Biochem 29 Flashcards

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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