body to reuse bile salts efficiently. 2. Portal vein 3. 15-30 g 4. 0.5 g/day (same is lost) 5. **Fecal excretion of bile salts** 6. When **gall stones** form in gall bladder - cholesterol crystals precipitate - due to deficiency of **bile salts** - to acid **chenodeoxy cholic acid (chenodiol)** (dissolution of gallstones occur)

Question 26

1. Vitamin D is synthesized by cholesterol when? 2. How much of cholesterol is esterified and how much is free? 3. What are the 5 classes of steroid hormones synthesized by cholesterol?

Answer 26

1. **7-dehydroxycholesterol** is converted to **Cholicalciferol** (vitamin D3) By UV rays in skin 2. **70-75%** esterified **25-30%** free 3. **Glucocorticoids**(cortisol) **Mineralocorticoids**(aldosterone) **Progestins**(progesterone) **Androgens**(testosterone) **Estrogens**(estradiol)

Question 27

1. Plasma cholesterol in adults Newborn 2. Why women have lower plasm cholesterol? 3. Total cholesterol can be measured by which method? 4. HDL cholesterol can be determined by? 5. VLDL is equivalent to _____ of TG? 6. LDL cholesterol can be calculated by? 7. In adults, normal LDL cholesterol and HDL cholesterol?

Answer 27

1. Adults----Range from **150-200 mg /dl** Newborn--**less than 100mg/dl** 2. Due to **estrogens** 3. Libermann-Burchard Carr & Dructor Cholesterol Oxidase 4. By precipitating LDL & VLDL with **polythylene glycol** 5. 1/5 6. **Friedwald formula** **LDL cholesterol = Total cholesterol - (HDL cholesterol + TG/5)** 7. LDL: **<100 mg /dl** HDL: **40 - 60 mg /dl**

Question 28

1. Hypercholesterolemia is increase in plasma cholesterol than? 2. Most dangerous fraction of LDL? 3. Effect of PUFA on cholesterol? Rich sources of PUFA? 4. Advised dietry intake of cholesterol? 5. Drug that inhibit intestinal cholesterol absorption? 6. Name the plant sterols with with esters that reduce plasma cholesterol? 7. How red wine is beneficial for lowering cholesterol? 8. Name the drugs that decrease intestinal absorption of bile salts? 9. Which drug increases the activity of lipoprotein lipase & lower the plasma cholesterol?

Answer 28

1. **>200 mg/dl** 2. Small dense LDL (sdLDL) 3. Lowers plasma cholesterol (Aiding transport & excretion by LCAT) **Rich sources** Cotton seed oil Soya bean oil Sunflower oil Corn oil Fish oil **Poor sources** Ghee Coconut oil 4.<300 mg/day 5. **Ezetimibe** 6. **Sitostanol esters** 7. Due to its **antioxidants** 8. **Cholestyramine** **Cholestypole** 9. **Clofibrate**

Question 29

1. Name the comlounds that decrease the formation of VLDL containing TG & cholesterol, by liver? 2. Name some statin drugs that inhibit HMG coA reductase? 3. Why statin are taken at night? 4. Nephrotic syndrome characterized by? & How does it affect cholesterol? 3. Diabetes mellitus occurs in which level of cholesterol? 4. Which of the following are associated with hypercholesterolemia & hypocholesterolemia; Hyperthyroidism Hypothyroidism Obstructive jaundice Hemolytic jaundice Diabetes mellitus Pernicious anemia Nephrotic syndrome Malabsorptive syndrome Atheroscelrosis Coronory heart disease

Answer 29

1. **Nictotinic acid** **Gemfibrozil** 2. Lovastatin Atrovastatin Simvastatin Fluvastatin Pravastatin 3. To ensure maximum activity (HMG coA activity is maximum abt 6 hrs after dark) 4. Increase in **plasma globulin**-----increase in **plasma lipoproteins**----increase in cholesterol 3. Hypercholesterolemia (More acetyl coA) 4 Hyperthyroidism---- hypocholesterolemia Hypothyroidism---- hypercholesterolemia Obstructive jaundice---- hypercholesterolemia Hemolytic jaundice---- hypocholesterolemia Diabetes mellitus---- hypercholesterolemia Pernicious anemia---- hypocholesterolemia Nephrotic syndrome---- hypercholesterolemia Malabsorptive syndrome---- hypocholesterolemia Atheroscelrosis---- hypercholesterolemia Coronory heart disease---- hypercholesterolemia

Question 30

1. Function of lipoprotein? 2. 5 classes of lipoprotein? 3. Free fatty acids in circulation are bound to? How many? 4. Which class of lipoprotein is not separated by electrophoresis? 5. Lipoprotein with least density and largest size? 6. Apolipoproteins? 7. Chylomicrons are synthesized in? And contain protein & lipid?

Answer 30

1. Transport lipid, cholesterol, triacylglycerols 2. Chylomicrons VLDL LDL HDL Free fatty acids---albumin 3. Albumin **20-30** to each albumin 4. Free fatty acids---albumin 5. Chylomicrons 6. Protein component of lipoprotein 7. Intestine Lipid ---99% Protein----1%

Question 31

1. chylomicrons contain apoprotein? 2. Nacent chylomicron & VLDL are converted to chylomicron & VLDL ehen? 3. Lipoprotein lipase is present in? Activated by? Function? 4. What is lipoprotein cascade pathway? 5. LDL binds to specific receptor pits which are stabilized by? 6. Which protein is responsible for recognition of LDL receptor sites? 7. Deficiency of LDL receptors lead to what condition?

Answer 31

1. **B48** (48% of protein is coded by apo B gene) 2. Combine with **Apo C II Apo E** Derived from HDL 3. Capillary wall of Adipose tissue Cardiac muscle Skeletal muscl -by **apo CII** - degrade triacylglycerol portion of chylomicrons & VLDL 4. Conversion of VLDL----IDL----LDL 5. **Clathrin** protein 6. **Apo B100** 7. **Type IIa hyperbetalipoproteinemia** ---high LDL-----high cholesterol----atherosclerosis

Question 32

1. Better predictor of cardiovascular disease is? 2. What is frieldwald equation used for? Becomes inaccurate when? 3. How non-HDL C is estimated? 4. How HDL plays an antioxidant role? 5. HDL with cholesterol enters hepatocytes with which transport? 6. HDL is synthesized in? And contains? 7. How to lower Non-HDL-C?

Answer 32

1. Non-HDL cholesterol (all other than HDL that is carried by VDL, LDL, IDL) 2. To detect LDL cholesterol in blood - When concentration of TG **exceeds 400 mg/dl** 3. Non HDL-C= Total cholesterol - HDL C 4. Due to enzyme **paroxanase** activity - protects LDL from getting oxidized 5. Receptor-mediated 6. Liver & intestine -free cholesterol -phospholipids (lecithin) -apoproteins (AI, AII, E, CII) 7. Reduction in consumption of; **Saturated & trans fatty acids & sugar** - food with high **w-3-fatty acids** are beneficial

Question 33

1. What is hyperlipoprotenemia? Also called? 2. hyperlipoprotenemia deficiency is due to what in; Type I Type II b Type IV 3. What is hyperbetalipoprotenemi? Due to? 4. What is broad beta disease? Due to? 5. In type V hyperlipoprotenemia, There's accumulation of? 6. What are the secondary types of hyperlipoprotenemia?

Answer 33

1. **Hyperlipoproteinemia** is a condition characterized by **elevated levels of lipoproteins (cholesterol and/or triglycerides)** in the blood. - **hyperlipidemias - dislipidemias** 2. Type I ---- **lipoprotein lipase** deficiency Type IIb ---- overproduction of **apo B** (accumulation of VLDL & LDL & cholesterol) Type IV ---- overproduction of **endogenous triacylglycerols** (rise in VLDL) 3. A **type IIa** hyperbetalipoprotenemia - defect in **LDL receptor** 4. **Type III** hyperlipoprotenemia - broad B band due to **intermediate density lipoprotein (IDL)** 5. Chylomicrons & VLDL 6. (That are due to other diseases) Type IIa Type IV Type V

Question 34

1. Fatty liver is due to? 2 main causes? 2. How alcohol leads to fatty liver? 3. VLDL formation requires what? 4. Deficiency of essential fatty acids will affects phospholipid as? 5. Name some chemicals that inhibit protein synthesis and cause fatty liver? Which protein do they block? 6. How Ethionine cause fatty liver? 7. Deficiency of which vitamin cause fatty liver? - what is a protective agent in such condition? 8. Non-alcoholic fatty liver disease (NAFLD) is caused by?

Answer 34

1.. Accumulation of **triacylglycerol (TAG)** (Doplets found in entire cytoplasm of liver) 2 main causes: **increased synthesis of TAGs Impairment in protein synthesis** 2. Inhibits fatty acids oxidation - promotes fat synthesis and deposition - (impair citric acid cycle---- acetyl coA accumulates--- FA synthesis) 3. Phospholipid & **apoprotein B** 4. Decreased synthesis 5. Puromycin Ethionine CCl4 Chloroform Lead Phosphorus - block **apoprotein B** synthesis 6. **Reduce availability of ATP** (for lipoprotein synthesis and release) - competes with **methionine** and traps ATP 7. Vitamin **E** - **Selenium** 8. Uncontrolled diabetes High fat diet

Question 35

1. What are lipotropic factors? Give examples of imp? Which of them are component of phospholipids? 2. What is Kwashiorkor? Leads to? Due to? 3. Non availability of which groups lead to fatty liver? 4. Most common affected arteries of atherosclerosis? 5. Which protein is identical to LDL and can cause coronary heart disease? How? And At what level suggest CHD? 6. Role of antioxidants in CHD? Give eg?

Answer 35

1. The mobilize fat from liver (prevent fatty liver) IMP are: **choline Betaine Methionine Inositol** Folic acid Vitamin B12 Glycine Serine - choline & Inositol (phospholipid) 2. Severe protein deficiency - fatty liver _ due to defect in synthesis of **Choline** (insufficient methionine (found in protein)) 3. **methyl groups** 4. Coronary arteries (---- Myocardial infarction) 5. **lipoprotein a** - inhibits fibrinolysis ( interefers with plasmjnogen activation---- intravascular thrombosis) - **> 30** - - - CHD 6. reduces CHD - decrease oxidation of **LDL** **Vitamin E, Vitamin C B-carotene**

Question 36

1. Alcohol is Oxidized in? To what? By? 2. Acetaldehyde to acid by? Inhibited by which drug for alcoholism? 3. What compound is responsible for manifestation of alcohol (harmful affects)? 4. What is MEOS? 5. What are barbiturates? Alternate? 5. What happens to uric acid in alcholism? 6. Alcoholic are more prone to what deficiencies? 8. What is wernicke-korsakoff syndrome?

Answer 36

1. In liver - to acetaldehyde - ADH--- alcohol dehydrogenase 2. Aldehyde dehydrogenase ( but less activity than Alc. Dehydrogenase) - **Disulfiram** 3. Acetaldehyde 4. **Microsomal Ethanol Oxidizing System** (family of cytochrome P450) - metabolize alcohols & barbiturate drugs 5. Depress CNS ( increase GABA effect Decrease brain activity) - anaesthesis - induce sleep - control seizures - alternate : **benzodiazepines** 5. Increased (inc. Purine metabolism - - - - - Inc. Uric acid) - reduced excretion 6. Vitamin deficiency B1 B6 C 8. In alcohics - due to **Thiamine (B1) deficiency** - Beri beri - **memory loss** - coordination defect

Question 37

1. Which vitamin boost HDL and lower LDL cholesterol 2. Cholelithiasis (gallstones) is due to? 3. Which apoprotein promotes the activity of LCAT? 4. What are hypolipoproteinemias? Name?

Answer 37

1. **Niacin** (vitamin B3) 2.. Defective absorption of **bile salts** from intestine Or biliary tract obstruction 3. **Apoprotein A** 4. Familial **hypo**-B-lipoproteinemia - impaired **apoprotein B** - **low** levels of LDL (B-lipoprotein) **A**betalipoproteinemia - - impaired **apoprotein B** - **total absence** of LDL (B-lipoprotein) Familial **alpha-lipoprotein** deficiency **(Tangier disease)** - **absent HDL** (alpha-lipoprotein) - accumulation of cholestryl esters - **absent apoprotein C II** (which activates lipoprotein Lipase)