Advanced Nutrition and Human Metabolism 5th Edition by Sareen S. Gropper - Test Bank

Advanced Nutrition and Human Metabolism 5th Edition by Sareen S. Gropper – Test Bank

 

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Sample Questions Are Posted Below

 

Chapter 5 – Lipids

 

Multiple-Choice

 

Key        Page(s)

d             132                         1.     The fatty acid chains found in foods and body tissues range from _____ carbon atoms.

1. 1 to 3
2. 2 to 6
3. 3 to 12
4. 4 to 24

 

b              132                         2.     Carbon-carbon double bonds in the trans form

1. result in a kinking of the fatty acid into a U-shape.
2. extend the fatty acid into a linear shape.
3. are required to create saturated fatty acids.
4. are the hallmark of essential fatty acids.

 

c              134                         3.     Which fatty acid is considered essential and must be supplied by the diet?

1. arachidonic acid
2. omega-9 fatty acid
3. linoleic acid
4. oleic acid

 

b              134                         4.     What antithrombotic n-3 fatty acid is found in fish oil?

1. alpha-linolenic
2. eicosapentaenoic
3. arachidonic
4. stearic

 

b              134                         5.     In what form is most body fat stored?

1. fatty acids
2. triacylglycerols
3. cholesterol
4. phospholipids

 

d             135                         6.     Triacylglycerols with saturated fatty acids of longer chain length tend to be _____ at room temperature.

1. liquid oils
2. emulsified
3. non-esterified fats
4. solid fats

 

 

c              135                         7.     What is the most common lipid characterized by a four-ring core structure?

1. prostaglandins
2. leukotrenes
3. cholesterol
4. glycolipids

 

a              136                         8.     Cholesterol serves as a precursor for all of the following EXCEPT _____.

1. phospholipids
2. estrogens and androgens
3. bile acids
4. vitamin D

 

b              138                         9.     Glycerophosphatides serve which of the following functions?

1. source of stored energy
2. constituent of cell and organelle membranes
3. precursor for long-chain n-3 fatty acids
4. constituent of myelin sheaths

 

c              138                         10.  Phospatidylinositol is a membrane phospholipid that can _____.

1. anchor surface proteins to the plasma membrane
2. create 2 second messengers in cell signaling
3. both a and b
4. none of the above

 

c              138                         11.  Sphingomyelins are important phospholipids in the _____.

1. pacemaker of the heart
2. kidney tubules
3. myelin sheath of nerves
4. human blood groups A, B and O

 

c              140                         12.  Gastric lipase is important for the suckling infant for all of the following reasons EXCEPT:

1. It can readily penetrate milk fat globules without bile salt stabilization.
2. It hydrolyzes short-chain fatty acids from the sn-3 position.
3. It requires an alkaline environment for optimal activity.
4. It is highly stable in an acid environment.

 

b              140                         13.  Undigested lipid in the stomach creates satiety because it

1. speeds the rate of emptying of the stomach.
2. delays the rate of emptying of stomach contents.
3. enhances gastric motility.
4. suppresses GIP and secretin.

 

 

d             141                         14.  All of the following are required for fat digestion EXCEPT _____.

1. pancreatic lipase
2. colipase
3. bile
4. lysolecithin

 

c              143                         15.  Polymolecular aggragates called micelles are small enough to _____.

1. enter the enterocytes
2. stabilize circulating lipoproteins in the blood
3. enter the intramicrovillus spaces to interact with the brush border
4. confer specificity for recognition by receptors on cells

 

d             143                         16.  The process by which bile salts are absorbed in the ileum and return to the liver is called _____ of the bile salts.

1. micelle induction
2. resecretion
3. conjugation
4. enterohepatic circulation

 

d             143                         17.  What is the carrier for short-chain fatty acids in portal circulation?

1. triacylglycerides
2. cholesterol
3. chylomicrons
4. albumin

 

c              144                         18.  What organ provides the major site for lipoprotein formation from exogenously derived lipids?

1. pancreas
2. adipocytes
3. intestine
4. liver

 

c              145-146                 19.  All of the following are functions of apolipoproteins EXCEPT:

1. stimulating enzymatic reactions that regulate the metabolic functions of lipoproteins.
2. stabilizing circulating lipoproteins in the blood.
3. decreasing the density of the lipoprotein.
4. conferring specificity for recognition by receptors on cells.

 

b              146                         20.  Which of the following lipoproteins are normally NOT present in blood in the fasting state?

1. VLDL
2. chylomicrons
3. LDL
4. HDL

 

c              150                         21.  Which of the following lipoproteins is the major carrier of cholesterol to tissues for use in construction of membranes or steroid hormones?

1. VLDL
2. HDL
3. LDL
4. chylomicrons

 

c              150-151                 22.  The key to the cell’s internalization of LDL is the interaction between the receptors and _____.

1. cholesterol acyltransferase
2. HMG COA reductase
3. apoprotein B-100
4. apoprotein C-100

 

d             152                         23.  Abnormal LDL receptors fail to remove cholesterol from the bloodstream resulting in familial hypercholesterolemia. How many different genetic mutations in these receptors have been identified to date?

1. 3
2. 5
3. 7
4. 10

 

d             152                         24.  Which drug therapy is associated with reduced cholesterol synthesis in the liver?

1. insulin
2. niacin
3. gene therapy
4. HMG COA reductase inhibitors

 

b              153                         25.  Reverse cholesterol transport that removes cholesterol from peripheral cells and carries it to the liver is carried out by _____.

1. LDL
2. HDL
3. VLDL
4. lipoprotein lipase

 

b              T 5.1(134),155     26.  What dietary fatty acid exerts anti-atherogenic properties?

1. palmitic acid
2. eicosapentaenoic acid (EPA)
3. myristic acid
4. stearic acid

 

 

c              156                         27.  Trans unsaturated fatty acids are now considered more atherogenic than saturated fatty acids because they

1. are unnatural and only formed during fat processing.
2. cause excess blood clotting.
3. elevate serum LDL while decreasing HDL.
4. were found to cause sudden cardiac arrest in women.

 

a              158                         28.  What is the carrier molecule needed for mitochondrial membrane transport of long-chain fatty acids and their CoA derivatives?

1. carnitine
2. creatine
3. creatinine
4. cysteine

 

c              158                         29.  What is formed when fatty acids are oxidized in the mitochondria (i.e. what is the end product of beta-oxidation)?

1. glycerol
2. pyruvate
3. acetyl CoA
4. triglyceride

 

b              158                         30.  When fatty acids are completely oxidized the end products are:

1. fatty acid and glycerol.
2. carbon dioxide, energy, and water.
3. urea and acetate.
4. carbon, hydrogen, and phosphate.

 

d             159                         31.  Ketones are produced from:

1. cholesterol.
2. hormones.
3. amino groups.
4. acetyl-CoA.

 

d             160                         32.  Ketogenesis would be the HIGHEST:

1. after a high-CHO meal.
2. after a high-protein meal.
3. after a high-fat meal.
4. during prolonged starvation.

 

c              162                         33.  What is the normal product of the fatty acid synthase system?

1. triacylglyceride
2. myristate
3. palmitate
4. butyrate

 

a              162                         34.  What is the most important unsaturated fatty acid serving as a precursor for eicosanoid synthesis?

1. arachidonic acid
2. linoleic acid
3. oleic acid
4. linolenic acid

 

b              164-165                 35.  Thromboxane A₂ is a hormone-like substance made from:

1. stearic acid.
2. arachidonic acid.
3. palmitic acid.
4. myristic acid.

 

a              164                         36.  Which group of 20-carbon fatty acid derivatives exhibit a range of physiological actions including lowering of blood pressure, diuresis, blood platelet aggregation and effects on the immune system?

1. prostaglandins
2. linoleic acid
3. palmitate
4. cholesterol

 

a              167                         37.  Which hormone is considered to be an antagonist of lipolysis?

1. insulin
2. epinephrine
3. glucagon
4. thyroxine

 

b              170                         38.  The mechanism by which Orlistat reduces absorption of dietary fat is _____

1. by replacing dietary fat with a synthetic, indigestible substitute.
2. by inhibiting the activity of pancreatic lipase.
3. by binding free fatty acids and causing their excretion.
4. by inhibiting HMG CoA reductase.

 

d             170                         39.  What is the toxic level of blood ethanol?

1. less than 10 mg/dL
2. 11 to 24 mg/dL
3. 25 to 45 mg/dL
4. 50 to 100 mg/dL

 

c              170                         40.  Which of these enzymes is the primary system for oxidizing alcohol after 1 drink?

1. catalase
2. microsomal ethanol oxidizing enzyme
3. alcohol dehydrogenase
4. aldehyde carboxylase

 

b              172                         41.  During starvation , or when following a very-low-carbohydrate diet, the consumption of alcohol may cause hypoglycemia because alcohol breakdown _____

1. depletes NADPH.
2. favors the reduction of DHAP to glycerol 3-phosphate
3. impairs the glutamate dehydrogenase reaction.
4. induces metabolic tolerance.

 

 

True/False

 

Indicate whether each of the following statements is true or false. If the statement is false, explain why it is false.

 

Key        Page(s)

F              140                         1.     Most Americans consume approximately half of their total dietary lipid as triacylglycerols, and the other half as cholesterol; very little is taken in as phospholipids.
Explanation: Dietary fat is mostly TGs (>90%).

T             134, 162-164        2.     Essential fatty acids are classified as such because we cannot synthesize them from other fatty acids and they are required for the synthesis of prostaglandins, thromboxanes, and leukotrienes.

F              160                         3.     Ketogenesis is the synthesis of ketone bodies from fatty acids for energy under conditions of excess glucose, such as in the fed state.
Explanation: Ketogenesis occurs when CHO levels are low.

T             167                         4.     HMG-CoA reductase is a key enzyme in the synthesis of cholesterol from acetyl-CoA.

F              143                         5.     Once a micelle, containing lipids and lipid-soluble compounds, enters the enterocyte, it is referred to as a chylomicron.
Explanation: A micelle delivers the FAs etc. to the enterocyte where they are taken up, reesterified to TGs by the enterocyte, and repackaged into a new lipoprotein called the CM.

T             150-153                 6.     The key organ in clearing (i.e., breaking down) lipoproteins is the liver.

T             138                         7.     One of the primary functions of a phospholipid is due to its structure, allowing it to be both hydrophobic and hydrophilic.

F              134, 162                8.     The conversion of linoleic acid (C18:2) to arachidonic acid (C20:4) involves the addition of 2 carbons to the methyl end and 2 double bonds at the n-3 and n-6 positions of the omega end.
Explanation: The addition of 2 carbons is at the carboxylic acid end and double bonds are placed no closer to the methyl carbon than the 9th carbon from the carboxylic acid end.

 

F              149                         9.     Adipocytes’ primary function is to store fat as triacylglycerol; thus they do not require glycolysis/ the TCA cycle for energy needs.
Explanation: Adipocytes are like all cells in that they require energy, and thus need glycolysis and the TCA cycle to produce ATP.

T             143                         10.  Unlike long-chain fatty acids, short-chain fatty acids from the diet leave the enterocyte via the portal vein and go directly to the liver.

F              158                         11.  Fatty acids are converted into glucose by gluconeogenesis and used for energy during starvation.
Explanation: FAs do not go to increase net glucose.

F              140                         12.  Bile is the GI enzyme that hydrolyzes dietary triacylglycerol into free fatty acids and glycerol.
Explanation: Bile is not an enzyme; lipase does this.

 

 

Matching

 

Enzymes: Match the enzymes with their functions in lipid metabolism.

 

Key	Page(s)	Enzyme	Function
b	147	1.     lipoprotein lipase	a.     creates a double bond in a fatty acid b.     removes triacylglycerol from plasma c.     mobilizes stored triacylglycerols from adipocytes d.    rate-limiting enzyme in cholesterol synthesis e.     creates prostaglandins
c	149	2.     intracellular lipase
d	167	3.     HMG CoA reductase
e	163	4.     cyclo-oxygenase
a	134	5.     desaturase

 

 

Fill-in-the-Blank

 

Page(s)

166 (T 5.5)            1.     Compounds affecting platelet anti-aggregation and aggregation are formed from the 20C:5 n-3 fatty acid. These compounds are: _____ and _____, respectively, and the locations in the body where they are produced are in _____ and _____, respectively.
Key: prostacyclin I₃, thromboxane A₃, vascular endothelium, platelets

 

Fill in the blanks with the appropriate information.

 

Process	Regulated by the hormone	Catalyzed by the enzyme	Location of the enzyme
2.             De novo lipogenesis	a.	b.	c.
3.             Lipolysis	a.	b.	c.
4.             Triglyceride storage	a.	b.	c.

 

                                Key:

161, 167                2.     a. insulin, b. acetyl CoA carboxylase and fatty acid synthase, c. adipocyte and hepatocyte cytoplasm

167                         3.     a. epinephrine or glucagon, b. hormone sensitive triacylglycerol lipase, c. adipocyte cytoplasm

149                         4.     a. insulin, b. lipoprotein lipase, c. endothelium of the capillaries

 

Usage of acetyl CoA in the cell depends on the metabolic/physiological state of humans. Identify 4 possible uses of acetyl CoA, the corresponding states of the human being and the organ and cellular locations where these processes occur.

 

Use of acetyl CoA	Metabolic/physiologic state	Organ & cellular site
5.             Ketogenesis	a.	b.
6.             a.	fed state	b.
7.             a.	b.	muscle mitochondria
8.             a.	fed state	b.

 

                                Key:

160                         5.     a. non-fed state or diabetes, b. liver mitochondria

166-167                 6.     a. Cholesterol synthesis, b. liver and intestine cytoplasm

158                         7.     a. TCA cycle oxidation, b. all the time (fed or fasted)

161                         8.     a. Free fatty acid synthesis, b. liver cytoplasm

 

166                         9.     A diet rich in simple sugars increases the hepatic formation of de novo fatty acids and then neutral lipids called _____ from glucose. These neutral lipids are transported from the liver to the adipose tissue by compound lipids called _____.
Key: triacylglycerols, VLDL

 

158                         10.  The carrier molecule required for the transport of long-chain fatty acids for fat oxidation is _____, which is located in the _____ membrane.
Key: carnitine, mitochondrial

 

145-47,150-54     11.  Lipoprotein Transport. List the four lipoproteins below and provide a BRIEF explanation of their function with respect to transportation of lipids and lipid-soluble compounds – your answer should include the tissue of origin, what they transport, and what they do with their cargo.

 

Lipoprotein	Function

 

 

Key:

Lipoprotein	Function
Chylomicron (CM)	synthesized in the enterocyte; dietary lipids (and other lipid-soluble substances from the diet) are put into the CM, which is sent first into the lymphatic system and then into the blood system to deliver its contents to tissues.
Very-low-density lipoprotein (VLDL)	synthesized in the liver; endogenous FAs are esterified to TGs and packaged in VLDL for delivery to tissues.
Low-density lipoprotein (LDL)	is the remnant of the VLDL after it has delivered its TGs; thus it contains predominantly cholesterol which it delivers to peripheral tissues for use by cells like those in the adrenal gland (to make cortisol); some LDL returns to the liver to be cleared from the circulation.
High-density lipoprotein (HDL)	are synthesized in the liver and sent out into the circulation to scavenge cholesterol and circulate back to the liver for clearance.

 

 

Short Answer (with suggested answer key)

 

Page(s)

149                         1.     Describe the process of fat storage (triacylglycerol synthesis) AND mobilization (triacylglycerol lipolysis) in adipose tissue – make sure to include how these processes are regulated (i.e., the signals involved).

Key:
Triacylglycerol synthesis – CM or VLDL, both containing TGs, deliver their contents to adipose tissue. Lipoprotein lipase is present on the capillary membrane that passes through the adipose tissue to hydrolyze the TGs inside to FAs, so they can cross the membrane and enter the adipocyte. Once inside, they are reassembled into TGs for storage. Insulin (fed state; high blood glucose) induces lipoprotein lipase activity and inhibits hormone sensitive triacylglycerol lipase (which breaks down stored TGs to FAs inside the adipocyte).

Triacylglycerol lipolysis – in the fasted state (low blood glucose), glucagon induces TG lipase – the resulting FAs in the adipocyte can leave the cell and are transported by albumin to tissues for use as energy.

[To answer this question, it is not necessary to talk about how insulin or glucagon stimulates FA synthesis or FA oxidation, respectively – just with respect to lipid storage and/or breakdown in adipose tissue.]

 

147-49,167-68     2.     A fed vs. fasted question – IN GENERAL, describe how opposing pathways are regulated during fasting vs. fed conditions. What are the primary signals involved? What would be an example of 2 opposing pathways? How is one pathway favored over the other (you don’t need to name specific proteins/ enzymes here)?

Key: A fed state is characterized by high blood glucose, which results in the pancreas releasing insulin into the circulation. Insulin promotes glucose uptake, glycolysis/TCA, glycogenesis, and lipogenesis by various mechanisms (including translocation, enzyme stimulation, enzyme induction, etc.). A fasted state is characterized by low blood glucose levels, resulting in the release of glucagon. Glucagon promotes gluconeogenesis, lipolysis, and glycogenolysis. Epinephrine also plays a role in this, but more so under exercise and stress conditions to promote glycogenolysis in muscle, rather than fasting conditions. [That was it, and that is what I meant by being general in your answer, rather than too specific with the naming of the enzymes involved in these pathways or other processes like transport.]

For both fed and fasting, all of these pathways also regulate themselves in the sense that high concentrations of products (e.g., ATP, citrate, NADH) allosterically inhibit many enzymes involved in their production, whereas high concentrations of substrates (e.g., ADP, NAD) allosterically stimulate these same enzymes.

 

168                         3.     Explain the regulation of the allosteric enzyme acetyl CoA carboxylase by citrate and palmitoyl CoA.

Key:
Citrate – allosterically stimulates acetyl CoA carboxylase to promote FA synthesis
Palmitate – allosterically inhibits acetyl CoA carboxylase in FA synthesis

 

 

Essay

 

Page(s)

133                         1.     Discuss three things that cannot be correct in the notation 18:2Δ^8,9,19 when using the delta system of designating fatty acids.[1]

149                         2.     Describe fat metabolism in the adipose cell following a meal.

161                         3.     Describe the transport system that allows for fatty acid synthesis and the molecules involved in transferring acetyl CoA into cytoplasm.

164                         4.     Prostaglandins have been described as being “hormone-like” in function. How do they actually differ from hormones?

167                         5.     Explain how the HMG CoA reductase regulates cholesterol synthesis.

168-169                 6.     Briefly describe the mechanism by which increased uncoupling protein opposes storage of energy as fat.

168,169                 7.     Aspirin at very high (acutely poisonous) doses can function to cause proton leaks from the intermembrane space back into the matrix of the mitochondria. Explain why a toddler who ate a bottle of about 50 flavored baby aspirin would develop a very high body temperature.

173                         8.     Explain the role of MEOS and cytochrome P450 in developing metabolic tolerance to ethanol.

171-173                 9.     Describe three detrimental physiological effects of excess alcohol consumption and three beneficial effects of moderate alcohol consumption.

Perspective – The Role of Lipids and Lipoproteins
in Atherogenesis

 

Multiple-Choice

 

Key        Page(s)

c              176                         1.     What are two major components implicated in the mechanism of atherogenesis?

1. growth factors and HDL
2. enterocytes and endothelial cells
3. cells of the immune system and serum lipids
4. primarily VLDL and IDL

 

d             176                         2.     Arterial fatty steaks are formed primarily due to

1. platelet aggregation at the endothelium.
2. smooth muscle proliferation.
3. toxicity of oxidized LDL to endothelial cells.
4. accumulation of foam cells filled with cholesterol.

 

a              176                         3.     Oxidized LDL is more atherogenic than native LDL because it _____

1. attracts blood monocytes into the subendothelial space.
2. oxidizes membrane fatty acids.
3. absorbs cholesterol readily to become foam cells.
4. delays clotting of platelets, which narrows the lumen, restricting blood flow.

 

 

Essay

 

Page(s)

176                         1.     Describe the mechanism by which oxidation of unsaturated fatty acids alters B-100 apoprotein on LDL to facilitate accelerated development of foam cells.

176                         2.     Discuss the factors that initiate the process that leads to plaque formation.

 

 

 

[1] Source: Brody T, Nutritional Biochemistry, 2nd ed. Academic Press, San Diego, CA, 1999. page 643.