A mixture of straight & branched-chain glucose polymers Amylase: straight Amylopectin: branched Glycogen: branched animal starch

DIGESTION & ABSORPTION I Flashcards by Lauren Nguyen

Mucosa of the small inestine

Epithelial layer: single layer of epithelial cells linked by tight junctions
- Endocrine & mucous cells
Lamina propria: connective tissue containing blood vessels, nerve fibers, and lymphatic ducts
Muscularis mucosae: thin layer of circular & longitudinal smooth muscle

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Submucosa of small inestine

Network of nerves, submucous plexus, blood, and lymphatic vessels

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Muscularis Externa of small intestine

Circular layer

Myenteric nerve plexus

Longitudinal layer

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Main layers of small intestine

Mucosa
- epithelial layer
- lamina propria
- muscularis mucosae
Submucosa - nerves, submucous plexus, blood, vessels
Muscularis externa
- circular layer
- myenteric nerve plexus
- longitudinal layer
Serosa

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Big structural & functional differences between small and large intestine

SI
- Longer
- Has more folds because it has villi
- Absorbs nutrients
LI
- Haustra
- K+ secretion

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Paneth cells are seen in small or large intestine?

Absorptive cells? Goblet cells? Stem cells? Enteric endocrine cells?

Paneth - Small

Absorptive, Goblet, Stem, and Enteric endocrine - both

Way more absorptive in the small intestine; way more goblet in large

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Gut-associated lymphoid tissue (GALT)

Organized aggregates of lymphoid tissue called Peyer patches that sample contents of intestinal lumen via endocytosis and secretes IgA

protects against pathogens
provides immunologic tolerance to dietary substances and the good bacteria in the large intestine
_{minor: mast cells can release histamine & cytokines}

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2 systems regulating GI function

Autonomic nervous system - Ach & norepinephrine

Enteric nervous system - sensory, interneurons, motor neurons; only in GI tract

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2 methods of regulating GI function

Hormones from enteroendocrine cells (G cells, I cells, S cells) in stomach & SI

Paracrine transmitters released from sensor cells to adjacent cells without entering the blood. Ex) Somatostatin & histamine

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Gastrin

Hormone family

Site of secretion

Stimuli for secretion

Actions

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Cholecystokinin (CKK)

Hormone family

site of secretion

stimuli

actions

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Secretin

Hormone family

Site of secretion

Stimuli for secretion

Actions

“fireman” alkalinizes the acidity

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Glucose-dependent insulinotropic peptide (GLIP/GIP)

Hormone family

Site of secretion

Stimuli for secretion

Actions

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Describe the structure and function of the components in a villus

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Starch

A mixture of straight & branched-chain glucose polymers

Amylase: straight
Amylopectin: branched

Glycogen: branched animal starch

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What kind of carbs can the SI absorb?

What kind of carbs can the LI absorb?

SI absorbs monosaccharides - nothing larger!

LI doesn’t absorb carbs

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Insoluble fibers are carbohydrate polymers that can’ tbe digested and get excreted

Soluble fibers are partially degraded by

enzymes from colonic bacteria

First phase of starch digestion

Luminal digestion of starch by a-amylase

Salivary amylase & *Pancreatic amylase*

hydrolyze internal a-1,4 bonds in amylose & amylopectin
CAN’T hydrolyze terminal bonds, a-1,6 bonds (branch points in amylopectin), or a-1,4 bonds immediately adjacent to a-1,6 bonds.

–> result: short oligomers of glucose

Maltose (dimer)
Malto triose (trimer)
a-limit dextrins (from amylopectin)

Second phase of starch digestion

Digestion of oligosaccharides at brushborder

Straight-chain oligomers (maltose & maltotriose)
- Digested by hydrolases:
  - glucoamylase
  - sucrase
  - isomaltase
a-limit dextrins
- Digested by isomaltase: cleaves a-1,4 and a-1,6

Result: free glucose monomers

Uptake of glucose & galactose across the enterocyte

Sodium/glucose transporter 1 (SGLT1)
1. Symporter that takes up glucose (and galactose) against its conc gradient by coupling to Na+
In the cytosol, glucose & galactose can stay for metabolism or leave across the basolateral GLUT2

Uptake of fructose across enterocytes

Why is it associated with lactose intolerance

Apical GLUT5 takes in fructose
Can stay or leave via basolateral GLUT2

Because it’s not coupled to Na+ like glucose & galactose, fructose uptake is inefficient and easily overwhelmed –> lactose-intolerance symptoms

Monosaccarides & disaccarides are completely absorbed in the SI.

The tiny amount of starch that does escape is metabolized by _____ into ____ taken up by ____

Metabolized by colonic bacteria into short chain fatty acids (acetate, proprionate, butyrate) taken up by colonic cells

Lactose intolerance

Lactase deficiency -> undigested lactose goes to the colon, where bacteria metabolize it and release gas that causes dirrhea & discomfort

Sucrase-Isomaltase deficiency

very low levels of sucrase and isomaltase activity in brush border

Glucose-galactose malabsorption syndrome

**Mutations in the SGLT1 gene** that result in a faulty or unexpressed protein or, more commonly, **failure of the protein to traffic appropriately to the apical membrane** of enterocytes. Gastrointestinal symptoms _{Oligosaccaridases are normal & fructose is well-tolerated}

3 types of enzymes that digest proteins

* **Luminal enzymes** from pancreas & stomach * Peptides -\> oligopeptides & aa * **Brush border enzymes** * Peptides -\> oligopeptides & aa * **Cytosolic enzymes** * Oligopeptides -\> aa

Name the luminal enzymes and what activates them

* _Gastric:_ Pepsinogen -\> **pepsin** 15%) * Activated by low pH * _Pancreas:_ Trypsinogen, chymotrypsinogen, proelastase, procarboxypepidase A & B -\> **Trypsin, Chymotrypsin, Elastase, Carboxypeptidases** * Activated by **trypsin** * Trypsinogen also activated by **enteropeptidase** (**enterokinase** from jejunum)

Differentiate between the endopeptidases and the exopeptidases

* **Endopeptidases** * Trypsin, Chymotrypsin, Elastase * cuts peptide bonds adjacent to specific aa --\> **oligopeptidases** * **Exopeptidases** * Carboxypeptidases A & B * cuts peptide bonds adjacent to the carboxyterminus -\> **aa**

* **Luminal proteases** convert dietary proteins to \_\_. * **Brush border peptidases** then convert those to * __ (70%) * Taken across brush border by \_\_\_ * __ (about 30%). * Taken across brush border by \_\_\_ * In the cytosol of the enterocyte, ___ are cleaved to single \_\_\_

* Luminal proteases convert dietary proteins to **oligopeptides.** * Brush border peptidases then convert oligopeptides to * **aa** (70%) * **Amino acid transporter** * **dipeptides** and **tripeptides** (30%). * **Small peptide transporter** * In the cytosol of the enterocyte, **dipeptides and tripeptides** are cleaved to single **amino acids**

Absorption of oligopeptides

1. **H+/oligopeptide cotransporter PepT1** (apical) 2. **Peptidases** in the cytoplasm digest oligpeptides -\> aa 3. **Na+/aa transporters** (basolateral) _{If free glycine is in the lumen, enterocyte absorbs it only via apical aa transporters; whereas, glycylglycine in the lumen wil also get absorbed by PepT1}

Absorption of aa across luminal membrane

**AA** enter the enterocyte via **Na-dependent (B^0,+**) and **Na-independent (b^0,+) transporters** on luminal membrane

**Peptidomimetic drugs** (antibiotics, cancer chemotherapy) are taken up by

PepT1

The movement of aa at the ___ membrane is bidirectional. Explain

basolateral membrane * aa **exit** the enterocyte via Na+-**independent** transporters * aa **enter** the enterocyte via Na+-**dependent** transporters

**Villous cells** vs **Crypt cell** How do they get their necessary aa?

**Villous cell** (absorptive): amino acid absorbed across the apical membrane are used for protein synthesis in the cell **Crypt cell** (secretory):does not absorb amino acids across the luminal side and needs to derive them from the blood across the basolateral membrane

10% of absorbed aa are used for protein synthesis in the ___ cell

villous cell

1. \_**_x_**\_ is the major apical transporter for neutral AA. 2. It is exploited by another apical transporter, \_**_y_**\_\_ which brings in \_**_z_**\_ in exchange for neutral AA. 1. Then z will exit the basolateral membrane via _w ._ 3. If y is defective, then ____ will compensate.

1. **Na-dependent B⁰** is the major apical transporter for neutral AA. 2. It is exploited by another apical transporter, **Na-independent b^0,+**which brings in **dibasic aa** & **cystine** in exchange for neutral AA. 1. Then dibasic aa & cystine will exit the basolateral membrane via **y⁺** 3. If b^0,+ is defective, then **PepT1** will compensate.

**Lysurinic protein intolerance** is assocaited with mutations in

basolateral y+L transporter

Hartnup disease

Defective **renal & intestinal B transporters** --\> **can't absorb neutral aa** * **Not protein deficient** because of normal absorption of oligopeptides * Suffer from **lack of niacin (vitamin B3)** which is synthesized from **tryptophan, a neutral aa lost in urine.**

Cystinuria

Disease caused by a defect in **renal & intestinal b⁰⁺ transporters**. Accumulation of cysteine in the urine causes kidney stones. No protein deficiency because of normal absorption of oligopeptides.