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Biochem 29

front 1

The major fat in the human diet is:
A. Cholesterol esters
B. Phospholipids
C. Triacylglycerols
D. Free fatty acids

back 1

C. Triacylglycerols

front 2

Triacylglycerols consist of three fatty acids esterified to a:
A. Glycerol backbone
B. Sphingosine backbone
C. Steroid nucleus
D. Glucose backbone

back 2

A. Glycerol backbone

front 3

The lipase secreted in the mouth is:
A. Pancreatic lipase
B. Cholesterol esterase
C. Phospholipase A2
D. Lingual lipase

back 3

D. Lingual lipase

front 4

The lipase secreted in the stomach is:
A. Lingual lipase
B. Gastric lipase
C. Pancreatic lipase
D. Phospholipase A2

back 4

B. Gastric lipase

front 5

In the intestine, fats are emulsified by:
A. Bile salts
B. Proteases
C. Bicarbonate
D. Intrinsic factor

back 5

A. Bile salts

front 6

Intestinal end products of triacylglycerol digestion are:
A. Glycerol and cholesterol
B. Phosphatidylcholine and bile
C. Ketone bodies and acetate
D. Free fatty acids, 2-monoacylglycerol

back 6

D. Free fatty acids, 2-monoacylglycerol

front 7

The intestinal hormone that stimulates gallbladder + pancreas secretion is:
A. Secretin
B. Cholecystokinin
C. Gastrin
D. Somatostatin

back 7

B. Cholecystokinin

front 8

Phospholipids are hydrolyzed in the intestinal lumen by:
A. Pancreatic lipase
B. Cholesterol esterase
C. Phospholipase A2
D. Pepsin

back 8

C. Phospholipase A2

front 9

Cholesterol esters are hydrolyzed in the intestine by:
A. Cholesterol esterase
B. Phospholipase C
C. Lipoprotein lipase
D. Acetylcholinesterase

back 9

A. Cholesterol esterase

front 10

Digestion products (FFA, cholesterol, etc.) form ____ with bile acids:
A. Liposomes
B. Chylomicrons
C. Lacteals
D. Micelles

back 10

D. Micelles

front 11

Micelles promote lipid entry mainly by interacting with the:
A. Brush border enzymes
B. Enterocyte membrane
C. Goblet cell mucus layer
D. Tight junction proteins

back 11

B. Enterocyte membrane

front 12

FFA and 2-monoacylglycerol are packaged with ____ into chylomicrons:
A. Apolipoprotein A-I
B. Apolipoprotein B-100
C. Apolipoprotein B-48
D. Apolipoprotein(a)

back 12

C. Apolipoprotein B-48

front 13

Newly formed chylomicrons are secreted first into:
A. Lymph
B. Portal vein
C. Hepatic sinusoids
D. Splenic circulation

back 13

A. Lymph

front 14

Intestinal lymph enters the bloodstream via the:
A. Cisterna chyli
B. Inferior vena cava
C. Right lymphatic duct
D. Thoracic duct

back 14

D. Thoracic duct

front 15

Chylomicrons receive which apoproteins from HDL?
A. ApoA-I and ApoB-48
B. ApoC-II and ApoE
C. ApoB-100 and ApoA-II
D. ApoE and ApoB-100

back 15

B. ApoC-II and ApoE

front 16

ApoC-II and ApoE acquisition converts chylomicrons into:
A. VLDL particles
B. LDL particles
C. Mature form
D. Remnant form

back 16

C. Mature form

front 17

ApoC-II activates which enzyme?
A. Lipoprotein lipase
B. Hormone-sensitive lipase
C. HMG-CoA reductase
D. Acetyl-CoA carboxylase

back 17

A. Lipoprotein lipase

front 18

Lipoprotein lipase is located primarily on:
A. Hepatocyte canalicular membranes
B. Enterocyte apical membranes
C. Lymphatic endothelial valves
D. Capillary endothelium, muscle/adipose

back 18

D. Capillary endothelium, muscle/adipose

front 19

LPL digestion of chylomicron triglycerides produces:
A. Cholesterol and bile acids
B. Free fatty acids and glycerol
C. Ketone bodies and lactate
D. Glucose and acetate

back 19

B. Free fatty acids and glycerol

front 20

Most released fatty acids enter nearby tissues for:
A. Bile acid synthesis
B. Urea cycle activation
C. Energy use or storage
D. DNA methylation

back 20

C. Energy use or storage

front 21

Chylomicron-derived glycerol is primarily:
A. Metabolized by the liver
B. Stored in adipose tissue
C. Excreted unchanged in urine
D. Converted to bile salts

back 21

A. Metabolized by the liver

front 22

After losing triglyceride, a chylomicron becomes:
A. HDL particle
B. VLDL particle
C. LDL particle
D. Chylomicron remnant

back 22

D. Chylomicron remnant

front 23

As triglyceride is removed, chylomicron density:
A. Decreases markedly
B. Increases
C. Stays constant
D. Becomes zero

back 23

B. Increases

front 24

The lymph system is best described as:
A. Arterioles supplying gut villi
B. Portal venous drainage network
C. Vessels around interstitial spaces
D. Coronary venous return vessels

back 24

C. Vessels around interstitial spaces

front 25

Sympathetic-chain–like lipid delivery to tissues depends critically on:
A. Capillary LPL activity
B. Gastric lipase secretion
C. RBC membrane transport
D. Cortisol receptor binding

back 25

A. Capillary LPL activity

front 26

A child has severe hypertriglyceridemia after meals. Most likely defect:
A. ApoA-I deficiency
B. ApoB-100 deficiency
C. CETP deficiency
D. ApoC-II deficiency

back 26

D. ApoC-II deficiency

front 27

Failure to form chylomicrons in enterocytes most directly implicates loss of:
A. ApoE
B. ApoC-II
C. ApoB-48
D. ApoA-II

back 27

C. ApoB-48

front 28

Thoracic duct obstruction would most directly impair:
A. Portal glucose delivery
B. Chylomicron entry to bloodstream
C. Hepatic urea production
D. Pancreatic enzyme secretion

back 28

B. Chylomicron entry to bloodstream

front 29

Lymph fluid is most similar in composition to:
A. Plasma
B. Urine
C. CSF
D. Bile

back 29

A. Plasma

front 30

Lymph differs from blood mainly because it lacks:
A. Electrolytes
B. Cells
C. Water
D. Proteins

back 30

B. Cells

front 31

Icteric yellow discoloration from bilirubin accumulation is:
A. Cholecystitis
B. Jaundice
C. Pancreatitis
D. Melena

back 31

B. Jaundice

front 32

Cholecystitis refers to:
A. Liver inflammation
B. Pancreatic inflammation
C. Gallbladder inflammation
D. Bile duct obstruction

back 32

C. Gallbladder inflammation

front 33

Amylase is produced only in:
A. Gastric glands and liver
B. Pancreas and duodenum
C. Salivary glands and pancreas acini
D. Salivary ducts and colon

back 33

C. Salivary glands and pancreas acini

front 34

Elevated lipase levels diagnose:
A. Gastritis
B. Pancreatitis
C. Cholangitis
D. Appendicitis

back 34

B. Pancreatitis

front 35

Lipases preferentially hydrolyze:
A. Aromatic fatty acids
B. Long-chain fatty acids
C. Very-long-chain fatty acids
D. Short/medium-chain fatty acids

back 35

D. Short/medium-chain fatty acids

front 36

Typical American diet calories from fat are about:
A. 18%
B. 25%
C. 38%
D. 50%

back 36

C. 38%

front 37

Recommended maximal fat intake is:
A. 10% of calories
B. 20% of calories
C. 30% of calories
D. 40% of calories

back 37

C. 30% of calories

front 38

Long-chain fatty acids predominate in:
A. Cow milk
B. Breast milk
C. Pancreatic juice
D. Bile

back 38

B. Breast milk

front 39

Dominant long-chain fatty acids in breast milk include:
A. Stearic, arachidonic, DHA
B. Palmitic, oleic, linoleic
C. Lauric, capric, butyric
D. Myristic, stearic, palmitoleic

back 39

B. Palmitic, oleic, linoleic

front 40

Infant human milk fat is readily absorbed because:
A. Bile salts are absent
B. Pancreatic lipase is high
C. Lingual/gastric lipases compensate
D. Esterases are inactive

back 40

C. Lingual/gastric lipases compensate

front 41

Bile salts are best described as:
A. Fully hydrophobic steroids
B. Amphipathic compounds
C. Purely hydrophilic ions
D. Enzyme cofactors only

back 41

B. Amphipathic compounds

front 42

Bile salts act as detergents by:
A. Destroying fatty acids
B. Binding to fat globules
C. Blocking peristalsis
D. Activating pepsin

back 42

B. Binding to fat globules

front 43

Pancreatic lipase is secreted with ____ in response to CCK:
A. Intrinsic factor
B. Secretin
C. Colipase
D. Elastase

back 43

C. Colipase

front 44

Secretin is released by the small intestine in response to:
A. Fat entering jejunum
B. Protein in ileum
C. Acid entering duodenum
D. Glucose in stomach

back 44

C. Acid entering duodenum

front 45

Secretin signals secretion of:
A. Bile acids
B. Bicarbonate
C. Pepsinogen
D. Gastrin

back 45

B. Bicarbonate

front 46

Bicarbonate raises lumen pH optimal for intestinal enzymes to:
A. pH 2
B. pH 4
C. pH 6
D. pH 8

back 46

C. pH 6

front 47

Bile salts can inhibit pancreatic lipase by:
A. Destroying colipase
B. Coating the substrate
C. Denaturing the enzyme
D. Lowering pH strongly

back 47

B. Coating the substrate

front 48

Colipase enhances lipase function by:
A. Blocking enzyme active site
B. Increasing bile salt coating
C. Relieving bile salt inhibition
D. Converting lipase to esterase

back 48

C. Relieving bile salt inhibition

front 49

Pancreatic lipase cleaves triglycerides mainly at positions:
A. 1 and 3
B. 1 and 2
C. 2 and 3
D. Only position 2

back 49

A. 1 and 3

front 50

Hydrolysis at positions 1 and 3 of triglycerides yields primarily:
A. Monoacylglycerol and FFAs
B. Glycerol and cholesterol
C. Lysophospholipid and bile
D. Fatty alcohols and ketones

back 50

A. Monoacylglycerol and FFAs

front 51

Enzymes that remove fatty acids from compounds are:
A. Kinases
B. Ligases
C. Oxidases
D. Esterases

back 51

D. Esterases

front 52

Secretin stimulates bicarbonate release from:
A. Liver, pancreas, intestinal cells
B. Colon and kidney
C. Spleen and stomach
D. Pancreas acini only

back 52

A. Liver, pancreas, intestinal cells

front 53

Acute right upper quadrant pain + fever suggests:
A. Cholecystitis
B. Pancreatitis
C. Appendicitis
D. Diverticulitis

back 53

A. Cholecystitis

front 54

Low pancreatic lipase in infants is partly offset by:
A. Pepsin secretion
B. Lingual and gastric lipase
C. Salivary amylase
D. Hepatic bile acids

back 54

B. Lingual and gastric lipase

front 55

Amphipathic bile salts contain:
A. Only hydrophobic groups
B. Only hydrophilic groups
C. Hydrophobic and hydrophilic parts
D. Only charged phosphate heads

back 55

C. Hydrophobic and hydrophilic parts

front 56

If bile salts are absent, dietary fat digestion mainly decreases due to:
A. Loss of pancreatic amylase
B. Failure of emulsification
C. Failure of lactase action
D. Excess bile inhibition

back 56

B. Failure of emulsification

front 57

Phospholipase A2 digestion produces:
A. Two free fatty acids
B. Free fatty acid + lysophospholipid
C. Cholesterol + bile acids
D. Glycerol + triglycerides

back 57

B. Free fatty acid + lysophospholipid

front 58

Micelles form when bile salts reach:
A. 1–3 mM
B. 3–5 mM
C. 5–15 mM
D. 15–30 mM

back 58

C. 5–15 mM

front 59

Bile salts recirculate to the liver via:
A. Portal venous shunt
B. Enterohepatic circulation
C. Lymphatic duct system
D. Systemic arterial supply

back 59

B. Enterohepatic circulation

front 60

Short/medium-chain fatty acid absorption does NOT require:
A. Bile salts
B. Water
C. Sodium
D. Glucose

back 60

A. Bile salts

front 61

Protein constituents of lipoproteins are:
A. Lipases
B. Esterases
C. Apolipoproteins
D. Phospholipids

back 61

C. Apolipoproteins

front 62

Apolipoproteins are synthesized mainly on:
A. Smooth ER
B. Rough ER
C. Golgi membrane
D. Mitochondria

back 62

B. Rough ER

front 63

Steatorrhea can result from insufficient:
A. Gastric acid secretion
B. Bile salt production/secretion
C. Salivary amylase production
D. Renal bicarbonate loss

back 63

B. Bile salt production/secretion

front 64

Olestra is best described as:
A. Absorbable long-chain triglyceride
B. Caloric fat emulsifier
C. Artificial noncaloric fat substitute
D. Bile salt binding resin

back 64

C. Artificial noncaloric fat substitute

front 65

Olestra yields no calories because it is:
A. Rapidly oxidized to ketones
B. Stored in adipose tissue
C. Hydrolyzed into glucose
D. Excreted intact in feces

back 65

D. Excreted intact in feces

front 66

A common side effect of olestra is:
A. Constipation
B. Bradycardia
C. Cramping and diarrhea
D. Hyperkalemia

back 66

C. Cramping and diarrhea

front 67

Chylomicrons float in plasma after centrifugation because they are:
A. Most dense particles
B. Least dense particles
C. Neutral density particles
D. High protein particles

back 67

B. Least dense particles

front 68

Chylomicrons are least dense because they have:
A. High triacylglycerol content
B. High cholesterol content
C. High phospholipid content
D. High protein content

back 68

A. High triacylglycerol content

front 69

Heparin dislodging LPL causes plasma:
A. Triglycerides to increase
B. Triglycerides to decrease
C. HDL protein to decrease
D. LDL to disappear

back 69

A. Triglycerides to increase

front 70

Chylomicrons appear in blood about:
A. 10–20 minutes
B. 1–2 hours
C. 4–6 hours
D. 12–24 hours

back 70

B. 1–2 hours

front 71

HDL contains the highest:
A. Triglyceride concentration
B. Cholesterol ester fraction
C. Protein concentration
D. Phospholipid concentration

back 71

C. Protein concentration

front 72

HDL also has the lowest:
A. Protein concentration
B. Triglyceride concentration
C. Cholesterol concentration
D. Phosphate concentration

back 72

B. Triglyceride concentration

front 73

Chylomicron triglycerides are digested by:
A. Hormone-sensitive lipase
B. Hepatic lipase
C. Lipoprotein lipase
D. Gastric lipase

back 73

C. Lipoprotein lipase

front 74

LPL is bound to endothelial basement membranes via:
A. Myosin filaments
B. Proteoglycans
C. Actin microtubules
D. Collagen IV pores

back 74

A. Myosin filaments

front 75

LPL is produced primarily by:
A. Liver and brain cells
B. Kidney and spleen cells
C. Adipose, muscle, mammary cells
D. Erythrocytes and platelets

back 75

C. Adipose, muscle, mammary cells

front 76

After a meal, LPL activity is highest in:
A. Adipose tissue
B. Cardiac valves
C. Renal cortex
D. Skeletal bone

back 76

A. Adipose tissue

front 77

Adipose LPL synthesis is stimulated by:
A. Glucagon
B. Epinephrine
C. Insulin
D. Cortisol

back 77

C. Insulin

front 78

A weight loss strategy targets inhibition of:
A. Bile salt transport
B. Pancreatic lipase
C. Lingual lipase
D. LPL at capillaries

back 78

B. Pancreatic lipase

front 79

Orlistat is a drug that inhibits:
A. Pancreatic lipase
B. Cholesterol esterase
C. Phospholipase A2
D. Lipoprotein lipase

back 79

A. Pancreatic lipase

front 80

Orlistat is derived from lipostatin, a natural inhibitor from:
A. Viruses
B. Bacteria
C. Fungi
D. Helminths

back 80

B. Bacteria

front 81

Alcohol-induced pancreatitis can occur due to:
A. Gallstone in cystic duct
B. Proteinaceous duct plugs
C. Excess bicarbonate secretion
D. Low pancreatic enzyme levels

back 81

B. Proteinaceous duct plugs

front 82

Proteinaceous plugs cause pancreatic injury by:
A. Decreasing enzyme synthesis
B. Back pressure and autodigestion
C. Increasing insulin secretion
D. Blocking bile salt recycling

back 82

B. Back pressure and autodigestion

front 83

Steatorrhea from bile salt deficiency is most likely due to:
A. Impaired micelle formation
B. Excess protein synthesis
C. Excess glucose absorption
D. Enhanced pancreatic lipase

back 83

A. Impaired micelle formation

front 84

A patient can taste olestra but gains no calories because:
A. It blocks insulin secretion
B. It is not metabolized
C. It converts to ketones
D. It binds bile salts strongly

back 84

B. It is not metabolized

front 85

Intestinal lymph enters bloodstream via the:
A. Portal vein
B. Hepatic vein
C. Right lymphatic duct
D. Thoracic duct

back 85

D. Thoracic duct

front 86

Chylomicron assembly in enterocyte ER requires:
A. MTP
B. LCAT
C. CETP
D. ApoA-I

back 86

A. MTP

front 87

Absent triglyceride transfer activity causes:
A. Tangier disease
B. Abetalipoproteinemia
C. Familial hypercholesterolemia
D. Type I hyperlipoproteinemia

back 87

B. Abetalipoproteinemia

front 88

MTP deficiency impairs assembly of:
A. LDL only
B. HDL only
C. Chylomicrons and VLDL
D. VLDL and LDL

back 88

C. Chylomicrons and VLDL

front 89

A child with abetalipoproteinemia most likely has:
A. Steatorrhea and vomiting
B. Jaundice and pruritus
C. Hematemesis and melena
D. Polyuria and polydipsia

back 89

A. Steatorrhea and vomiting

front 90

Intestinal phospholipid digestion uses:
A. Pancreatic lipase
B. Cholesterol esterase
C. Phospholipase A2
D. Lingual lipase

back 90

C. Phospholipase A2

front 91

Chylomicron triglycerides are hydrolyzed by:
A. Gastric lipase
B. Phospholipase A2
C. Cholesterol esterase
D. LPL

back 91

D. LPL

front 92

LPL action on chylomicrons yields:
A. Cholesterol and bile salts
B. Fatty acids and glycerol
C. Ketones and acetate
D. Glucose and lactate

back 92

B. Fatty acids and glycerol

front 93

Amylase is made only by:
A. Liver and bile ducts
B. Salivary glands and pancreas
C. Stomach and duodenum
D. Colon and ileum

back 93

B. Salivary glands and pancreas

front 94

Parotid swelling with high amylase suggests:
A. Pancreatitis
B. Appendicitis
C. Cholecystitis
D. Mumps

back 94

D. Mumps

front 95

Pancreatic amylase is produced by:
A. Acinar cells
B. Islet beta cells
C. Duct epithelial cells
D. Stellate cells

back 95

A. Acinar cells

front 96

Lingual/gastric lipases prefer hydrolyzing:
A. Very-long-chain fatty acids
B. Odd-chain fatty acids
C. Short/medium-chain fatty acids
D. Polyunsaturated fatty acids

back 96

C. Short/medium-chain fatty acids

front 97

Pancreatic lipase is co-secreted with:
A. Colipase
B. Enteropeptidase
C. Intrinsic factor
D. Pepsinogen

back 97

A. Colipase

front 98

CCK release from intestine stimulates:
A. Secretin and bicarbonate
B. Gastrin and acid secretion
C. Histamine release from ECL
D. Lipase and colipase secretion

back 98

D. Lipase and colipase secretion

front 99

Bile salts inhibit pancreatic lipase by:
A. Lowering intestinal pH
B. Denaturing lipase enzyme
C. Coating the substrate surface
D. Blocking lipase gene transcription

back 99

C. Coating the substrate surface

front 100

Bile salts are reabsorbed mainly in:
A. Ileum
B. Duodenum
C. Jejunum
D. Colon

back 100

A. Ileum

front 101

C4–C12 fatty acids can absorb without:
A. Micelles
B. Bile salts
C. Water
D. Sodium

back 101

B. Bile salts

front 102

Protein components of lipoproteins are:
A. Apolipoproteins
B. Triacylglycerols
C. Steroid esters
D. Bile acids

back 102

A. Apolipoproteins

front 103

Heparin reduces LPL activity by:
A. Increasing ApoC-II binding
B. Dislodging LPL from capillaries
C. Blocking LPL gene expression
D. Enhancing LPL proteolysis

back 103

B. Dislodging LPL from capillaries

front 104

Heparin dislodging LPL causes plasma:
A. Triglycerides to increase
B. Triglycerides to decrease
C. HDL protein to decrease
D. LDL to disappear

back 104

A. Triglycerides to increase

front 105

A noncaloric fat substitute is:
A. Cholic acid
B. Colipase
C. Lipostatin
D. Olestra

back 105

D. Olestra

front 106

Olestra allows fat taste but:
A. Raises amylase strongly
B. Requires bile salts absorption
C. Adds no dietary fat calories
D. Activates pancreatic lipase

back 106

C. Adds no dietary fat calories

front 107

Which statement best fits abetalipoproteinemia?
A. ApoE deficiency impairs remnants
B. CETP mutation raises HDL
C. MTP loss blocks chylomicrons
D. LCAT loss lowers HDL

back 107

C. MTP loss blocks chylomicrons

front 108

VLDL assembly fails in abetalipoproteinemia because:
A. LDL receptors are absent
B. ApoA-I cannot form HDL
C. CETP cannot exchange lipids
D. Hepatic MTP-dependent transfer fails

back 108

D. Hepatic MTP-dependent transfer fails

front 109

Loss of chylomicron formation causes:
A. Increased LDL cholesterol
B. Lipid malabsorption with steatorrhea
C. Hyperglycemia after meals
D. Respiratory alkalosis at rest

back 109

B. Lipid malabsorption with steatorrhea

front 110

LPL-mediated triglyceride removal mainly supports:
A. Fatty acid uptake by tissues
B. Bile salt formation in liver
C. Glucose entry into enterocytes
D. Protein digestion in lumen

back 110

A. Fatty acid uptake by tissues