Biochem II Exam 1 Flashcards by Charles L

What is the common property of lipids? Why is the term amphipathic used to describe lipids? Why is this property important in the behavior of lipids in aqueous media?

What is the common property of lipids? Why is the term amphipathic used to describe lipids? Why is this property important in the behavior of lipids in aqueous media?

Lipids are hydrophobic, and their amphipathic property causes lipids to form into globules (micelle).

Properties (of fatty acids)

Amphipathic - have both polar and non polar properties.
melting points, solubility related to chain length and degree of saturation. (eg increasing melting point w/ increasing length, decreasing solubility as hydrophobic character dominates)
Unsaturated chains are especially sensitive to oxidation

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Identify the major classes of lipids and the kind of structure or activity in which each class is important.

Identify the major classes of lipids and the kind of structure or activity in which each class is important.

Fatty acids - store energy, get attached to the glycerol backbone, and are included in lipids used to build cell membranes. Water insoluble

glycerides - are esters formed from glycerol and fatty acids

Sphingolipids>>>They also make membranes (sphingosine backbone)

Ketone bodies: water soluble – understood as fatty acid breakdown products.

Cholesterol: used to build cell membranes.

steroids: signaling molecules as hormones. Cholesterol is precursor.

Eicosanoids - also used as signaling molecules derived from lipid precursors.

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Provide a general definition of a fatty acid. What is meant by a saturated fatty acid? Define unsaturated and polyunsaturated fatty acids? What is the configuration of the double bond in most naturally occurring unsaturated fatty acids?

Provide a general definition of a fatty acid. What is meant by a saturated fatty acid? Define unsaturated and polyunsaturated fatty acids? What is the configuration of the double bond in most naturally occurring unsaturated fatty acids?

Polyunsaturated fats are lipids in which the constituent hydrocarbon chain possesses two or more carbon–carbon double bonds. Polyunsaturated fat can be found mostly in nuts, seeds, fish, algae, leafy greens, and krill.

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What is the relationship of fatty acid chain length to membrane fluidity and to melting point? What is the relationship of the degree of fatty acid unsaturation to membrane fluidity and to melting point?

What is the relationship of fatty acid chain length to membrane fluidity and to melting point? What is the relationship of the degree of fatty acid unsaturation to membrane fluidity and to melting point?

Increased fluidity - increased pour-ability!

If we increase the chain length for saturated fatty acids, this will reduce fluidity (more packing). If we increase the chain length for UNsaturated fatty acids, this will increase fluidity (less packing).

Increasing FA chain length, INCREASING melting point.

Decreasing solubility as hydrophobic character dominates.

Closer packing w/ trans double bonds than cis double bonds. Also, with double bonds, the FAs are further apart, and more likely to
melt!

Lipids with shorter chains are less stiff and less viscous because they are more susceptible to changes in kinetic energy due to their smaller molecular size and they have less surface area to undergo stabilizing van der Waals interactions with neighboring hydrophobic chains. Lipid chains with double bonds are more fluid than lipids that are saturated with hydrogen and thus have only single bonds

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Be able to identify and name fatty acids based on delta and omega naming conventions.

Be able to identify and name fatty acids based on delta and omega naming conventions.

non-conjugated - 2 double bonds separated by more than one single bond.

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Compare the saturated and unsaturated content of human adipose tissue.

Compare the saturated and unsaturated content of human adipose tissue.

Most E store is in FA chains. Small amt. of carb stores is glycogen (mostly liver and muscle) and glucose (body fluids).Fraction of proteins can be used for E!

Most is palmitic acid (16:0) for saturated, and oleic acid (18:1) for unsaturated!

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Name the essential fatty acids? Why are they essential?

Name the essential fatty acids? Why are they essential?

The body can synthesize most of the fats it needs from the diet. However, two essential fatty acids, linolenic and linoleic acid, cannot be synthesized in the body and must be obtained from food. These basic fats, found in plant foods, are used to build specialized fats called omega-3 and omega-6 fatty acids.

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Is there a difference between triacylglycerols and triglycerides?

Is there a difference between triacylglycerols and triglycerides?

NO!

Triglyceride (triacylglycerol, TAG or triacylglyceride) is an ester composed of a glycerol bound to three fatty acids. It is the main constituent of vegetable oil and animal fats.

A. Fatty acids are stored in adipose tissue as Triglycerides (tracylglycerols)

glycerides are esters of glycerol and FAs
triglycerides are less dense than water
are a concentrated form of E
do not cause osmotic problems in the body

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Fatty Acid Synthesis

What does the acetyl-CoA shuttle accomplish? What is the carrier of free fatty acids (FFA) in the general circulation?

Fatty Acid Synthesis

What does the acetyl-CoA shuttle accomplish? What is the carrier of free fatty acids (FFA) in the general circulation?

Fatty Acid synthesis is the polymerization of mitochondrial acetyl CoA
2. Requires NADPH from the pentose pathway; “malic enzyme”

ATP is required

4. the acetyle CoA shuttle transports 2-carbon units as citrate out of the mitochondria

Ablumin is the carrier of FFA in the general circulation

Picture: Fatty Acid Synthesis

OAA - begins gluconeogenesis. Also, this is an anaplerotic reaction, and allows us to increase the amt. of OAA, reversing what we did in the matrix and increasing intermediates for Kreb’s cycle.

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Outline the steps of fatty acid biosynthesis. Where does this process occur in the cell? What is the most important organ for fatty acid biosynthesis? Why do most naturally occurring fatty acids have an even number of carbons?

Outline the steps of fatty acid biosynthesis. Where does this process occur in the cell? What is the most important organ for fatty acid biosynthesis? Why do most naturally occurring fatty acids have an even number of carbons?

FA synthesis occurs mainly in the LIVER (but also mammary glands and adipose tissue).

In the cell, FA synthesis occurs in the CYTOSOL!

FA Synthesis occurs mainly in cytosol of the liver cells but also in fat cells. The cytosol also contains the necessary acetyl CoA, malonyl CoA, and reducting agent (NADPH). But the elongation of fatty acids would occur in the smooth ER.
8 acetyl CoA + 7 ATP + 14 NADPH + 14 H+ >> Palmitate + 7 ATP + 7 P + 8 CoASH + 14 NADPH

Requires BIOTIN! Uses citrate as a carbon donor. Series of carboxylation, condensation, reduction, dehydration, reduction.
Extra notes:
Beta oxidation occurs mainly in the mitochondria of the liver and muscle. Having the synthesis and degradation in two different places of the cell adds a layer of regulation. Malonyl CoA shuts down beta oxidation transport from the mitochondria inner membrane.

Fatty acids are made from glucose, 2. preferred fueld of heart, 3 stored in adipose tissue, 4. major site of synthesis is the liver, 5. enzymes are in the cytosol

Why do most naturally occurring fatty acids have an even number of carbons?

Fatty acids are generally made using a complex called fatty acid synthase. This complex grabs a 3 carbon molecule in the first step (Malonyl-CoA) and adds to it a 2 carbon molecule (Acetyl-CoA). In this ajoinment, one carbon is lost as carbon dioxide, leaving a four carbon unit at the end of the first round. The fatty acid continues to grow by adding additional Malonyl-CoA molecules, sacrificing one carbon to join with the parent chain in each round. Therefore, the chain grows by two carbon units, giving us the plethora of even numbered fatty acids. Additional reactions are required to add odd numbered units to the chain, so the path of least resistance generates more even numbered chains than odd numbered chains in nature. When fatty acids are broken down by B-oxidation (most common), the chain degrades two carbons at a time.

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What vitamin-derivatives are required for fatty acid synthesis? What is the role of biotin in fatty acid synthesis? What is the energy input required for each cycle of fatty acid biosynthesis?

What vitamin-derivatives are required for fatty acid synthesis? What is the role of biotin in fatty acid synthesis? What is the energy input required for each cycle of fatty acid biosynthesis?

Requires: Biotin (B7). This is required in Acetyl CoA carboxylase.

B5 - pantothenic acid - ACP (acetyl cysteinyl group) - required to activate acetyl CoA >> Acetyl-ACP for FA synthesis

ATP: The activation of Acetyl CoA>>Malonyl CoA requires 1 ATP each step. This occurs 7X. So to make 1 palmitate, it takes 7ATP

Reactions in FA synthesis: 8 acetyl CoA + 7ATP+ 14 NADPH + 14 H+ + H2O >> palmitate + 7 ADP + 7 Pi + 8 CoASH + 14 NADP-

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What is the key regulatory enzyme for fatty acid biosynthesis? What metabolites are responsible for regulating this pathway? Hormonal regulators?

What is the key regulatory enzyme for fatty acid biosynthesis? What metabolites are responsible for regulating this pathway? Hormonal regulators?

Regulation of FA synthesis

Acetyl CoA carboxylase is the rate-limiting enzyme

A. Activators: citrate, insulin

B. synthesis induced by high-carbohydrate diet, fat free diet

C. Inhibitors: palmitoyl CoA, glucagon

D. Decrease synthesis with high-fat diet, fasting

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Where in the cell does fatty acid desaturation and elongation occur? What vitamins are required for these processes? What other small molecular species is required for desaturation to occur (molecular weight = 32)?

Where in the cell does fatty acid desaturation and elongation occur? What vitamins are required for these processes? What other small molecular species is required for desaturation to occur (molecular weight = 32)?

V. Elongation and Desaturation of FAs

ER elongation system adds acetyl CoA units via malonyl CoA onto palmitate. 2. Double bonds are introduced proximal to carbon 9 by desaturates (Triangle 9,6,5,4 desaturases) which require O2 and NADH. 3. Fatty acyl-CoA and NADH undergo oxidation. 4. Enzymes are in the membrane of the smooth ER.

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Where in the cell does fatty acid desaturation and elongation occur? What vitamins are required for these processes? What other small molecular species is required for desaturation to occur (molecular weight = 32)? II

Where in the cell does fatty acid desaturation and elongation occur? What vitamins are required for these processes? What other small molecular species is required for desaturation to occur (molecular weight = 32)?

FA desaturation & elongation occurs in the Endoplasmic reticulum. Also, it requires NADH (niacin, B3), O2, and H+!

Triangle Desaturatse adds double bond, malonyl CoA elongates!

V. Elongation and Desaturation of FAs

Endoplasmic reticulum elongation system adds acetyl CoA units via malonyl CoA onto palmitate. 2. Double bonds are introduced proximal to carbon 9 by desaturates (Triangle 9,6,5,4 desaturases) which require O2 and NADH. 3. Fatty acyl-CoA and NADH undergo oxidation. 4. Enzymes are in the membrane of the smooth ER.

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Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

Picture: Carnitine Shuttle system

Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

I. Introduction: 1. FAs are E source. 2. Oxidation yields NADH, FADH2, acetyl CoA. 3. Liver, heart, skeletal muscle are principal sites of FA oxidation.

II. Beta oxidation is the major route of FA catabolism.

Name indicates formation of B-keto acid.
Free FAs must be activated to enter metabolic pathways. A. ER acyl CoA synthetase activate long-chain FAs (12-20 carbons). B. Mitochondrial acyl CoA synthetases (matrix) activates medium and short chain fatty acids.

FA + ATP + CoASH >> acyl CoA + PPi + AMP

activated long chain FAs are transported into the mitochondrial matrix by a carnitine shuttle system. A. carnitine palmitoyl transferase (CPT 1) adds carnitine to the FA chain. B. Carnitine acylcarnitine translocase transports acylcarnitine into matrix of mitochondria. C. Carnitine palmitoyl transferase II (CPT II) regenerates acyl CoA. D. Carnitine is available in red meats and dairy, can also be synthesized from the AA lysine in the body. E. Enzymes for this system are located in the outer and inner mitochondrial membranes.
Reactions of Beta oxidation: repeated 4-step process removes 2-carbon units. A. acyln CoA + FAD >> enoyl CoA + FADH2, B. enoyl CoA >> 3-hydroxyacyl CoA, C. 3-hydroxylacyl CoA + NAD+ >> 3-ketoacyl CoA + NADH, d. 3-ketoacyl CoA + CoASH >> acetyl CoA + acyln-2 CoA
Stoichiometry + Energetics

palmitoyl CoA + 7 CoA + 7FAD + 7NAD+ + 7H2O >> 8 acetyl CoA + 7 FADH2 + 7NADH + 7H+

8 acetyl CoA X 12 ATP/Kreb’s Cycle = 96 ATP

7 FADH2 x 2 ATP/FADH2 = 14 ATP; 7 NADH x 3 ATP/ATP/NADH = 21 ATP.

ACTIVATION: Uses 2 high energy bonds (equivalent to 2ATP to ADP conversion

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Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

I. Introduction: 1. FAs are E source. 2. Oxidation yields NADH, FADH2, acetyl CoA. 3. Liver, heart, skeletal muscle are principal sites of FA oxidation.

II. Beta oxidation is the major route of FA catabolism.

Name indicates formation of B-keto acid.
Free FAs must be activated to enter metabolic pathways. A. ER acyl CoA synthetase activate long-chain FAs (12-20 carbons). B. Mitochondrial acyl CoA synthetases (matrix) activates medium and short chain fatty acids.

FA + ATP + CoASH >> acyl CoA + PPi + AMP

activated long chain FAs are transported into the mitochondrial matrix by a carnitine shuttle system. A. carnitine palmitoyl transferase (CPT 1) adds carnitine to the FA chain. B. Carnitine acylcarnitine translocase transports acylcarnitine into matrix of mitochondria. C. Carnitine palmitoyl transferase II (CPT II) regenerates acyl CoA. D. Carnitine is available in red meats and dairy, can also be synthesized from the AA lysine in the body. E. Enzymes for this system are located in the outer and inner mitochondrial membranes.
Reactions of Beta oxidation: repeated 4-step process removes 2-carbon units. A. acyln CoA + FAD >> enoyl CoA + FADH2, B. enoyl CoA >> 3-hydroxyacyl CoA, C. 3-hydroxylacyl CoA + NAD+ >> 3-ketoacyl CoA + NADH, d. 3-ketoacyl CoA + CoASH >> acetyl CoA + acyln-2 CoA
Stoichiometry + Energetics

palmitoyl CoA + 7 CoA + 7FAD + 7NAD+ + 7H2O >> 8 acetyl CoA + 7 FADH2 + 7NADH + 7H+

8 acetyl CoA X 12 ATP/Kreb’s Cycle = 96 ATP

7 FADH2 x 2 ATP/FADH2 = 14 ATP; 7 NADH x 3 ATP/ATP/NADH = 21 ATP.

ACTIVATION: Uses 2 high energy bonds (equivalent to 2ATP to ADP conversion

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Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

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Fatty Acid Oxidation

Be able to lay out the reaction sequence in the conversion of a long chain fatty acid via b–oxidation to acetyl CoA. Be able to calculate the energy production from fatty acid oxidation for any fatty acid chain length. How does b–oxidation of a mono-unsaturated fatty acid differ from that of a saturated fatty acid? How does the net energy production differ for these two types of fatty acids?

I. Introduction: 1. FAs are E source. 2. Oxidation yields NADH, FADH2, acetyl CoA. 3. Liver, heart, skeletal muscle are principal sites of FA oxidation.

II. Beta oxidation is the major route of FA catabolism.

Name indicates formation of B-keto acid.
Free FAs must be activated to enter metabolic pathways. A. ER acyl CoA synthetase activate long-chain FAs (12-20 carbons). B. Mitochondrial acyl CoA synthetases (matrix) activates medium and short chain fatty acids.

FA + ATP + CoASH >> acyl CoA + PPi + AMP

activated long chain FAs are transported into the mitochondrial matrix by a carnitine shuttle system. A. carnitine palmitoyl transferase (CPT 1) adds carnitine to the FA chain. B. Carnitine acylcarnitine translocase transports acylcarnitine into matrix of mitochondria. C. Carnitine palmitoyl transferase II (CPT II) regenerates acyl CoA. D. Carnitine is available in red meats and dairy, can also be synthesized from the AA lysine in the body. E. Enzymes for this system are located in the outer and inner mitochondrial membranes.
Reactions of Beta oxidation: repeated 4-step process removes 2-carbon units. A. acyln CoA + FAD >> enoyl CoA + FADH2, B. enoyl CoA >> 3-hydroxyacyl CoA, C. 3-hydroxylacyl CoA + NAD+ >> 3-ketoacyl CoA + NADH, d. 3-ketoacyl CoA + CoASH >> acetyl CoA + acyln-2 CoA
Stoichiometry + Energetics

palmitoyl CoA + 7 CoA + 7FAD + 7NAD+ + 7H2O >> 8 acetyl CoA + 7 FADH2 + 7NADH + 7H+

8 acetyl CoA X 12 ATP/Kreb’s Cycle = 96 ATP

7 FADH2 x 2 ATP/FADH2 = 14 ATP; 7 NADH x 3 ATP/ATP/NADH = 21 ATP.

ACTIVATION: Uses 2 high energy bonds (equivalent to 2ATP to ADP conversion

Where does b–oxidation of fatty acids occur in the cell? In what tissues/organs is b– oxidation prominent?

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Where does b–oxidation of fatty acids occur in the cell? In what tissues/organs is b– oxidation prominent? The liver, heart, and skeletal muscle are principal sites of FA oxidation. Beta oxidation (the major route of FA catabolism) begins when FAs are activated to enter metabolic pathways (by ER acyl CoA synthetase for long chain FAs, and mitochondrial acyl CoA synthetase (matrix) for medium and short chain FAs). Activated long chain FAs are transported into the mitochondrial matrix by a carnitine shuttle system.

Reactions of Beta oxidation: repeated 4-step process removes 2-carbon units. A. acyln CoA + FAD >> enoyl CoA + FADH2, B. enoyl CoA >> 3-hydroxyacyl CoA, C. 3-hydroxylacyl CoA + NAD+ >> 3-ketoacyl CoA + NADH, d. 3-ketoacyl CoA + CoASH >> acetyl CoA + acyln-2 CoA
Stoichiometry + Energetics

palmitoyl CoA + 7 CoA + 7FAD + 7NAD+ + 7H2O >> 8 acetyl CoA + 7 FADH2 + 7NADH + 7H+

8 acetyl CoA X 12 ATP/Kreb’s Cycle = 96 ATP

7 FADH2 x 2 ATP/FADH2 = 14 ATP; 7 NADH x 3 ATP/ATP/NADH = 21 ATP.

ACTIVATION: Uses 2 high energy bonds (equivalent to 2ATP to ADP conversion

How do phosphoglycerides, sphingomyelins, glycosphingolipids and triglycerides differ? In what tissues are sphingolipids and glycolipids most abundant? What is sphingosine? Identify 2 ways membranes are asymmetric.

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How do phosphoglycerides, sphingomyelins, glycosphingolipids and triglycerides differ? In what tissues are sphingolipids and glycolipids most abundant? What is sphingosine? Identify 2 ways membranes are asymmetric..

phosphoglycerides (or phospholipids) - Have a glycerol backbone attached to two FAs, and P + Head Group (2nd one over in pic)

sphingomyelins are phospholipids (form lipid bilayers)– and they are made of a sphingosine (long backbone) attached to a a FA & a P + Head group (Second from furthest to the right)

glycosphingolipids–Sphingosine backbone (long) attached to a FA and a carbohydrate. (Furtherest to the Right)
triglycerides - made up of glycerol backbone and fatty acids. FAs are stored in adipose tissue as TAG. 1. glycerides are esteres of glycerol and FAs, 2. triglycerides are less dense than water, 3. are a concentrated form of E, 4. do not cause osmotic problems in the body.

Sphingolipids (which make up glycosphingolipids and sphingophospholipids (sphingomyelin) —> are another type of membrane lipid. 1. Are concentrated in neural tissue, esp. white matter of brain, 2. are based on sphingosine as the backbone structure, 3. sphingomyelins are phospholipids, 4. glycosphingolipids contain carbohydrates. A. cerebrosides = monohexose, B. globosides = 2 or more sugars, C. ganlgiosides = contain sialic acid, D. sulfatides = sulfate containing sugars

Sphingosine (2-amino-4-octadecene-1,3-diol) is an 18-carbonamino alcohol with an unsaturated hydrocarbon chain, which forms a primary part of sphingolipids, a class of cell membrane lipids that include sphingomyelin, an important phospholipid.

Differences: See picture: Major Forms of Lipids Containing Fatty Acids

What controls the rate of fatty acid oxidation? What is the role of carnitine in fatty acid oxidation? Is carnitine a vitamin derivative? What are its sources?

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What controls the rate of fatty acid oxidation? What is the role of carnitine in fatty acid oxidation? Is carnitine a vitamin derivative? What are its sources?

Fatty acid oxidation “breakdown” has the key enzyme of CPT 1. Also, it’s inhbited by malonyl CoA. It is also activated by glucagon, and inhibited by insulin (hormonal regulation).

Also, activated long chain fatty acids are transported into the mitochondrial matrix by a carnitine shuttle system. Canitine is available in red meats and dairy, and can also be synthesized from the amino acid lysine in the body. Carnitine is NOT a vitamin derivative.

Derivatives of which vitamins are required for fatty acid oxidation?

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Derivatives of which vitamins are required for fatty acid oxidation?

Niacin - NADPH (B3)

Riboflavin - FAD B2

pantothenic acid B5

biotine B7

B12 (for odd chain)

Cobalt (in B12)

How does the complete oxidation of odd-chain length fatty acids differ from oxidation of even-chain fatty acids? What intermediate does the Krebs cycle and b–oxidation of odd chain fatty acids have in common? Identify a source of odd-chain fatty acids in human nutrition.

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How does the complete oxidation of odd-chain length fatty acids differ from oxidation of even-chain fatty acids? What intermediate does the Krebs cycle and b–oxidation of odd chain fatty acids have in common? Identify a source of odd-chain fatty acids in human nutrition.

The Kreb’s cycle and b-oxidation of odd chainf atty acids have SUCCINYNL CoA in common. Odd chain fatty acids are found in butter, chicken fat, cream, some fish oils, lard, and olive oil.

II. Oxidation of Odd-chain length fatty acids

B-oxidation is used up to final 3 carbon fragment, proprionyl CoA
Carboxylation of propionyl CoA to methylmalonyl CoA; biotin is the coenzyme.
Racemization of D-methylmalonyl CoA
L-methylmalonyl CoA is converted into succinyl CoA in a vitamin B12-dependent reaction enzyme: methylmalonyl CoA mutase
Succinyl CoA is metabolized via Kreb’s cycle

Ketone Body Metabolism

What three compounds are called ketone bodies? What is the organ of ketone body formation? In which cellular compartment are ketone bodies made? Under what conditions are ketone bodies made? Why are ketone bodies produced? By what mechanism do ketone bodies enter the circulation?

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Ketone Body Metabolism

What three compounds are called ketone bodies? What is the organ of ketone body formation? In which cellular compartment are ketone bodies made? Under what conditions are ketone bodies made? Why are ketone bodies produced? By what mechanism do ketone bodies enter the circulation?

>Ketone bodies are acetoacetate, beta-hydroxybutyrate, and acetone.

>Ketone bodies are produced mainly in the mitochondria of liver cells, and synthesis can occur in response to an unavailability of blood glucose

>Provide a means for brain to use enery stored in fatty acids

>Energy source during starvation.

>Synthesis in the liver mitochondria; liver does NOT use ketone bodies for energy; synthesis during times of high fatty acid oxidation.

> Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the TCA cycle and mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle or if activity in the TCA cycle is low due to low amounts of intermediates such as oxaloacetate, acetyl-CoA is then used instead in biosynthesis of ketone bodies via acetoacyl-CoA and β-hydroxy-β-methylglutaryl-CoA (HMG-CoA).

What are the 4 most prominent types of phosphoglycerides? Which group is called lecithins? What lecithin is a component of lung surfactant? What is the role of lung surfactant?

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What are the 4 most prominent types of phosphoglycerides? Which group is called lecithins? What lecithin is a component of lung surfactant? What is the role of lung surfactant?

The 4 major classes of glycerophospholipids based on head group are the following:

A. phosphatidylcholine - member of lecithin group! >>major component in lung surfactant

B. phosphatidylserine

C. phosphatidyl ethanolamine

D. phosphatidylinositol

phospholipids are components of cellular membranes. 1. Contain phosphate group and a hydrophilic head group. 2. Some are esters of glycerol-3-phosphate and fatty acids, 3. are amphipathic, 4. Major classes of glycerophospholipids based on head group.

Lecithin that’s a component of lung surfactant: DIPALMITOYLphosphatidylcholine! Lung surfactants are important because they reduce the surface tension of water lining the surface of the alveolar sac., preventing collapse. They are produced in babies @ 24 weeks of life!

Picture: Major Forms of lipids containing Fatty Acids

10. How do phosphoglycerides, sphingomyelins, glycosphingolipids and triglycerides differ? In what tissues are sphingolipids and glycolipids most abundant? What is sphingosine? Identify 2 ways membranes are asymmetric The composition of the inside/outside leaflets of membrane differ Outside of membrane: phosphatidylcholine, sphingomyelin, glycolipid, saturated FAs. Inside: Pohsphatidylserine, phosphatidyl ethantamine, phosphatidyl insoitol, unsaturated FA, sulfhydryl (-SH)

11. Note the use of different nucleotides (GTP, ATP, CTP, UTP) as fuel molecules or as activators of reactants.

11. Note the use of different nucleotides (GTP, ATP, CTP, UTP) as fuel molecules or as activators of reactants. UDP: Used in glycogenesis (conversion of glucose to glycogen) CDP: Used in LIPID METABOLISM (aka synthesis of glycerophospholipids) GTP - is used for energy in cell signaling pathways ATP - the energy currency Picture: Synthesis of Glycerophospholipids

14. What are the enzyme defects in the most common lysosomal storage disorders (Tay-Sachs, Gaucher's)? What products accumulate in these 2 disorders?

14. What are the enzyme defects in the most common lysosomal storage disorders (Tay-Sachs, Gaucher's)? What products accumulate in these 2 disorders? Lysosomal storage disorders (sphingolipidoses): 1. Degradation of sphingolipids occurs in lysosomes. 2 The rates of synthesis and degradation are normally balanced. 3. Sphingolipids accumulate when there is a defective lysosomal hydrolase, an enzyme of degradation. 4. The lipid that accumulates depends on the impaired enzyme. these disorder are rare except for Tay-Sachs and Gaucher's disease. **\>Hexosaminidase A is the defective enzyme in Tay-Sachs** **\>\>\>\>This enzyme is used to attach sugar to cerebroside (monohexose), or detach from ganglioside (contains sialic acid). Gm2 ganglioside accumulation** **\>Beta-glucosidase is defective in Gaucher's disease - cannot remove sugar from cerebroside (monohexose) to create cermide. Accumulation of cerebroside** Tay-Sachs and Gaucher's disease occur w/ high frequency in Ashkenazi Jewish populations. Clinical picture: **GM2 ganglioside accumulation**, progressive neurodegeneration, blindness, muscle weakness, seizures. Picture: Degradation of Sphingolipids is associated w/ multiple clinical conditions.

2. What is the precursor of ketone bodies? What is the product of ketone body breakdown? Why might the breath of an untreated diabetic have the odor of acetone? What organ has a heavy dependence on ketone bodies during starvation? Ketone body synthesis occurs in the liver, and they are synthesized from 2 acetyl CoA. The product of ketone body breakdown (or oxidation) is 2 Acetyl CoA. This process requires NAD & Succinyl CoA. The breath of an untreated diabetic might have the odor of acetone because they're not synthesizing the blood glucose, so their body think they are fasting. Also, the brain utilizes ketones for the majority of fuel riequirement (50-70 percent. The brain uses ketone bodies during starvation! Picture: ketone body oxidation

What do phosphoplipases accomplish? What bond is trageted by phospholipase A?

What do phosphoplipases accomplish? What bond is trageted by phospholipase A? Phospholipases are in the membrane and lysosome. They are required to degrade glycerophospholipids. Phospholipase A1 cleaves FA chain right next to C1 Phospholipase A2 cleaves the middle FA chain Phospholipase C cleaves off the phosphate group Phospholipase D cleaves off the head group from phosphate

1. Describe the formation of triglycerides. Where are triglycerides stored in adipocytes? How do WAT and BAT differ? How does BAT generate heat? What are the key enzymes for breakdown of triglycerides? How is triglyceride breakdown regulated hormonally? WAT Predominant type, found in subcutaneous and in visceral regions surrounding the internal organs. Store triglycerides as a large fat droplet in cytosol. The droplet is coasted w/ proteins. WAT can be stimulated to acquire phenotypic features of BAT BAT has non shivering thermogenesis as its primary role. Store lipids in multiple small lipid droplets, have numerous mitochondria, produce and uncoupling protein (UCP-1 or thermogenin) which promotes thermogenesis. Is found in neonates and has been recently confirmed in human adults.-- Fat storage: formation of triacylglycerols 1. Activated FAs are esterified w/ G3P 2. glycerol can be activated for esterification in the liver not not in adipose tissue. 3. DHAP from glycolysis is the soruce of glycerol-phosphate in adipose tissue. 4. Glucose entry into adipose tissue is insulin-independent FA chains are NOT USED to form glucose ---- Lipolysis (breakdown) of triacylglycerols is mediated by lipases 1. adipose triglyceride lipase (ATGL) initiates basal lipolysis of triacylglycerols in adipose tissue 2. hormone-sensitive lipase (HSL) primarily targets diacylglycerols and is activated by hormones, epinephrine, glucagon (inhibited by insulin) 3. hormonal activation of HSL occurs via cAMP-dependent protein kinase A. 4. phosphorylated HSL attaches to surface of lipid droplet5. Insuilin stimulates the phosphatase that reverses phosphorylation and thereby INHIBITS lypolysis! ALSO: Monacylglycerol Lipase (MGL) - lyses final FA!

2. In which organ, in which pathway, and at which step does the glycerol liberated by the hydrolysis of a triglyceride enter intermediary metabolism? Why isn’t the glycerol utilized by the adipocytes? What advantages do triglycerides have over carbohydrates as an energy storage form? What fraction of energy reserves are triglycerides? Phospholipases remove FA chains, freeing glycerol in the liver. \>Not used by adipocytes because they do not have the enzyme glycerol kinase to break it down. Breakdown of triacyglycerols is mediated by lipases in adipose tissue. 3 lipases: 1. Adipose Triglyceride Lipase (ATGL): basal lipolysis 2. Hormone sensitive Lipase (HSL): targets diacylglycerols. Uses cAMP dependent protein kinase A to be activated \>\> phosphorylated. \>activated by epinephrine, glucagon, inhibited by insulin. 3. Monoacylglycerol Lipase (MGL): lyses final FA ENERGY STORAGE: Carbs are stored as glycogen... Forming alpha 1,4 and alpha 1,6 linkages by dehydration. Water gets placed in plasma as H20 drops out... throwing off osmotic balance if glycogen was a major energy source. Need to oxidize glucose... You do GAIN ATPs, however... FATS: break of 2 carbon units to create Acetyl CoA \>\> Krebs, and this does NOT require ATP. You have twice the net GAIN of ATP from fat breakdown vs. CARB breakdown. Fats are HIGHLY reduced, so lots of E is released. No water is involved. ++++Triglycerides are the highest form of E reserve in the body, and are an important source during exercise & starving states.

Cholesterol Metabolism 1. What roles are played by steroids in human physiology? What is the parent compound of steroids in the body? Where is most of the cholesterol in the human body found?

Cholesterol Metabolism 1. What roles are played by steroids in human physiology? What is the parent compound of steroids in the body? Where is most of the cholesterol in the human body found? Steroids contain four fused carbon rings. A. Sterols are a class of steroids with 1. a hydroxyl function at carbon 3 2. an aliphatic chain at carbon 17 B. Cholesterol is the main sterol in the human body 1. is a structural component of cell membranes and lipoproteins 2. Is the precursor of steroid hormones (estrogen, cortisol, testosterone, aldosterone), bile salts (digestion), and vitamin D! --- We see that steroids in the body can act as hormones, and, therefore, their presence can impact a number of things from your growth to your sexual development. It could be said that the most important steroid molecule in your body ischolesterol, because cholesterol is the parent compound from which steroids are derived. It is basically the precursor for steroid hormones and other steroids. -- The human body contains about 100 g of cholesterol. Most of this is incorporated in the membranes from which cells are constructed and is an indispensable component of them. The insulating layers of myelin wound around neurons are especially rich in cholesterol. In far smaller quantities, but no less important, cholesterol is starting ingredient for the synthesis of the steroid hormones: progesterone; estrogens; androgens (e.g., testosterone); glucocorticoids (e.g., cortisol); mineralocorticoids (e.g., aldosterone).

2. What organ is responsible for most cholesterol biosynthesis?

2. What organ is responsible for most cholesterol biosynthesis? Biosynthesis of cholesterol 1. The LIVER is the major site of cholesterol synthesis 2. ALL carbons of cholesterol are derived from acetyl group of acetyl CoA 3. Enzymes are located in the cytosol and ER. 4. There are 5 key stages in cholesterol biosynthesis. A. formation of mevalonate from acetyl units, B. conversion of mevalonate into activated isoprene, C. adding isoprenes together to form squalene (30 C chain), D. cyclization of squalene to lanosterol, E. modification of lanosterol to form cholesterol 5. Cholesterol synthesis requires many NADPH and high energy phosphate bonds (around 22 ATP and 27 NADPH) PICTURE: Biosynthesis of cholesterol

**4. What is the rate limiting step in cholesterol synthesis? What enzyme catalyzes this step? Describe the regulation of cholesterol synthesis.** In what other pathway does HMG-CoA appear? Do these pathways intersect? In what form is cholesterol stored? What 2 enzymes are involved in storage? How is cholesterol removed from the body? B. REgulation of cholesterol biosynthesis 1. Rate limiting enzyme: HMG CoA reductase (btwn. HMG CoA & Mevalonic acid) 2. Fasting REDUCES synthesis activity 3. Feeding of cholesterol reduces liver synthesis 4. Feeding carbohydrates or fat elevates cholesterol synthesis 5. hormonal actions: A. glucagon INHIBITS cholesterol formation B. Insulin PROMOTES cholesterol formation

In what form is cholesterol stored? What 2 enzymes are involved in storage? How is cholesterol removed from the body?

In what form is cholesterol stored? What 2 enzymes are involved in storage? How is cholesterol removed from the body? C. Storage forms of cholesterol 1. Most tissue and plasma cholesterol is esterified w/ long chain fatty acids 2. ACAT esterifies cellular cholesterol 3. LCAT (lecithin:cholesterol acyltransferase) forms cholesterol esters in plasma lipoproteins.

5. Why do statins reduce blood cholesterol levels? Identify 3 commercial statin formulations? Why might statins be associated with skeletal muscle problems?

5. Why do statins reduce blood cholesterol levels? Identify 3 commercial statin formulations? Why might statins be associated with skeletal muscle problems? Statins INHIBIT HMG CoA Reductase (key regulatory enzyme), which inhibits the formation of of mevalonate. The reason that many people have muscle pain issues when they take statins since this pathway also produces CoQ10, which is important in muscle energy production in the ETC. Sometimes, they recommend taking CoQ10 w/ statins to limit this possibility!

6. What intermediate in the mevalonate pathway is the branch point for a number of final products, including lipid-soluble vitamins (in plants), dolichols, and CoQ (ubiquinone)? What are the roles of dolichol and CoQ? FPP (C15) is the branch point for a number of final products, including lipid soluble vitamins in plant, dolichols, and CoQ10 (ubiquinone). Dolichol-P is used in glycosylation of prtoeins. A major part of glycoproteins are those for our emotions, our neuropeptides. CoQ10 It is a component of the electron transport chain and participates in aerobic cellular respiration, generating energy in the form of ATP. Ninety-five percent of the human body’s energy is generated this way.[1][2]Therefore, those organs with the highest energy requirements—such as the heart, liver and kidney—have the highest CoQ10 concentrations.

**7. What are bile acids? Where are primary and secondary bile acids made in the body? What role do bile salts play in digestion? Where do conjugation and de-conjugation of bile salts occur? Why are bile salts conjugated? What amino acids are used for conjugation of bile salts? Discuss the entero-hepatic circulation of bile acids.** ## Footnote Bile acids are steroid acids found predominantly in the bile of mammals and other vertebrates. Different molecular forms of bile acids can be synthesized in the liver by different species.[1][2][3] Bile acids are conjugated with taurine or glycine in the liver, forming bile salts. Primary bile acids are those synthesized by the liver. Secondary bile acids result from bacterial actions in the colon. -- bile salts emulsify fats, promote micelle formation Detergent property due to ampiphilic character --- Removing cholesterol: biosynthesis and enterohepatic circulation of bile salts. 1. Primary bile salts (cholic acid and chenodeoxycholic acid) are synthesized from cholesterol in the liver. 2. Only hepatocytes express high levels of 7 alpha hydroxylase, the key regulator enzyme for bile synthesis. 3. Primary bile salts are converted into secondary bile salts (deoxycholic acid and lithocholic acid) by intestinal bacteria. 4. Secondary bile salts are absorbed from the GI tract after formation by bacteria. 5. Both primary and secondary bile salts are conjugated in the liver w/ glycine or taurine. 6. primary and secondary bile salts are secreted into the gallbladder and into the small intestines w/ food intake. 7. In the intestines, both primary and secondary bile salts are DECONJUGATED (By intestinal bacteria), reabsorbed across the intestinal wall, and returned to the liver via the portal vein. 8. Liver reconjugates the bile salts and secretes all four of them into the bile. 9. Secretion of bile, re-absorption and return to the liver, and re-secretion into the gut forms the enterohepatic circulation of bile salts 10. The steroid nucleus cannot be oxidized to carbon dioxide and water. 11. The main route of cholesterol excretion is through fecal loss of bile salts. --- WHY? What is the purpose of conjugation of bile acids? Bile acids are conjugated with taurine or glycine in the liver, forming bile salts. E. Solubility of cholesterol in bile 1. Bile contains cholesterol which is not very water soluble 2. Bile salts and phospholipids solubilize cholesterol in the bile 3. Gallstones can result from elevated cholesterol or reduced bile salts in the bile (cholelithiasis)

7. What are bile acids? Where are primary and secondary bile acids made in the body? What role do bile salts play in digestion? Where do conjugation and de-conjugation of bile salts occur? Why are bile salts conjugated? What amino acids are used for conjugation of bile salts? Discuss the entero-hepatic circulation of bile acids. Bile acids are steroid acids found predominantly in the bile of mammals and other vertebrates. Different molecular forms of bile acids can be synthesized in the liver by different species.[1][2][3] Bile acids are conjugated with taurine or glycine in the liver, forming bile salts. Primary bile acids are those synthesized by the liver. Secondary bile acids result from bacterial actions in the colon. -- bile salts emulsify fats, promote micelle formation Detergent property due to ampiphilic (water loving and fat loving) character --- Removing cholesterol: biosynthesis and enterohepatic circulation of bile salts. 1. Primary bile salts (cholic acid and chenodeoxycholic acid) are synthesized from cholesterol in the liver. 2. Only hepatocytes express high levels of 7 alpha hydroxylase, the key regulator enzyme for bile synthesis. 3. Primary bile salts are converted into secondary bile salts (deoxycholic acid and lithocholic acid) by intestinal bacteria. 4. Secondary bile salts are absorbed from the GI tract after formation by bacteria. 5. Both primary and secondary bile salts are conjugated in the liver w/ glycine or taurine. 6. primary and secondary bile salts are secreted into the gallbladder and into the small intestines w/ food intake. 7. In the intestines, both primary and secondary bile salts are DECONJUGATED (By intestinal bacteria), reabsorbed across the intestinal wall, and returned to the liver via the portal vein. 8. Liver reconjugates the bile salts and secretes all four of them into the bile. 9. Secretion of bile, re-absorption and return to the liver, and re-secretion into the gut forms the enterohepatic circulation of bile salts 10. The steroid nucleus cannot be oxidized to carbon dioxide and water. 11. The main route of cholesterol excretion is through fecal loss of bile salts. --- WHY? What is the purpose of conjugation of bile acids? Bile acids are conjugated with taurine or glycine in the liver, forming bile salts. E. Solubility of cholesterol in bile 1. Bile contains cholesterol which is not very water soluble 2. Bile salts and phospholipids solubilize cholesterol in the bile 3. Gallstones can result from elevated cholesterol or reduced bile salts in the bile (cholelithiasis)

Biochem II Exam 1 Flashcards

(42 cards)