19 Nutrition of Carbohydrates, Proteins, and Lipids (2) Flashcards Preview

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Flashcards in 19 Nutrition of Carbohydrates, Proteins, and Lipids (2) Deck (18):
1

Protein Digestion and Absorption

  • although an adult may ingest about 100 g of protein per day, the quantity digested and absorbed/
  • Desquamation of mucosal cells contributes/
  • the enzymes in the digestive juices contribute/
  • The nitrogen remaining in daily fecal material is equivalent to/
  • protein digested and absorbed each day

  • In terms of the quantity of protein digested by the gastrointestinal tract each day, although an adult may ingest about 100 g of protein per day, the quantity digested and absorbed is much greater.
  • Desquamation of mucosal cells contributes 35 g
  • the enzymes in the digestive juices contribute a further 35 g per day.
  • The nitrogen remaining in daily fecal material is equivalent to about 10 g,
  • therefore, 160 g of protein are digested and absorbed each day.

2

Protein Digestion and Absorption:
Stomach (p.39)

  • Protein digestion first begins in/
  • In order to initiate protein digestion, first it must be/
  • Exposure to an acidic environment will/
  • The stomach therefore provides/
  • The gastric chief cells secrete/
  • the parietal cells secrete/
  • The bicarbonate buffered mucus secretions of the stomach surface cells become a necessity to/

  • Protein digestion first begins in the stomach.
    • The stomach employs a complementary system of digestion.
  • In order to initiate protein digestion, first it must be denatured.
  • Exposure to an acidic environment will uncoil 4o and 3o structure.
  • The stomach therefore provides
    • the acidic compartment
    • a peptidase, pepsin, that is enzymatically active at an acidic pH.
  • The gastric chief cells secrete the inactive proenzyme pepsinogen,
  • the parietal cells secrete HCl.
  • The bicarbonate buffered mucus secretions of the stomach surface cells become a necessity to prevent self-digestion.

3

Protein Digestion and Absorption:
Pancreas (p.40)

  • Pancreatic proenzymes are emptied into/
    • Pancreatic proenzymes are emptied into/
    • Trypsin then activates/
  • Pancreatic secretions contain
    • Endopeptidases
      • Trypsin
      • Chymotrypsin
      • Elastase
    • Exopeptidases
      • Carboxypeptidases A and B
      • Carboxypeptidase A
      • Carboxypeptidase B

  • Pancreatic proenzymes are emptied into the duodenum.
    • They must encounter enterokinase, an intestinal brush border enzyme that cleaves trypsinogen.
    • Trypsin then activates the remainder of the pancreatic enzymes, as well as the brush border enzymes.
  • Pancreatic secretions contain
    • Endopeptidases
      • Trypsin: cleaves peptide bonds on the carboxyl side of basic amino acids (lysine and arginine)
      • Chymotrypsin: cleaves peptide bonds on the carboxyl side of aromatic amino acids (tryosine, phenylalanine and tryptophan)
      • Elastase: cleaves peptide bonds on the carboxyl side of aliphatic amino acids (alanine, leucin, glycine, valine, isoleucine)
    • Exopeptidases
      • Carboxypeptidases A and B: zinc-containing metallo-enzymes that remove single amino acids from the carboxyl-terminal ends of proteins and peptides.
      • Carboxypeptidase A: polypeptides with free carboxyl groups are cleaved to lower peptides and aromatic amino acids
      • Carboxypeptidase B: polypeptides with free carboxyl groups are cleaved to lower peptides and dibasic amino acids

4

Protein Digestion and Absorption:
Small Intestine (p.41-44)

  • Peptidases within the enterocyte brush-border glycocalyx/
  • About 20 peptidases have been identified, acting as/
  • Also present in the lateral edges of the microvilli are/
  • Imported di- and tri-peptides are digested in/
    • Ninety percent of absorbed amino acids are/
    • The remaining 10% are used for/
  • Protein digestion and absorption in the small intestine/

  • Peptidases within the enterocyte brush-border glycocalyx hydrolyze the oligo peptides generated by intraluminal digestion into free amino acid and di- and tri-peptides.
  • About 20 peptidases have been identified, acting as endopeptidases, exopeptidases, aminopeptidases and carboxypeptidase.
  • Also present in the lateral edges of the microvilli are the transport proteins for amino acid assimilation, often coupled with Na+ import.
  • Imported di- and tri-peptides are digested in lysosomes and exported as single amino acids.
    • Ninety percent of absorbed amino acids are released into the portal blood.
    • The remaining 10% are used for local protein synthesis and as the major respiratory fuels for the small intestine (especially glutamine, glutamate and aspartate).
  • Protein digestion and absorption in the small intestine
    • 1. brush-border membrane peptidases
    • 2. brush-border membrane amino acid transporters
    • 3. brush-border membrane di- and tripeptide transporters
    • 4. intracellular peptidases
    • 5.basolateral-membrane amino acid carriers
    • 6. basolateral membrane di- and tripeptide carriers

5

Protein Digestion and Absorption:
Portal Vein and Liver (p.45-46)

  • Assimilated amino acids are carried away by/
  • Amino acids are absorbed first by/
  • The liver synthesizes/
  • The liver also deaminates amino acids to form/

  • Assimilated amino acids are carried away by veins that coalesce to become the hepatic portal vein.
  • Amino acids are absorbed first by liver transporters.
  • The liver synthesizes all the major plasma proteins (albumin, prealbumin, transferrin, apoproteins, fibrinogen, prothrombin and alpha & beta globulins).
  • The liver also deaminates amino acids to form ammonia (NH3), which it then combines with glutamine and converts to the less toxic form, urea.

6

Utilization of Protein as an Energy Source (p.47)

  • If all the components of the body are considered strictly for their caloric value, in the average 70 kg man, the break down would be:
  • the first to be mobilized
    • However, after simply an overnight fast, these/
  • In mild starvation, liver carbohydrate reserves/
    • This limits energy supplies to/
  • In the early post absorptive period, 8-16 hours after eating, glucagon levels/
  • Although fatty acids are the highest caloric yield per weight, they cannot/
    • This means that those organs dependant on glucose metabolism: the brain, red blood cells, peripheral nerves and the renal medulla, must rely on/
  • As there are no true reserve stores of protein, only half of the potential caloric value/
    • Depletion of total body protein below 50%/
  • The first organs to manifest inadequate protein/
  • the most common cause of death in an epidemic of starvation is typically/
  • A nutritional evaluation for protein status will include/

  • If all the components of the body are considered strictly for their caloric value, in the average 70 kg man, the break down would be:
    • Triglycerides (adipose) 135,000 Calories
    • Protein (viscera & muscles) 54,000 Calories
    • Carbohydrate (liver & muscle) 1,200 Calories
  • the first to be mobilized are the glycogen stores of the liver.
    • However, after simply an overnight fast, these are nearing depletion.
  • In mild starvation, liver carbohydrate reserves are totally oxidized within three days.
    • This limits energy supplies to fats and proteins.
  • In the early post absorptive period, 8-16 hours after eating, glucagon levels begin to rise and increase lipolysis for energy, thus sparing proteins.
  • Although fatty acids are the highest caloric yield per weight, they cannot be converted to glucose.
    • This means that those organs dependant on glucose metabolism: the brain, red blood cells, peripheral nerves and the renal medulla, must rely on glucose produced via amino acid conversion through gluconeogenesis.
  • As there are no true reserve stores of protein, only half of the potential caloric value can be extracted.
    • Depletion of total body protein below 50% is incompatible with life.
  • The first organs to manifest inadequate protein are the liver and the immune system.
  • the most common cause of death in an epidemic of starvation is typically simple bacterial pneumonia.
  • A nutritional evaluation for protein status will include assessments of liver proteins, immune function and lean body mass.

7

Assessment of Protein Nutrition:
Liver (p.48)

  • Albumin 
    • accounts for/
    • contributes/
    • half-life
  • Transferrin
    • half-life
    • is increased during/
  • Prealbumin 
    • half-life
    • can be used to/
    • has been more accurately renamed/

  • Albumin
    • accounts for 50% of the proteins synthesized in the liver, totaling 20 g of albumin per day.
    • contributes essential functions as a carrier protein and as the major contribution to plasma oncotic pressure.
    • has a relatively long half-life of 20 days in circulation, and does not reflect recent alterations in nutritional status, but rather long-term shifts.
  • Transferrin
    • has a half-life of 8.8 days,
    • is increased during iron deficiency, which may accompany a decrease in protein intake.
  • Prealbumin
    • has a half-life of only 24-48 hours,
    • can be used to reflect changes in nutritional status over the short-term as patients receive therapeutic nutritional support.
    • has been more accurately renamed transthyretin to reflect its unique functions in the plasma transport of thyroxin and retinol-binding protein.

8

Assessment of Protein Nutrition:
Immune Function and Lean Body Mass (p.49-50)

  • Immune function:
    • Inadequate protein/
    • Absolute lymphocyte counts/
    • hypersensitivity reactions using skin test allergens/
    • Routine skin allergens tested are chosen based on/
    • caution must be added for those individuals with/
  • Lean Body Mass:
    • The status of lean body mass can be assessed by measuring/
    • Creatinine production is directly proportional to/

  • Immune function:
    • Inadequate protein impairs the immune system.
    • Absolute lymphocyte counts decrease significantly,
    • hypersensitivity reactions using skin test allergens are delayed.
    • Routine skin allergens tested are chosen based on the wide spread exposure to common antigens that could therefore be expected to elicit a skin reaction (tuberculin PPD, mumps, Candida albicans).
    • caution must be added for those individuals with disease states that alter the ability of the immune system to respond, such as Hodgkin’s disease or HIV.
  • Lean Body Mass:
    • The status of lean body mass can be assessed by measuring urinary creatinine excretion over 24 hours.
    • Creatinine production is directly proportional to skeletal muscle mass, provided there is no rapid turnover due to severe sepsis or trauma and verifying appropriate kidney function.

9

Lipids (p.51-53)

  • Lipids
    • ?
    • In a typical Western diet, an average adult consumes/
    • These consist primarily of/
  • Lipids serve many functions :
  • The challenge in the assimilation of lipids
    • Absorption
    • subsequent distribution of absorbed lipids throughout the body/

  • Lipids
    • hydrophobic molecules that are more soluble in organic solvents than in water.
    • In a typical Western diet, an average adult consumes 120-150 g of lipid a day.
    • These consist primarily of triglycerides (with fatty acids of at least 12 carbons) , and lesser amounts of phospholipids, plant sterols and cholesterol.
  • Lipids serve many functions :
    • Denser in caloric value than carbohydrates or protein (9 Kcal/g vs 4 Kcal/g) and serve as an important storage form of energy
    • Vitamins A,D, E, K are lipids
    • Biological membranes are built of lipids
    • Signaling molecules are derived from arachadonic acid ( a long-chain fatty acid)
    • Volatile lipids make food palatable and tasty
  • The challenge in the assimilation of lipids, is how water–soluble lipolytic enzymes access these hydrophobic molecules for digestion.
    • Absorption becomes less of a challenge because the small products of lipolysis readily diffuse across plasma membranes.
    • However, subsequent distribution of absorbed lipids throughout the body occurs via a different mechanism than carbohydrates and proteins.

10

Lipid Digestion:
Gastric Digestion (p.54-55)

  • Digestion of dietary lipids begins/
  • Shearing action, especially of the antrum, produces/
    • This increased surface area is then/
  • Gastric lipase
    • functions at/
    • is resistant to/
    • functions independent of/
    • cleaves/
  • At the acidic stomach pH, however, the free fatty acids/
  • Thus, gastric digestion of lipids/
  • In an adult, gastric digestion of lipids/
    • In neonates, however, pancreatic maturity/
    • Steatorrhea

  • Digestion of dietary lipids begins in the stomach with the powerful tituration of the gastric musculature.
  • Shearing action, especially of the antrum, produces a fine emulsion of small lipid droplets.
    • This increased surface area is then attacked by gastric lipase, a secretion of chief cells in the body/fundus of the stomach.
  • Gastric lipase
    • functions at a low pH of 4.0-5.5
    • is resistant to proteolytic cleaveage by pepsin (also released by the chief cells).
    • functions independent of any cofactors
    • cleaves triglycerides at the C1 of the glycerol backbone to produce a free fatty acid and a 2,3-diglyceride.
  • At the acidic stomach pH, however, the free fatty acids become protonated and migrate into the center of oil droplets.
  • Thus, gastric digestion of lipids is incomplete, and shields the very products that could diffuse through a plasma membrane.
  • In an adult, gastric digestion of lipids is not essential; pancreatic enzymes alone can accomplish lipid digestion.
    • In neonates, however, pancreatic maturity is often delayed and there is a much greater dependence on gastric lipase for lipid breakdown.
    • Steatorrhea (fat in the stools) is therefore common in newborns as well as in patients with pancreatic diseases.

11

Lipid Digestion:
Intestinal Digestion (p.56)

  • Acidic chyme/
  • Fatty acids now become/
  • Fatty acids in the lumen of the duodenum are a potent stimulus for the release of cholecystokinin (CCK):
    • Secreted in response to/
    • Secondary stimulus for/
    • Stimulates/
    • Decreases/
    • Relaxes/
  • Diet can affect CCK release:
    • Long-chain triglycerides/
    • Medium-chain triglycerides/
    • Oleic acid/

  • Acidic chyme is slowly released into the duodenum where it is neutralized by bicarbonate secretions from the pancreas, biliary ducts and Brunner’s glands.
  • Fatty acids now become ionized and shift to the outer surface of the oil droplet, with a few molecules dissociating and diffusing through the intestinal mucosa.
  • Fatty acids in the lumen of the duodenum are a potent stimulus for the release of cholecystokinin (CCK):
    • Secreted in response to fats (and polypeptides) in the duodenum
    • Secondary stimulus for exocrine pancreas secretion of digestive enzymes (via CCK receptors on afferents nerves to acetylcholine released from the vagus)
    • Stimulates gallbladder contraction, releasing bile into the small intestine
    • Decreases stomach contractions (slows delivery)
    • Relaxes sphincter of Oddi
  • Diet can affect CCK release:
    • Long-chain triglycerides increases CCK
    • Medium-chain triglycerides increases CCK
    • Oleic acid (major FA in olive oil) most potent stimulus for CCK release

12

Lipid Digestion:
Intestinal Digestion:
Pancreatic acinar cells produce two proteins necessary for fat digestion (p.57-58)

  • Pancreatic lipase 
    • active at/
    • cleaves/
    • Of the pancreatic enzymes, lipase is most susceptible to/
    • in a patient with pancreatic diseases/
    • colonic bacteria can digest/
    • Any reason for fat malabsorption in the small intestine results in/
  • Both gastric and pancreatic lipases are inhibited by/
    • sphincter of Oddi
  • pancreatic colipase

  • Pancreatic lipase
    • active at a neutral pH.
    • cleaves triglycerides at both the 1 and 3 site of the glycerol base forming esterified fatty acids and a 2-monoglyceride.
    • Of the pancreatic enzymes, lipase is most susceptible to degradation at an acidic pH.
    • in a patient with pancreatic diseases, where delivery of bicarbonate is restricted and lipase becomes inactivated, the earliest clinical symptom is steatorrhea.
    • colonic bacteria can digest any remaining carbohydrates, but the anaerobic nature of the colon prevents bacterial oxidation and digestion of fatty acids.
    • Any reason for fat malabsorption in the small intestine results in steatorrhea.
  • Both gastric and pancreatic lipases are inhibited by bile salts.
    • This is usually not an issue in the stomach, but pancreatic enzymes and bile share a common delivery system through the sphincter of Oddi.
  • When bile salts coat the lipid droplet, lipase is displaced.
    • The solution for this dilemma is pancreatic colipase.
    • Colipase binds to both bile acids and to lipase, locking the digestive enzyme on to the lipid surface.

13

Lipid Digestion:
Intestinal Digestion:
Two other lipolytic enzymes are synthesized by the pancreas (p.59-61)

  • Like colipase (but not lipase), they are/
  • Phospholipase A2/
  • Cholesterol esterase

  • Like colipase (but not lipase), they are secreted as pro-peptides that become activated within the duodenum.
  • Phospholipase A2 cleaves the fatty acid from the 2-position of glycerol.
  • Cholesterol esterase
    • a nonspecific enzyme capable of degrading esters of cholesterol, esters of vitamins A, D and E, as well as the total cleavage of all three fatty acids from triglycerides.
    • requires the presence of bile salts to assemble into its active tetramer.

14

Lipid Absorption:
Bile Salts (p.58)

  • Bile again plays an important role in/
  • These lipids are truly in solution within/
  • Bile mixed micelles
    • on their outer face
    • easily mix into/
  • Critical micellar concentrations of bile are the rate limiting factor in/

  • Bile again plays an important role in solubilizing the end products of lipid digestion.
  • These lipids are truly in solution within the mixed micelles, not merely emulsified into smaller droplets, as was the case in the stomach.
  • Bile mixed micelles
    • are hydrophilic on their outer face
    • easily mix into the aqueous environment of the brush border, presenting high concentrations of lipid products for uptake.
  • Critical micellar concentrations of bile are the rate limiting factor in assimilation of lipids and the fat-soluble vitamins, A, D, E and K.

15

Lipid Absorption:
Enterocyte Absorption & Re-esterification (p.61-64)

  • The products of lipid digestion diffuse/
  • Fatty acids are re-esterified into/
  • Short-chain fatty acids (< 10 C) diffuse/
  • Cholesterol uptake is also facilitated by/
  • The NPC1L1 is the target of/
  • The bile salts remain/

  • The products of lipid digestion diffuse across the apical membrane of the enterocytes.
  • Fatty acids are re-esterified into triglycerides and onto cholesterol.
    • FA + CoA + ATP --> FA-CoA + AMP + PPi (fatty acyl CoA synthetase)
    • FA-CoA + 2-monoglyceride --> TG (fatty acyl CoA transferase)
    • FA-CoA + cholesterol --> cholesterol ester (ACAT)
  • Short-chain fatty acids (< 10 C) diffuse directly into the portal blood and are carried by albumin.
  • Cholesterol uptake is also facilitated by a specific carrier, the Niemann Pick C1 Like1 (NPC1L1) transporter.
  • The NPC1L1 is the target of ezetimibe, a recently approved drug that blocks uptake of cholesterol from the small intestine.
  • The bile salts remain behind in the intestinal lumen, until the terminal ileum, where a specific enterocyte receptor binds and transcytoses the bile

16

Lipid Absorption:
Chylomicrons & Transport of Dietary Fats (p.66+68)

  • Chylomicrons are assembled in/
    • The inner core is composed of/
    • The hydrophilic outer shell is composed of/
    • The only apoprotein carried by chylomicrons upon secretion into the lymph
  • Chylomicron Composition

  • Chylomicrons are assembled in the enterocyte.
    • The inner core is composed of triglycerides, with smaller amounts of cholesterol esters and fat-soluble vitamins.
    • The hydrophilic outer shell is composed of phospholipids, free cholesterol and apoproteins.
    • The only apoprotein carried by chylomicrons upon secretion into the lymph is Apo B48.
  • Chylomicron Composition
    • Triglyceride 88%
    • Phospholipid 8%
    • Cholesterol ester 3%
    • Cholesterol 1%
    • Apoprotein 1-2%

17

Lipid Absorption:
Chylomicrons & Transport of Dietary Fats (p.69-70)

  • Chylomicrons are carried/
  • In the systemic circulation, the chylomicrons gain/
  • the types of apoproteins on all the lipoprotein particles:
    • Apo A
    • Apo B
    • Apo C
    • Apo D
    • Apo E

  • Chylomicrons are carried in the lymph to the thoracic duct and into the right atrium.
  • In the systemic circulation, the chylomicrons gain Apo E and Apo CII from HDLs.
  • the types of apoproteins on all the lipoprotein particles:
    • Apo A
      • HDL Reverse cholesterol transport 
      • (LCAT cofactor)
    • Apo B
      • LDL receptor binding and clearance(B100)
      • Chylomicron assembly (B48)
    • Apo C
      • Cofactor for LpL
    • Apo D
      • HDL cholesterol ester transfer (CETP cofactor)
    • Apo E
      • Remnant receptor binding and clearance

18

Lipid Absorption:
Chylomicrons & Transport of Dietary Fats (p.70)

  • Lipoprotein lipase (LpL)
    • ?
    • requires/
  • Triglycerides of chylomicrons (and VLDLs & IDLs)
    • ?
    • the products, FAs and glycerol, enter adipose tissue to be
  • A chylomicron remnant
    • produced by/
    • Apo CII/
    • This remnant is taken into the liver/
    • ApoE- remnant receptors are found/

  • Lipoprotein lipase (LpL)
    • an extracellular enzyme attached to the endothelial walls of capillaries, especially in adipose tissue, heart and skeletal muscle.
    • requires Apo C II as a co-factor.
  • Triglycerides of chylomicrons (and VLDLs & IDLs)
    • hydrolyzed
    • the products, FAs and glycerol, enter adipose tissue to be reconstructed and stored as triglycerides, or enter muscle to be oxidized for energy.
  • A chylomicron remnant
    • produced by further hydrolysis.
    • Apo CII is returned to HDL.
    • This remnant is taken into the liver via the ApoE- remnant receptor interaction.
    • ApoE- remnant receptors are found only in the liver.