EXAM #1: BIOCHEMISTRY OF THE GI TRACT Flashcards

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
Q

What is lactose hydrolyzed into via lactase?

A

1) Glucose

2) Galactose

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26
Q

What is maltose hydrolyzed into via maltase?

A

2x Glucose

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27
Q

What is sucrose hydrolyzed to via sucrase/isomaltase?

A

1) Glucose

2) Fructose

28
Q

What transporter transports glucose across the membrane of the enterocyte for absorption?

A

Na+/Glucose cotransporter SGLT1

29
Q

What transporter transports fructose across the enterocyte membrane for absorption?

A

Facilitated diffusion transporter, GLUT5

30
Q

What is the role of Na+/K+ ATPase pumps in the absorption of monosaccharides?

A
  • Cotransporters use Na+ as the driving force

- Concentration gradient is maintained by Na+/K+ ATPase

31
Q

Which monosaccharide transporter requires ATP? Which does NOT?

A
SGLT1= ATP 
GLUT5= NO ATP
32
Q

Once monosaccharides are in the enterocyte, how do they get into the circulation?

A

Facilitated diffusion transporter, GLUT2

33
Q

Where does protein digestion begin? What enzyme?

A

Stomach via pepsin

34
Q

What activates pepsinogen into pepsin?

A

Low pH from HCl secreted via parietal cells

35
Q

What is the specific molecular function of pepsin?

A

Pepsin breaks proteins into large fragments

36
Q

What happens to proteins in the small intestine?

A

Further breakdown into amino acids, dipeptides, and tripeptides

37
Q

What pancreatic enzymes breakdown proteins in the small intestine?

A

Chymotrypsin
Trypsin
Carboxypeptidases
Elastase

38
Q

What enzymes are produced by enterocytes of the small intestine to breakdown proteins?

A

Aminopeptidase
Dipeptidase
Endopeptidase

39
Q

Which enzymes are zymogens, pancreatic proteases or small intestine proteases?

A

Pancreatic

40
Q

What is the difference between an Endoprotease and an Exoprotease? Which pancreatic proteases are Endoproteases and which are Exoproteases?

A

Endoprotease= hydrolyze internal peptide bonds

  • Trypsin
  • Chymotrypsin
  • Elastae

Exoprotease= hydrolyze only terminal peptide bonds
- CARBOXYPEPTIDASE

41
Q

What enzyme in the small intestine enterocyte beings conversion of pancreatic zymogens to active proteases?

A

Enteropeptidase

42
Q

What is the function of enteropeptiase?

A

Conversion of Trypsinogen to Trypsin

43
Q

What is the general role of the pancreatic proteases? What is the follow-up role of the proteases produced by the small intestine enterocytes?

A

Pancreatic= large fragments into oligopeptides

Small intestine= oligopeptides into di/tripeptides and amino acids

44
Q

Where does the further digestion of di/tripeptides occur?

A

Intracellularly i.e. in the enterocyte

45
Q

What prevents Trypsin activation in the pancreas?

A

Trypsin inhibitor in the pancreas

46
Q

What happens when pancreatic ducts are blocked i.e. how does this lead to acute pancreatitis?

A

Blocked ducts lead to an accumulation of Trypsinogen that overwhelms inactivating enzymes; activation occurs in the pancreas and leads to tissue damage

47
Q

What disease of the pancreas is associated with CF?

A

Pancreatic insufficiency

48
Q

How does CF lead to pancreatic insufficiency?

A

1) CFTR mutation= decreased Sodium Bicarboante
2) Dehydrates pancreatic juice/ thickens it
3) Thickened pancreatic juice reduces production of pancreatic digestive enzymes

49
Q

What is the manifestation of pancreatic insufficiency?

A

Insufficient digestion of:

1) Lipids
2) Proteins
3) Carbohydrates

Plus symptoms excess FAT in the large intestine

50
Q

Describe the etiology of Celiac Disease.

A
  • 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
Q

What transporter is present on the luminal membrane of the intestine and facilitate the uptake of amino acid, di and tripeptides?

A

SLC type transporters

52
Q

What disease does a defect in SLC3A1/7A9 result in?

A

Cystinuria

53
Q

Describe the etiology of Cystinuria.

A
  • 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
Q

What do TAGs need to be digested into for uptake?

A

2x fatty acids

1x glycerol

55
Q

What three enzymes facilitate TAG digestion? Which does the bulk of the work?

A

1) Lingual lipase
2) Gastric lipase
3) Pancreatic lipase*

*Pancreatic lipase does most of the digestion of lipids in the small intestine

56
Q

What happens to lipids in the small intestine?

A

Emulsifiaction by bile acids to prevent the formation of large lipid droplets

57
Q

What prevents pancreatic lipase from being denatured by bile acids?

A

Binding to colipase in the small intestine

58
Q

What reaction is catalyzed by pancreatic lipase?

A

Hydrolysis of 2 fatty acids from TAG to form:

  • Monoglycerol
  • 2x fatty acids
59
Q

Where are bile acids formed, stored, and secreted?

A
  • Formed= liver from cholesterol
  • Stored= gallbladder
  • Secreted= duodenum
60
Q

Where are bile acids reabsorbed for intrahepatic circulation/ recycling?

A

Ileum

61
Q

What happens to fatty acids once they are absorbed into enterocytes?

A

Resynthesis to TAG in the endoplasmic reticulum

62
Q

What happens to TAGs in the enterocyte, once they have been re-synthesized?

A

Packaging into Chylomicrons

63
Q

What apolipoprotein facilitates the packacking of TAGs into chylomicrons?

A

Apo B-48

64
Q

Where are chylomicrons secreted once formed in the enterocytes?

A

Lymphatic system

65
Q

What is Steatorrhea?

A

Lipid malabsorption resulting in increased lipids in the feces

66
Q

What are the causes Steatorrhea?

A

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