Biochem B: Chapter 16

Ketone bodies can be used as an alternative fuel source by the liver. True or False?

False

β-oxidation of unsaturated fatty acids yields the same amount of energy as saturated fatty acids with the same number of carbons. True or false?

False

From the ATP yield of palmitate oxidation, what is the metabolic efficiency of the biological oxidation, in terms of kilojoules saved as ATP per kilojoule released? (Ignore the cost of fatty acid activation.)

Metabolic efficiency = 35.5%

Clathrin is a self-associating protein, which is able to form cage-like structures, which facilitate receptor-mediated endocytosis. True or False?

True

HMG-CoA reductase, the major control point of cholesterol biosynthesis is regulated by transcriptional and post-transcriptional mechanisms mediated by Insig proteins bound in the endoplasmic reticulum membrane. True or false?

True

Mono- and poly-unsaturated fatty acids are produced in the endoplasmic reticulum by desaturase enzymes. True or false?

True

The liver is the central organ in animals for processing lipoproteins whether they are derived from the diet or from biosynthetic pathways. True or false?

True

How many moles of glucose are required to provide the carbon for the synthesis of one mole of palmitate?

4 mol of glucose

How many moles of glucose are required if all of the glucose first proceeds through the pentose phosphate pathway before proceeding through the rest of glycolysis on its way to pyruvate?

4.8 mol of glucose

Calculate the number of ATPs generated by the complete metabolic oxidation of tripalmitin (tripalmitoylglycerol). Hydrolysis of the triacylglycerol occurs at the cell surface. Consider the energy yield from catabolism of glycerol, as well as from the fatty acids.

412.0 ATPs

How many tritium atoms (3H) are incorporated into palmitate when fatty acid synthesis is carried out in vitro with the following labeled substrate?

7 tritium atoms

________ is taken up by cells using receptor-mediated endocytosis, which involves the recognition of the B-100 apolipoprotein component of LDL.

Cholesterol

Sort the phrases into the appropriate bins depending on whether they describe exocytosis, endocytosis, or both. Options: -requires cellular energy -forms vesicles from inward folding of the plasma membrane -requires fusion of vesicles with the plasma membrane -decreases the surface area of the plasma membrane -transported substances never physically cross the plasma membrane -increases the surface area of the plasma membrane -secretes large molecules out of the cell

Exocytosis: -increases the surface area of the plasma membrane -secretes large molecules out of the cell -requires fusion of vesicles with the plasma membrane Endocytosis: -decreases the surface area of the plasma membrane -forms vesicles from inward folding of the plasma membrane Both: -requires cellular energy -transported substances never physically cross the plasma membrane

Elongation of fatty acids from palmitate occurs only in the mitochondrion. True or False?

False

Excess cholesterol is metabolically degraded in the liver. True or false?

False

Based on the metabolism of such molecules, what quantity of a C−19 fatty acid would be required to produce 1 g of glucose?

Mass = 3.3 g

Considering that odd-chain fatty acids make up approximately 1% of the fat in our diet, what quantity of fatty acids would be needed to produce 1 g of glucose?

Mass = 330 g

Calculate the grams of fat necessary to sustain a 20-hr nonstop flight.

Mass = 1.6 g

Under conditions where ketone bodies are being produced in the liver, how many ATPs can be produced from a molecule of palmitic acid if all resulting molecules of acetyl-CoA are converted into β-hydroxybutyrate?

Net yield = 16.0 ATP

Calculate the number of ATPs generated from the metabolic oxidation of the four carbons of acetoacetyl-CoA to CO2.

Net yield = 20.0 ATPs

Now consider the homolog derived from oxidation of an odd-numbered carbon chain, namely propionoacetyl-CoA. Calculate the net ATP yield from oxidation of the five carbons of this compound to CO2.

Net yield = 20.5 ATPs

If the birds relied on carbohydrate for this energy, how much additional weight would they have to start the flight with?

Weight = 10g

Calculate the ATP yield from oxidation of palmitic acid, taking into account the energy needed to activate the fatty acid and transport it into mitochondria.

Yield = 106.0 ATPs

Calculate the ATP yield from oxidation of linoleic acid.

Yield = 116.0 ATPs

Calculate the ATP yield from oxidation of oleic acid.

Yield = 118.5 ATPs

Calculate the ATP yield from oxidation of stearic acid.

Yield = 120.0 ATPs

Calculate the energy yield from glucose.

Yield = 5.3 ATPs per carbon atom

Calculate the ATP yield per carbon atom oxidized.

Yield = 8.1 ATPs per carbon atom

The β-oxidation of odd-numbered FAs presents a small problem in that once most of the oxidation has occurred, the last component is propionyl-CoA rather than acetyl CoA. This has one more carbon and as such cannot be utilized any further. Outline the events that control the metabolism of this unit in their proper order: 1) Methylmalonyl-CoA epimerase converts S-methylmalonyl-CoA to R-methylmalonyl-CoA. 2) Methylmalonyl-CoA mutase demethylates R-methylmalonyl-CoA to succinyl-CoA. 3) Propionyl-CoA carboxylase catalyzes the addition of CO2 to propionyl-CoA. 4) The odd-carbon FA is metabolized to propionyl-CoA. a. 4-3-1-2 b. 4-1-3-2 c. 3-1-4-2 d. 2-1-3-4

a. 4-3-1-2

Which of the following statements regarding the β-oxidation of FA is NOT correct? a. Acyl-CoA dehydrogenase catalyzes the synthesis of a cis α,β-unsaturated CoA thioester. b. 3-L-hydroxyacyl-CoA dehydrogenase catalyzes the oxidation of the 3-hydroxyacetyl CoA ester to the corresponding 3-ketone. c. Enoyl-CoA hydratase catalyzes the hydration of the α,β-unsaturated CoA thioester to a β-hydroxy CoA thioester. d. Thiolase catalyzes the thiolytic cleavage of a 3-ketoacyl CoA ester to release acetyl CoA and a new FA with two fewer carbons.

a. Acyl-CoA dehydrogenase catalyzes the synthesis of a cis α,β-unsaturated CoA thioester.

Identify and briefly discuss each mechanism ensuring against simultaneous fatty acid synthesis and oxidation in the same cell. Check all that apply. a. Fatty acyl-CoAs, the substrates for fatty acid oxidation, inhibit fatty acid synthesis by interfering with the polymerization of acetyl-CoA carboxylase. b. Malonyl-CoA, a key intermediate in fatty acid synthesis, inhibits carnitine acyltransferase I, thereby blocking the entry of fatty acyl units into the mitochondrion for oxidation. c. Citrate is an inhibitor of fatty acid synthesis, acting as an allosteric activator of acetyl-CoA carboxylase. Also it carries the acetyl units, which are important intermediates for oxidation of fatty acids, from the mitochondria to the cytoplasm. d. Pyruvate, the source of acetyl-CoA for fatty acid synthesis, can be converted into oxaloacetate which consumes acetyl-CoA, competing with AMP-dependent protein kinase during fatty acids oxidation. e. AMP-activated protein kinase switches off fatty acid synthesis by inhibiting acetyl-CoA carboxylase, whereas acetyl-CoA carboxylase is essential for fatty acid degradation. f. Hormonal effects on adipocytes: insulin promotes fatty acid synthesis by several mechanisms, while glucagon promotes fat breakdown and fatty acid oxidation.

a. Fatty acyl-CoAs, the substrates for fatty acid oxidation, inhibit fatty acid synthesis by interfering with the polymerization of acetyl-CoA carboxylase. b. Malonyl-CoA, a key intermediate in fatty acid synthesis, inhibits carnitine acyltransferase I, thereby blocking the entry of fatty acyl units into the mitochondrion for oxidation. f. Hormonal effects on adipocytes: insulin promotes fatty acid synthesis by several mechanisms, while glucagon promotes fat breakdown and fatty acid oxidation.

The diagram below shows the transport functions of four types of lipoproteins. For example, one type of lipoprotein transports triacylglycerols (TAGs) from the liver to the peripheral tissues. Identify the type of lipoprotein associated with each function. a. VLDL remnants -> Liver b. Liver -> TAGs to peripheral tissues c. Cholesterol from dead or dying cells -> liver d. Liver -> cholesterol to peripheral tissues Options: LDL IDL VLDL HDL

a. IDL b. VLDL c. HDL d. LDL

Choose a pathway whereby some of the carbon from a fatty acid with an odd-numbered carbon chain could undergo a net conversion to carbohydrate. a. Propionyl−CoA⟶methylmalonyl−CoA⟶succinyl−CoA⟶oxaloacetate⟶PEP⟶glucose b. Propionyl−CoA⟶methylmalonyl−CoA⟶pyruvate⟶malonyl−CoA⟶PEP⟶glucose c. Propionyl−CoA⟶acetoacetyl−CoA⟶β−hydroxybutyrate⟶oxaloacetate⟶PEP⟶glucose d. Propionyl−CoA⟶methylmalonyl−CoA⟶malonyl−CoA⟶malate⟶oxaloacetate⟶PEP⟶glucose

a. Propionyl−CoA⟶methylmalonyl−CoA⟶succinyl−CoA⟶oxaloacetate⟶PEP⟶glucose

Explain your answer. a. This is a nonhydrolyzable analog of glycerol-3-phosphate, so it is acylated without difficulty to give the phosphonate analog of diacylglycerol. b. 3,4-Dihydroxybutyl-1-phosphonic acid competes with glycerol-3-phosphate when it binds to glycerophosphate acyltransferase. This process completely suppresses the further acylation. c. 3,4-Dihydroxybutyl-1-phosphonic acid binds to glycerol-3-phosphate causing the whole process to stop. d. 3,4-Dihydroxybutyl-1-phosphonic acid consumes all fatty acyl-CoA during the acylation process. The further esterification is impossible without the substrate.

a. This is a nonhydrolyzable analog of glycerol-3-phosphate, so it is acylated without difficulty to give the phosphonate analog of diacylglycerol.

Part complete Because PS must be present in the membrane to serve as an intermediate, how might you explain its failure to accumulate to a significant extent? a. Under sertain conditions PS could never accumulate, because, once formed by phosphatidylserine synthase, it would immediately be converted to PE by phosphatidylserine decarboxylase. b. The biosynthesis of phosphatidylethanolamine from CDP-diacylglycerol and serine occurs at the two active sites of a single enzyme. PS could never be accumulated, because this process is not sterically restricted. c. PS is a very unstable intermediate. It could never be accumulated, because it would spontaneously decompose back to serine and CDP-diacylglycerol. d. PS is a very unstable intermediate. It could never be accumulated, because it would undergo spontaneous decarboxylation to PE.

a. Under sertain conditions PS could never accumulate, because, once formed by phosphatidylserine synthase, it would immediately be converted to PE by phosphatidylserine decarboxylase.

Linoleic acid a. linoleate+25.5O2+118ADP+116Pi→18CO2+117ATP+AMP+135.5H2O b. linoleate+25.5O2+117ADP+108Pi→16CO2+108ATP+9AMP+138H2O c. linoleate+25.5O2+116.5ADP+115Pi→16CO2+115.5ATP+AMP+77.5H2O d. linoleate+25.5O2+120ADP+120Pi→20CO2+118ATP+2AMP+136.5H2O

a. linoleate+25.5O2+118ADP+116Pi→18CO2+117ATP+AMP+135.5H2O

What would you expect to happen to levels of mevalonate in human plasma if an individual were to go from a meat-containing diet to a vegetarian diet? a. mevalonate levels increase b. mevalonate levels decrease c. mevalonate levels do not change

a. mevalonate levels increase

Part complete Using Figure 16.9 on page 515 in the text, arrange the order of events for the internalization of LDL particles into cells: 1) A combination of cholesterol and apolipoprotein binds to LDL receptors and becomes internalized as endocytotic vesicles. 2) The environment of the endosome becomes acidic, which causes the LDL to dissociate from its receptor; additionally, the endosome fuses with a lysosome. 3) Several endocytotic vesicles fuse to form an endosome. 4) The LDL particle is degraded by the lysosome. 5) LDL receptors migrate to the cell surface and cluster in clathrin-coated pits. a. 5-4-1-3-2 b. 5-1-3-2-4 c. 5-2-3-1-4 d. 1-5-3-2-4

b. 5-1-3-2-4

The overall net synthesis of palmitate starting from acetyl CoA requires: a. 8 acetyl-CoA, 8 ATP and 16 NADPH and 16H+. b. 8 acetyl-CoA, 7 ATP and 14 NADPH and 7 H+. c. 8 acetyl-CoA, 8 ATP and 14 NADPH and 7 H+. d. 8 acetyl-CoA, 7 ATP and 14 NADPH and 14 H+. e. 8 acetyl-CoA, 7 ATP and 16 NADPH and 8 H+.

b. 8 acetyl-CoA, 7 ATP and 14 NADPH and 7 H+.

Which of the following statements about β-oxidation of fatty acids is CORRECT? a. Both dehydrogenation reactions use FAD as the electron acceptor. b. All fatty acids must be activated to acyl-CoAs before entering the pathway. c. Both dehydrogenation reactions produce a C=C double bond. d. Fatty acids of any length are oxidized by exactly the same enzymes. e. Thiolytic cleavage releases acetyl-CoA and a free fatty acid in the final step of the cycle.

b. All fatty acids must be activated to acyl-CoAs before entering the pathway.

When cultured in the presence of LDL, normal cells showed low activity of HMG−CoA reductase. After removal of lipopoteins, including LDL, HMG−CoA reductase activities increased some 50- to 100-fold in normal cells (panel a). This high level of enzyme activity was rapidly suppressed upon addition of LDL back to normal cells (panel b). a. Cholesterol blocks the pores in the membrane of the cell, so no components necessary for the action of HMG−CoA reductase can enter into the cell, thus its the activity is reduced. b. Cholesterol is normally transported into the cell, where it regulates its own synthesis by suppressing the activity of HMG−CoA reductase, the rate-limiting enzyme. c. Cholesterol is normally transported into the cell, where it deplaces water, which in turn dries HMG−CoA reductase, and without water its activity is very low.

b. Cholesterol is normally transported into the cell, where it regulates its own synthesis by suppressing the activity of HMG−CoA reductase, the rate-limiting enzyme.

Which of the following statements about the lipoproteins given in the introduction are true? Check all that apply. a. HDL has a high lipid-to-protein ratio. b. Lipoprotein densities vary because lipoproteins have different lipid-to-protein ratios. c. Lipoprotein densities increase in the following order: chylomicrons, VLDLs, LDLs, HDLs, IDLs. d. Lipoproteins are complexes of lipids and proteins. e. Lipoproteins can be distinguished by their densities and composition. f. HDL is termed "bad" cholesterol because it can deposit excess cholesterol in the arteries. g. Chylomicrons are the only lipoproteins that exclusively carry dietary lipids.

b. Lipoprotein densities vary because lipoproteins have different lipid-to-protein ratios. d. Lipoproteins are complexes of lipids and proteins. e. Lipoproteins can be distinguished by their densities and composition. g. Chylomicrons are the only lipoproteins that exclusively carry dietary lipids.

How do FAs of different carbon lengths cross into the mitochondrial matrix for oxidation? 1) Small FAs of 10 carbons or fewer can freely diffuse through the membrane. 2) Large FAs are cleaved into two smaller units that are actively transported across the membrane. 3) A membrane-bound transferase catalyzes the conversion of long-chain FAs to FA-carnitine esters, which are transported across the membrane via a specific carrier. 4) The breakdown of large FAs starts outside the matrix, allowing for smaller particles to pass easily through the membrane. a. Only statements 1 and 4 are correct. b. Only statements 1 and 3 are correct. c. Only statements 1, 2 and 3 are correct. d. All of the listed statements are correct.

b. Only statements 1 and 3 are correct.

Explain these observations. a. To stabilize the subunits in vitro we should use the double amount of NADPH which completely supresses the reduction of β-ketoacyl-ACP. b. The acyl-ACP produced by one subunit undergoes the next round of reductive two-carbon addition on the other subunit. c. The produced D-3-hydroxyacyl-ACP is oxidized by oxygen from the air making the overall synthesis of palmitate impossible. d. This reaction requires two acyl-ACP units that cannot be produced by one separated subunit.

b. The acyl-ACP produced by one subunit undergoes the next round of reductive two-carbon addition on the other subunit.

Compare these two values. a. The energy yield from tripalmitin is smaller than the energy yield from glucose. b. The energy yield from tripalmitin is larger than the energy yield from glucose. c. These values are equal.

b. The energy yield from tripalmitin is larger than the energy yield from glucose.

Which step in lipid metabolism would you expect to be affected by 3,4-dihydroxybutyl-1-phosphonic acid (shown here)? a. The ATP-dependent phosphorylation of glycerol by glycerol kinase. b. The esterification of glycerol-3-phosphate with fatty acyl-CoA, catalyzed by glycerophosphate acyltransferase. c. The reduction of the glycolytic intermediate dihydroxyacetone phosphate, catalyzed by glycerol-3-phosphate dehydrogenase. d. The hydrolysis of diacylglycerol-3-phosphate to 1,2-diacylglycerol.

b. The esterification of glycerol-3-phosphate with fatty acyl-CoA, catalyzed by glycerophosphate acyltransferase.

What is the most likely site of inhibition by 2-bromopalmitoyl-CoA? a. acyl-CoA synthetase b. carnitine palmitoyltransferase I c. carnitine palmitoyltransferase II d. the carnitine-acylcarnitine translocase

b. carnitine palmitoyltransferase I

Choose a balanced equation for the synthesis of sn-1-stearoyl-2-oleoylglycerophosphorylserine, starting with glycerol, the fatty acids involved, and serine. a. glycerol+stearicacid+oleicacid+3ATP+CMP+serine→sn−1−stearoyl−2−oleylglycerophosphorylserine+ADP+PPi+CTP b. glycerol+stearicacid+oleicacid+3ATP+CTP+serine→sn−1−stearoyl−2−oleylglycerophosphorylserine+ADP+2AMP+3PPi+CMP c. glycerol+stearicacid+oleicacid+ATP+3CTP+serine→sn−1−stearoyl−2−oleylglycerophosphorylserine+ADP+3PPi+3CMP d. glycerol+stearicacid+oleicacid+3ATP+serine→sn−1−stearoyl−2−oleylglycerophosphorylserine+ADP+AMP+6Pi+cAMP

b. glycerol+stearicacid+oleicacid+3ATP+CTP+serine→sn−1−stearoyl−2−oleylglycerophosphorylserine+ADP+2AMP+3PPi+CMP

Which of the following compounds is NOT derived from cholesterol? a. Glycocholate b. α-tocopherol c. Cortisol d. Aldosterone e. 1,25-dihydroxycholecalciferol

b. α-tocopherol

In some instances, the levels of LDL cholesterol exceed the ability of the body to maintain homeostasis, and as a result, the excess material accumulates into fatty deposits that harden into plaques. Arrange in the correct order the sequence of events that leads to this condition, known as atherosclerosis: 1) The plaques harden, blocking the flow of blood in major arteries. 2) White blood cells become engorged with fatty deposits. 3) Excess LDL cholesterol accumulates in the interior of arterial walls. 4) Macrophages are drawn to this site. a. 3-2-4-1 b. 3-1-2-4 c. 3-4-2-1 d. 1-3-4-2

c. 3-4-2-1

Arrange the order of events in the fatty acid (FA) metabolism pathway in the correct order: 1) The modified FA is transported across the inner membrane of the mitochondrion. 2) Dehydration occurs to generate an α,β-unsaturated FA. 3) The free FA is converted to acetyl CoA ester. 4) Thiolytic cleavage occurs, releasing a molecule of acetyl CoA and a new FA with two fewer carbon atoms. 5) The FA CoA ester is converted to its carnitine ester. 6) Hydration occurs to yield a β-hydroxy ester. 7) The FA CoA ester is regenerated. a. 3-6-4-7-2-1-5 b. 3-5-2-7-1-6-4 c. 3-5-1-7-2-6-4 d. 3-6-1-2-7-5-4

c. 3-5-1-7-2-6-4

Present pathways by which this could come about. a. Acetyl−CoA⟶citricacidcyclepyruvate⟶Pyruvatecarboxylaseoxaloacetate⟶PEPcarboxykinasePEP⟶gluconeogenesisglucose b. Acetyl−CoA⟶citricacidcyclemalate⟶PEPcarboxykinasePEP⟶gluconeogenesisglucose c. Acetyl−CoA⟶citricacidcycleoxaloacetate⟶PEPcarboxykinasePEP⟶gluconeogenesisglucose d. Acetyl−CoA⟶citricacidcyclefumarate⟶PEPcarboxykinasePEP⟶gluconeogenesisglucose

c. Acetyl−CoA⟶citricacidcycleoxaloacetate⟶PEPcarboxykinasePEP⟶gluconeogenesisglucose

What kinds of experiments could test your proposed explanation? a. Doubling the amount of phosphatidylserine synthase in this system leads to doubling of PE production. b. Inhibition of phosphatidylserine synthase and further addition of radiolabeled PS to an enzyme system leads to formation of labeled PE. c. Addition of radiolabeled PS to an enzyme system would not label PE, because phosphatidylserine decarboxylase would act only on PS generated by phosphatidylserine synthase. d. Inhibition of phosphatidylserine decarboxylase leads to an accumulation of PS generated by phosphatidylserine synthase.

c. Addition of radiolabeled PS to an enzyme system would not label PE, because phosphatidylserine decarboxylase would act only on PS generated by phosphatidylserine synthase.

Cells from FH individuals exhibited high levels of reductase activity, regardless of the presence or absence of LDL in the culture medium. a. Cells from FH individuals were activated by the LDL in the culture medium; after activation, the LDL served no other role by being present in the culture medium. b. Cholesterol did not take part in any processes of cells from FH individuals. c. Cells from FH individuals were deficient in their ability to take up cholesterol from the culture medium.

c. Cells from FH individuals were deficient in their ability to take up cholesterol from the culture medium.

Glucagon secretion causes inhibition of intracellular acetyl-CoA carboxylase activity by several mechanisms. Name all you can think of. Check all that apply. a. Glucagon increases the activity of citrate synthase which consumes acetyl-CoA in the tricarboxylic acid cycle. As a result, the substrate level is reduced and the enzyme activity is decreased. b. Glucagon stops glycolysis yielding decrease in ATP production, hence carbonyl-phosphate formation is lowered and this prevents carboxylation of the enzyme. c. Glucagon activates phosphorylation of pyruvate dehydrogenase, which inhibits the formation of acetyl-CoA, the substrate for the enzyme. d. Glucagon promotes triacylglycerol breakdown, yielding increased levels of fatty acids, which could prevent polymerization and activation of acetyl-CoA carboxylase. e. Glucagon decreases the activity of biotin carboxylase, reducing the N-carboxybiotinyl-enzyme formation.

c. Glucagon activates phosphorylation of pyruvate dehydrogenase, which inhibits the formation of acetyl-CoA, the substrate for the enzyme. d. Glucagon promotes triacylglycerol breakdown, yielding increased levels of fatty acids, which could prevent polymerization and activation of acetyl-CoA carboxylase.

Which regulatory effects are results of internalized cholesterol? 1) It activates acyl-CoA:cholesterol acyltransferase. 2) It increases endogenous cholesterol synthesis. 3) It downregulates the production of LDL receptors. 4) It inhibits HMG-CoA reductase. a. Statements 2, 3, and 4 are direct results of the internalization of cholesterol. b. Statements 1, 2, and 4 are direct results of the internalization of cholesterol. c. Statements 1, 3, and 4 are direct results of the internalization of cholesterol. d. Statements 1 and 4 are direct results of the internalization of cholesterol.

c. Statements 1, 3, and 4 are direct results of the internalization of cholesterol.

Discuss the metabolic rationale for phosphorylation of acetyl-CoA carboxylase by AMP-activated protein kinase (AMPK) and cyclic AMP-dependent protein kinase (PKA). a. This could be a way for a cell to activate fatty acid synthesis in the case of acetyl-CoA deficiency. b. This could be a way for a cell to control fatty acid synthesis in the case of glucose high level in cytosol. c. This could be a way for a cell to inhibit fatty acid synthesis under conditions where substrates are needed for oxidation. d. This could be a way for a cell to avoid the excess of ATP production during the fatty acid oxidation.

c. This could be a way for a cell to inhibit fatty acid synthesis under conditions where substrates are needed for oxidation.

Stearic acid a. stearate+28O2+108ADP+60PPi→16CO2+120ATP+AMP+78H2O b. stearate+22O2+124ATP+AMP→12CO2+124ADP+124Pi+118H2O c. stearate+26O2+122ADP+120Pi→18CO2+121ATP+AMP+138H2O d. stearate+24O2+106ADP+100Pi→20CO2+122ATP+cAMP+120H2O

c. stearate+26O2+122ADP+120Pi→18CO2+121ATP+AMP+138H2O

Oleic acid a. oleate+28O2+118ATP+AMP→20CO2+118ADP+118Pi+148H2O b. oleate+26O2+122ADP+59.25PPi→8CO2+120ATP+2AMP+170H2O c. oleate+25.5O2+120.5ADP+118.5Pi→18CO2+119.5ATP+AMP+135.5H2O d. oleate+22.5O2+118.5ADP+120.5Pi→16CO2+120.5ATP+cAMP+130.5H2O

c. oleate+25.5O2+120.5ADP+118.5Pi→18CO2+119.5ATP+AMP+135.5H2O

Describe the probable effect in adipocytes of insulin-stimulated uptake of glucose into these cells. Increased glucose levels in the ________ stimulate glycolysis, which provides ________ for oxidation in the ______________. The resultant acetyl-CoA can return to the __________ (as _______) and can generate precursors for increased fatty acid synthesis. The increased intracellular glucose also stimulates glycogen synthesis. options: cytosol pyruvate malate oxaloacetate citrate mitochondrion

cytosol; pyruvate; mitochondrion cytosol; citrate

One pathway that appears to relate elevated cholesterol levels to atherosclerosis involves the oxidation of LDL. Which of the following are consequences of this process? a. The presence of scavenger receptors on macrophages allows unlimited cholesterol uptake, leading to its conversion to foam cells. b. Though the mechanism by which this occurs is not completely understood, this oxidation includes the peroxidation of fatty acids, the hydroxylation of cholesterol, and the oxidation of amino acids. c. Oxidized LDL products induce an immune response that includes recruitment of monocytes and T lymphocytes. d. All of the listed responses are consequences of this process.

d. All of the listed responses are consequences of this process.

Which of the following enzymes are required for the oxidation of unsaturated FA? a. acyl-CoA dehydrogenase b. 2,4-Dienoyl-CoA reductase c. enoyl-CoA isomerase d. All of the listed responses are correct.

d. All of the listed responses are correct.

Which of the following are key discoveries of the experiments conducted by Brown and Goldstein? 1) Cholesterol is taken into cells through the action of a specific receptor. 2) The receptor for the LDL particle recognizes B-100 apolipoprotein. 3) The entire receptor complex, unlike hormones involved in signaling pathways, enters the cell via endocytosis. 4) Familial hypercholesterolemia patients have defective or deficient LDL receptors. a. Statements 1, 2, and 4 are correct. b. Statements 1, 2, and 3 are correct. c. Only statements 1 and 4 are correct. d. All of the listed statements are true.

d. All of the listed statements are true.

Explain why a deficiency of steroid 21-hydroxylase leads to excessive production of sex steroids (androgens and estrogens). a. 21-hydroxylase competes with 17α-hydroxylase, so deficiency of 21-hydroxylase leads to increasing 17α-hydroxylase activity and to excessive production of sex steroids. b. By shutting down the pathway leading to aldosterone, this deficiency increases the supply of dehydroepiandrosterone that converted directly to sex steroids. c. 21-hydroxylase competes with 17,20-lyase, so deficiency of 21-hydroxylase leads to increasing 17,20-lyase activity and to excessive production of sex steroids. d. By shutting down the pathway leading to aldosterone, this deficiency increases the supply of progesterone available for conversion to sex steroids.

d. By shutting down the pathway leading to aldosterone, this deficiency increases the supply of progesterone available for conversion to sex steroids.

Which of the following statements is FALSE? a. Chylomicrons are lipoproteins that transport dietary fat from intestine to peripheral tissues. b. VLDL transports triacylglycerol synthesized in the liver to peripheral tissues. c. Some fatty acids become complexed with serum albumin for transport in the blood to peripheral cells. d. The cholesterol ester content of HDL is generally less than that of chylomicrons. e. LDL is the main form in which cholesterol is transported to tissues.

d. The cholesterol ester content of HDL is generally less than that of chylomicrons.

Palmitic acid a. palmitate+25O2+120ADP+60PPi→14CO2+110ATP+5AMP+60H2O b. palmitate+24O2+110ADP+110Pi→16CO2+109ATP+AMP+120H2O c. palmitate+20O2+106ADP+AMP→18CO2+107ATP+107Pi+106H2O d. palmitate+23O2+108ADP+106Pi→16CO2+107ATP+AMP+122H2O

d. palmitate+23O2+108ADP+106Pi→16CO2+107ATP+AMP+122H2O

Free fatty acids are released from the adipocyte after mobilization of fat stores by: a. monoacylglycerol lipase. b. adipose triglyceride lipase. c. hormone sensitive lipase. d. lipoprotein lipase. e. A, B, and C.

e. A, B, and C.

Insulin stimulates fatty acid synthesis by which of the following mechanisms? a. Stimulation of dephosphorylation of pyruvate dehydrogenase b. Activation of citrate lyase c. Dephosphorylation of acetyl-CoA carboxylase d. Stimulation of a glucose transport across the plasma membrane e. All of the above

e. All of the above

The shuttle system for transfer of acetyl-CoA generated in the mitochondrial matrix to the cytosol includes: a. citrate from the citric acid cycle. b. citrate lyase in the cytosol. c. ATP hydrolysis. d. the production of NADPH by malic enzyme. e. all of the above.

e. all of the above.

Part complete If mevalonate labeled with 14C in the carboxyl carbon were administered to rats, which carbons of cholesterol would become labeled? Check all that apply. a. C-1 b. C-2 c. C-3 d. C-4 e. C-5 f. C-6 g. C-6 h. none

h. none

cis-Vaccenate is an 18-carbon unsaturated fatty acid abundant in E. coli membrane lipids. Propose a metabolic route for synthesis of this fatty acid, in light of the fact that stearic acid, the C18 saturated analogous fatty acid, is virtually absent from E. coli lipids. Options: a. NAD+ + 2H2O b. CoA - SH + 2NADP+ + H2O + CO2 c. palmitoleoyl - CoA d. palmitoyl - CoA Δ9 desaturase e. stearoyl - CoA Δ9 desaturase f. C2 elongation g. stearoyl - CoA h. malonyl - CoA + 2NADPH + 2H+ i. NADH + H+ + O2

i. NADH + H+ + O2 d. palmitoyl - CoA Δ9 desaturase a. NAD+ + 2H2O c. palmitoleoyl - CoA h. malonyl - CoA + 2NADPH + 2H+ f. C2 elongation b. CoA - SH + 2NADP+ + H2O + CO2

What would be the effect on fatty acid synthesis of an increase in intramitochondrial oxaloacetate level? Briefly explain your answer. Increase in citrate levels would _________ generation of acetyl-CoA in cytosol, hence _____________ fatty acid synthesis. options: stimulating inhibiting decrease increase

increase; stimulating

Propionyl-CoA, the end product of β-oxidation of odd-chain fatty acids can enter the citric acid cycle after being converted to ________.

succinyl-CoA