EXAM #1: BIOCHEMISTRY OF THE GI TRACT Flashcards

(66 cards)

1
Q

What enzymes are contained in the mouth that begin the breakdown of food?

A

1) Alpha-amylase

2) Lingual lipase

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2
Q

What is the function of alpha-amylase?

A

Breakdown of starch in the mouth

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3
Q

What is the function of lingual lipase?

A

Breakdown of TAGs in the mouth

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4
Q

What macronutrient is NOT brokendown in the mouth?

A

Protein

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5
Q

What are the components of gastric juice that breakdown food?

A

1) HCl

2) Pepsin

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6
Q

What is the inactive zymogen form of pepsin?

A

Pepsinogen

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7
Q

What converts pepsinogen into its active form?

A

Secretion of HCl that lowers the pH of the gastric juice

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8
Q

What are the three functions of HCl in the stomach?

A

1) Initial breakdown of protein
2) Activation of pepsinogen to pepsin
3) Kill microorganisms

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9
Q

What enzymes are produced by the pancreas?

A

Amylase
Lipase
Peptidase

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10
Q

In addition to enzymes, what else does the pancreas secrete?

A

NaCl

NaHCO3

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11
Q

What pancreatic enzyme is secreted in its active form?

A

Pancreatic alpha-amylase

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12
Q

What is the function of bile acids?

A

Emulsificaiton of aggregated lipids to make them more accessible for lipid digestion enzymes

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13
Q

What form must carbohydrates be absorbed in in the small intestine?

A

Monosaccharide

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14
Q

What are the common sources of glucose?

A

Honey
Fruit
Corn syrup

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15
Q

What are the common sources of fructose?

A

Honey

Fruit

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16
Q

What is the common source of sucrose?

A

Table sugar

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17
Q

What is amylose?

A

Plant carbohydrate/ starch with alpha 1,4 glycosidic bonds

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18
Q

What is amylopectin?

A

Plant carbohydrate/starch with alpha 1,4 glycosidic bonds AND alpha 1,6 branches

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19
Q

What is the specific molecular function of alpha-amylase?

A

Hydrolysis of non-terminal alpha-1,4 linkages

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20
Q

What is the function of pancreatic alpha-amylase?

A

Conversion of branched polysaccharides into oligosaccharide units in the small intestine

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21
Q

What are the end products of pancreatic alpha-amylase digestion?

A

1) Maltose
2) Maltotriose
3) alpha-limit dextrins

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22
Q

What is cellulose? Why can’t humans breakdown cellulose?

A

Polysaccharide plant cell wall component with BETA 1,4 GLYCOSIDIC BONDS

**Humans don’t have BETA 1,4 ENDOGLYOCSIDASES to breakdown cellulose

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23
Q

What is Chitin? Why can’t humans breakdown Chitin?

A

Polymer of N-acetyl-glucosamine with Beta 1,4 Glycosidic bonds that we do not have the enzymes to breakdown

Comes from fungi and arthropods*

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24
Q

How are the oligosaccharides made by alpha-amylase broken down into monosaccharides?

A

Membrane bound glycosidases on the luminal side of small intestine enterocytes

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25
What is lactose hydrolyzed into via lactase?
1) Glucose | 2) Galactose
26
What is maltose hydrolyzed into via maltase?
2x Glucose
27
What is sucrose hydrolyzed to via sucrase/isomaltase?
1) Glucose | 2) Fructose
28
What transporter transports glucose across the membrane of the enterocyte for absorption?
Na+/Glucose cotransporter SGLT1
29
What transporter transports fructose across the enterocyte membrane for absorption?
Facilitated diffusion transporter, GLUT5
30
What is the role of Na+/K+ ATPase pumps in the absorption of monosaccharides?
- Cotransporters use Na+ as the driving force | - Concentration gradient is maintained by Na+/K+ ATPase
31
Which monosaccharide transporter requires ATP? Which does NOT?
``` SGLT1= ATP GLUT5= NO ATP ```
32
Once monosaccharides are in the enterocyte, how do they get into the circulation?
Facilitated diffusion transporter, GLUT2
33
Where does protein digestion begin? What enzyme?
Stomach via pepsin
34
What activates pepsinogen into pepsin?
Low pH from HCl secreted via parietal cells
35
What is the specific molecular function of pepsin?
Pepsin breaks proteins into large fragments
36
What happens to proteins in the small intestine?
Further breakdown into amino acids, dipeptides, and tripeptides
37
What pancreatic enzymes breakdown proteins in the small intestine?
Chymotrypsin Trypsin Carboxypeptidases Elastase
38
What enzymes are produced by enterocytes of the small intestine to breakdown proteins?
Aminopeptidase Dipeptidase Endopeptidase
39
Which enzymes are zymogens, pancreatic proteases or small intestine proteases?
Pancreatic
40
What is the difference between an Endoprotease and an Exoprotease? Which pancreatic proteases are Endoproteases and which are Exoproteases?
Endoprotease= hydrolyze internal peptide bonds - Trypsin - Chymotrypsin - Elastae Exoprotease= hydrolyze only terminal peptide bonds - CARBOXYPEPTIDASE
41
What enzyme in the small intestine enterocyte beings conversion of pancreatic zymogens to active proteases?
Enteropeptidase
42
What is the function of enteropeptiase?
Conversion of Trypsinogen to Trypsin
43
What is the general role of the pancreatic proteases? What is the follow-up role of the proteases produced by the small intestine enterocytes?
Pancreatic= large fragments into oligopeptides Small intestine= oligopeptides into di/tripeptides and amino acids
44
Where does the further digestion of di/tripeptides occur?
Intracellularly i.e. in the enterocyte
45
What prevents Trypsin activation in the pancreas?
Trypsin inhibitor in the pancreas
46
What happens when pancreatic ducts are blocked i.e. how does this lead to acute pancreatitis?
Blocked ducts lead to an accumulation of Trypsinogen that overwhelms inactivating enzymes; activation occurs in the pancreas and leads to tissue damage
47
What disease of the pancreas is associated with CF?
Pancreatic insufficiency
48
How does CF lead to pancreatic insufficiency?
1) CFTR mutation= decreased Sodium Bicarboante 2) Dehydrates pancreatic juice/ thickens it 3) Thickened pancreatic juice reduces production of pancreatic digestive enzymes
49
What is the manifestation of pancreatic insufficiency?
Insufficient digestion of: 1) Lipids 2) Proteins 3) Carbohydrates Plus symptoms excess FAT in the large intestine
50
Describe the etiology of Celiac Disease.
- Exact cause is unknown, but there is a peptidase defect - Small peptides are present in the intestine that are toxic to mucosal cells - Ingestion of gluten causes an inflammatory response
51
What transporter is present on the luminal membrane of the intestine and facilitate the uptake of amino acid, di and tripeptides?
SLC type transporters
52
What disease does a defect in SLC3A1/7A9 result in?
Cystinuria
53
Describe the etiology of Cystinuria.
- Defect in the amino acid transporter that catalyzes the reuptake of cystine in the kidney - Cystine accumulates in the urine - Cytine is insoluble and forms kidney stones
54
What do TAGs need to be digested into for uptake?
2x fatty acids | 1x glycerol
55
What three enzymes facilitate TAG digestion? Which does the bulk of the work?
1) Lingual lipase 2) Gastric lipase 3) Pancreatic lipase* *Pancreatic lipase does most of the digestion of lipids in the small intestine
56
What happens to lipids in the small intestine?
Emulsifiaction by bile acids to prevent the formation of large lipid droplets
57
What prevents pancreatic lipase from being denatured by bile acids?
Binding to colipase in the small intestine
58
What reaction is catalyzed by pancreatic lipase?
Hydrolysis of 2 fatty acids from TAG to form: - Monoglycerol - 2x fatty acids
59
Where are bile acids formed, stored, and secreted?
- Formed= liver from cholesterol - Stored= gallbladder - Secreted= duodenum
60
Where are bile acids reabsorbed for intrahepatic circulation/ recycling?
Ileum
61
What happens to fatty acids once they are absorbed into enterocytes?
Resynthesis to TAG in the endoplasmic reticulum
62
What happens to TAGs in the enterocyte, once they have been re-synthesized?
Packaging into Chylomicrons
63
What apolipoprotein facilitates the packacking of TAGs into chylomicrons?
Apo B-48
64
Where are chylomicrons secreted once formed in the enterocytes?
Lymphatic system
65
What is Steatorrhea?
Lipid malabsorption resulting in increased lipids in the feces
66
What are the causes Steatorrhea?
1) Disruption in delivery of bile acids to the duodenum 2) Compromised pancreas function e.g. CF 3) Defective intestinal mucosa 4) Products such a Olestra, a fat substitute that cannot be digested