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SF4 - Test 1 > 2 - Digestion and Absorption of Carbs, Proteins, Lipids, Iron > Flashcards

2 - Digestion and Absorption of Carbs, Proteins, Lipids, Iron Flashcards

1
Q

Objectives: Describe how carbohydrates are digested and absorbed

Digestion

Starches

Sucrose

Lactose

Trehalose

Cellulose

A
  • Carbohydrates must be digested into monosaccharides before being absorbed
  • Starches (Amylopectin / Amylose)
    • Converted by Salivary and Pacreatic a-amylase to maltose, maltotriose, and a-limit dextrins
    • Hydrolyzed to glucose by glucoamylase, isomaltase, and maltase in brush border membrane
  • Sucrose
    • Cleaved by sucrase in brush border to glucose/fructose
  • Lactose
    • Cleaved by lactase in brush border to glucose/galactose
  • Trehalose (glucose dimer)
    • Cleaved by trehalase in brush border to glucose
  • Cellulose
    • Not digested by human enzymes
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2
Q

Objectives: Describe how carbohydrates are digested and absorbed

Absorption

Glucose / Galactose

Fructose

A
  • Intestine will only absorb monosaccharides (glucose, galactose, fructose)
  • Glucose / Galactose:
    • ​Absorbed into enterocyte by common Na+-dependent active transport system (SGLT-1)
    • Almost all absorbed in intestine
    • Cell to blood via facilitated diffusion
  • Fructose:
    • ​Cannot be absorbed against concentration gradient
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3
Q

Objectives: Describe how carbohydrates are digested and absorbed

Clinical Disorders

Lactose Intolerance

Sucrase-Isomaltase Deficiency

Glucose / Galactose Malabsorption

A
  • Lactose Intolerance
    • Deficiency in lactase
    • Lactose remains in GI tract; leads to diarrhea
    • Colonic bacteria metabolize; leads to gas
  • Sucrase-Isomaltase Deficiency
    • Inherited disorder, cannot digest sucrose/isomaltase
  • Glucose / Galactose Malabsorption
    • Genetic defect in SGLT1
    • Cannot absorb glucose / galactose
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4
Q

Objectives: Describe how proteins are disgested and absorbed

Overview

Sources

A
  • Sources:
    • Endogenous - Secretory proteins and cells shed into GI tract lumen
    • Exogenous - Dietary proteins
  • Proteins absorbed as amino acids, dipeptides, and tripeptides; larger peptides poorly absorbed
  • All ingested protein assimilated
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5
Q

Objectives: Describe how proteins are disgested and absorbed

Digestion

Endopeptidases

Pepsin, Trypsin - Role of Enterokinase?

A
  • Endopeptidases - Hydrolyze Interior Peptide Bonds
    • ​Pepsin digests small amount of ingested protein
    • Pancreatic Enymes secreted as Inactive precursors
      • Trypsinogen converted to trypsin by enterokinase, secreted by brush border in small intestine
      • Trypsin autocatalyzes:
        • ​Trypsinogen
        • Chrymotrypsin
        • Elastase
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6
Q

Objectives: Describe how proteins are disgested and absorbed

Exopeptidases

A
  • Exopeptidase: Hydrolyze ONE amino acid at a time from C-terminus of proteins and peptides
    • ​Carboxypeptidases A and B
    • Secretec from pancrease as proenzymes
    • Trypsin activates
  • Peptidases in brush border cleave peptides produced by pancreatic proteases to oligopeptides and amino acids
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7
Q

Objectives: Describe how proteins are disgested and absorbed

Absorption; Transport Mechanism(s)+Method(s)?

Enterocytes: Di- and Tri- Peptide Absorption; Transporter

Food Allergies

A
  • Most amino acid absorbed into enterocytes by Na-Depenent Co-transport
  • Separate tx for Neutral, Acidic, Basic, and Imino Amino Acids
  • Transported via facilitated diffusion
  • Enterocytes:
    • Transport of di- and tri- peptides faster, more efficient
      • ​Uses H+ dependent co-transporter (PEPT1)
      • Majority of protein absorbed in di- tri- peptides
    • Peptides hydrolyzed to amino acids by cytoplasmic peptidases
  • Whole proteins can lead to food allergies
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8
Q

Objectives: Describe how proteins are disgested and absorbed

Abnormalities

A
  • Trypsin Deficiency
    • Congenital lack of trypsin or pancreatic disease
  • Defect in Transport
    • ​Cystinuria - Basic Amino Acids (Aginine, Lysine, Ornithine)
    • Hartnup Diease - Neutral Amino Acids
    • Familial Iminoglycinuria - Proline, Hydroxyproline
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9
Q

Objectives: Descrie how lipids are digested and absorbed

Digestion overview (stomach)

What is key hormone to ensure lipids are given time to digest?

A
  • Lipids must be made water soluble before they can be absorbed
  • Digestion:
    • Lipids will separate out into oily phase
    • Stomach mixing breaks into droplets (increase total surface area)
    • CCK slows gastric emptying to allow sufficient time for digestion and absorption in duodenum
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10
Q

Objectives: Descrie how lipids are digested and absorbed

Small Intestine

Pancreatic Enzymes: Pancreatic Lipse, Cholestero ester Hydrolase, Phospholipase A2, Colipase

A
  • Emulsification: Neurtal / Alkaline Environment
    • Detergent action of bile salts, lecithin, and increased surface area
  • Pancreatic Enzymes: Hydrolyze lipids
    • Pancreatic Lipase
      • ​Cleaves fatty acids from 1 / 3 position in TAGs
      • = 2x FAs , 2-monoglyceride
      • Requires Colipase
    • Cholesterol Ester Hydrolase
      • ​Cleaves fatty acid from cholesterol ester
      • = Cholesterol, 1x FA
    • Phospholipase A2
      • ​Releases FA from 2 position in phospholipids
      • = 1x FA, lysophospholipid
    • Colipase (inactive) - Needed for Pancreatic Lipase
      • Activated by trypsin
      • Prevents inhibition of pancreatic lipase by bile salts
      • Acts as anchor for lipase; binds 1:1 ratio
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11
Q

Objectives: Descrie how lipids are digested and absorbed

Absorption

A
  • Emulsified products of lipolysis form water-soluble mixed micelles with bile
  • Bring into contact with microvilli on surface of enterocytes
  • Diffuse across luminal membrane into cells
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12
Q

Objectives: Descrie how lipids are digested and absorbed

Intracellular Processing

Monoglyceride Acylation Pathway

Phosphatidic Acid Pathway

Lysophospholipid Combination

Cholesterol

A
  • Enterocytes:
    • Products (think TAG building blocks) reesterified to TAGS and Phospholipids
  • Monoglyceride Acylation Pathway
    • TAGs synthesized from 2-monoglycerides and CoA-activated FAs
    • Reesterification in smooth ER
    • ***Medium-Chain FAs absorbed directly into bloodstream w/out resynthesis into TAG***
  • Phosphatidic Acid Pathway
    • 2-Acyl CoA + a-Glycerophosphate to Phosphatidic Acid
    • Phsphatidic Acid + Acyle CoA to TAG + P
  • Lysophospholipid
      • FA = Phospholipid
  • Cholesterol
    • Absorbed in free form
    • Reesterified with FA in enterocytes
    • Both free, reesterified TX’ed in chylomicron
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13
Q

Objectives: Describe how the products of lipid digestion are normally processed

Chylomicron Formation

Chylomicron Transportatio

A
  • Resynthesized TAGs, Cholesterol / Cholesterol Esters, and Phospholipids form Chylomicrons
    • ​Core: TAGs, Esterefied Cholesterol, Fat-Soluble Vitamins
    • Surface: Phospholipids, Apoproteins, Free Cholesterol
  • Transportation
    • Out of Cell: Exocytosis
    • Lymphatic System: Enter via gaps between endothelial cells
    • Larger Than Capillaries?
      • Reach blood via thoracic duct
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14
Q

Objectives: Describe how the products of lipid digestion are normally processed

Lipid Malabsorption: Steatorrhea

Causes:

Failure of Digestion

Absence of Bile Salts

Defect in Absorbing Cells

Failure of Synthesis of Apoproteins

A
  • Steatorrhea: Excretion of high fat in feces
  • Failure of Digestion
    • Pancreatic enzymes not secreted
    • Pancreatitis, Pancreatic Cancer, Cystic Fibrosis
  • Absence of Bile Salts
    • Liver disease, obstruction of bile ducts (gallstones), bacterial obergrowth in small intestine, low diodenum pH
    • Treated with feeding of medium chain FAs (absorbed directly into bloodstream)
  • Defect in Absorbing Cells
    • Tropical Sprue
    • Gluten Enteropathy / Celiac Sprue
      • Gluten Allergy
      • Loss of villi lining small intestine
      • Malabsorption of carbs, proteins
      • Treated by gluten free diet
  • Failure of Synthesis of Apoproteins
    • ApoB protein component of chylomicron not synthesized
    • Chylomicrons do not form, or cannot be transported
    • Fats, Cholesterol, Fat-soluble vitamins not absorbed
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15
Q

Objectives: Describe how iron stores are regulated

Background

Heme Iron vs Free Iron (two forms)

Digestion, Transport

A
  • Background
    • Amount absorbed = Amount lost
    • Absorbed as heme (bound to hemoglobin or myoglobin from meat) or as free iron
  • Heme Iron
    • Most easily absorbed
    • Taken up by endocytosis or TX protein (HCP1)
    • Heme broken down by heme-oxygenase to release free iron
  • Free Iron
    • Forms:
      • Ferrous (Fe2+) - easier absorption
      • Ferric (Fe3+) - insoluble; ppt easily; most dietary iron
    • Digestion:
      • Gastric acid dissolves iron; complexes with Ascorbic Acid (Vitamin C)
        • ​Vit C reduces Ferric to Ferrous
      • Dcytb (Duodenal Cytochrome b) reduces ferric to ferrous
    • Transportation:
      • Ferrous Iron - DMT1 Transporter
      • Binds to Apoferritin as Ferritin for storage (prevents toxicity)
      • May be transported out by ferroportin
      • Converted to ferric iron to bind to plasma protein for TX to other tissues
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16
Q

Objectives: Describe how iron stores are regulated

Regulation

A
  • Absorption is regulated
  • Hepcidin: Liver derived peptide for regulation
    • Regulates entry of iron into plasma by binding ferroportin–blocks cellular iron export and reduces plasma iron
    • Iron Low = Hepcidin Low
      • ​Increased asorption and elevated iron release from enterocytes
    • Iron High = Hepcidin High
      • ​Decrease export of iron from enterocytes; enterocytes containing ferritin bound iron lost into intestin
17
Q

Objectives: Describe how iron stores are regulated

Disorders

A
  • Iron Deficiency very prevalent globally; most common cause of anemia
  • Hemochromatosis: Chronic Absorption
    • Hereditary = most common genetic disorder
    • Defect in HFE gene causes hepcidin levels to drop
    • Excess iron collects in liver; cirrhosis; eventually cancer
    • Diabetes (damages pancrease)
    • Coronary disease
    • Must periodically remove blood
18
Q

What occurs as the GI tract ages?

A
  • Mouth
    • Lose taste, muscles of mastication weakened, lose teeth
  • Esophagus
    • Harder to swallow, LES f(x) declines
  • Stomach
    • Lose parietal cells, increased ulcers from NSAIDs
  • Small Intestine
    • Decrease in motility, increase malabsorption
  • Colon
    • Decrease in motility, increase in polyps
19
Q
A

SF4 - Test 1 (18 decks)

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