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PHSI 208 - Resp., Renal, Acid/Base, Blood, GI, Repro. > GI Tract Lectures (8) > Flashcards

GI Tract Lectures (8) Flashcards

1
Q

Primary function of the gastrointestinal tract?

GI1

A

move nutrients, water and electrolytes from external enviro (lumen of GI) into body’s internal enviro

  • central to regulation and integration of metabolic processes throughout body (whole-body homeostasis)
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2
Q

Anatomy involved in the GI tract?

GI1

A
  • long tube with muscular walls lined by transporting/secretory epithelial cells
  • mouth –> esophagus –> stomach –> SI -> LI -> anus
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3
Q

Digestion is?

GI1

A

mechanical/chemical breakdown of food joined by secretions from accessory glandular organs (salivary glands, liver, gallbladder, pancreas)

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4
Q

Digestion begins in the ___ with _____.

GI1

A

Begins in the mouth with mastication (chewing breaks down big macro’s) and addition of saliva

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5
Q

4 functions of 3 pairs of salivary glands?

GI1

A
  • moisten and lubricate food
  • amylase: partially digests polysaccharides into simpler CHOs
  • dissolve some food molecules
  • Lysozyme: kills bacteria immunoglobulins with some saliva
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6
Q

3 types of salivary glands and their location?

GI1

A

Parotid - upper jaw (by place where your contour goes)
Sublingual - under tongue
Submandibular - under jaw bond (by chin)

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7
Q

Esophagus basic info
- sphincters
- type of muscle in walls
GI1

A
  • passageway mouth-stomach
  • upper esophagus sphincter: lowers during swallowing
  • lower/cardiac esophageal sphincters: lets food into stomach, prevents backflow
  • top 1/3 of esophagus is skeletal muscle voluntary
  • bottom 2/3 is smooth muscle **once distention occurs in walls, peristaltic waves occur to move food down into stomach
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8
Q

Why is swallowing considered a reflex?

GI1

A

initiated voluntarily, then cannot stop it as peristaltic contractions take over
- moves to smooth muscle (non-voluntary control)

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9
Q

Parts of the stomach

GI1

A

fundus –> body –> antrum –> valve (pylorus) sphincter

contains gastric folds known as RUGAE (inc SA)

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10
Q

Digestion occuring in stomach mixes food with acid and enzymes, creating ____.
GI1

A

Chyme

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11
Q 
Pylorus sphincter (valve) function?
GI1
A

permits slow movements of chyme from stomach into SI

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12
Q

Small intestine basics

GI1

A
  • majority of digestion occurs here, 9ft long in live person
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13
Q

Small intestine parts

GI1

A
  • Duodenum (25cm) w sphincter where exocrine secretions from liver/pancreas enter. empties into:
  • Jejunum –> ileum (remaining 8ft): mechanically/chemically breakdown chyme in circular contractions
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14
Q

Large Intestine basics and parts

GI1

A
  • larger diameter, shorter than SI (150cm)
  • Ileocecal sphincter –> cecum -> ascending colon –> transverse colon –> descending colon –> sigmoid colon –> rectum –> anal canal –> anus
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15
Q

___L of watery chyme passes through the large intestine each day
GI1

A
  1. 5L

- absorption of water and electrolytes occurs to create semi-solid feces

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16
Q

GI layers within walls
- serosa layer info
GI1

A

lumen of the gastrointestinal tract to:

  • Mucosa layer –> submucosa layer –> muscularis externa –> serosa layer
  • *Submucosa and muscularis makeup enteric nervous system

Serosa: dense covering of connective tissue that’s a continuation of peritoneal memb (lines abdominal cavity). Sheets of mesentery hold intestines in place. Where ducts from external exocrine glands (liver, pancreas, salivary glands) release secretions into lumen

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17
Q

Mucosa Layers makeup

GI1

A
  • epithelium (mucous membrane): Transports substances from lumen to blood. where hormones/mucus/enzyme production occurs
  • lamina propria next: subepithelial tissue with small blood/lymph vessels, nerve fibres to stimulate secretions
  • muscularis mucosae last: thin layer of smooth able to alter SA for absorption
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18
Q

Submucosa and muscularis externa layer makeup (ENS)

GI1

A 
submucosa layer (middle layers): major blood/lymph vessels
-submucosal plexus: one of major nerve networks in ENS

muscularis externa layer:

  • circular muscle layer
  • myenteric plexus
  • longitudinal muscle
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19
Q

Where are villi located in the SI? Crypts?

GI1

A

line lumen i.e. mucosa layer
- when the muscularis externa layer contracts, it pulls villi together to dec SA and absorption.

If villi are mountains, crypts are valleys in b/n. “opening” to inside the mucosa layer

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20
Q

What are Plicae?

GI1

A

large folds lining the lumen

  • larger than rugae
  • inc SA
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21
Q

Epithelium layer of the mucosa layer

GI1

A

most variable

  • transporting epithelial cells (enterocytes), enterendocrine and exocrine secretory cells
  • most transport is transcellular w paracellular junctions in SI
  • short lifespan of few days
  • GI stem cells constantly replacing ~17 billion cells daily *why colorectal cancer rates are so high: in 5 days all cells replaced
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22
Q

Muscularis externa jobs

GI1

A
  • major movement muscle
  • 2-3 layers of smooth muscle that when contracted…
    circular = decrease diameter
    longitudinal = decrease length

contractions alternate

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23
Q

4 basic digestive functions and processes

GI1

A
  1. digestion: breakdown of food into absorbable units
  2. secretion: water/ions move from cells into lumen, cells into ECF, ECF into lumen
  3. absorption: movement of water/ions lumen to ECF
  4. motility: movement of materials through GI tract
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24
Q

Challenges of digestive system (3)?

GI1

A
  1. avoiding autodigestion: once food is broken into small molecules, w/o digesting cells of the GI, it could be absorbed
  2. mass balance: absorption = secretion but secrete more than absorb. Feces is mostly bacteria
  3. defense: absorb water/nutrients while preventing pathogens entry via mucus, digestive enzymes, acid, lymphoid tissue (*80% of lymphocytes exist in SI)
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25
Q

Fluid input and output (mass balance)

GI1

A

ingestion: 2L food/drink
secretions (7L): 0.5L bile, 2L gastric secretions, 1.5L pancreatic secretions, 1.5L intestinal secretions.
Total input = 9L

absorption: 7.5L from SI, 1.4L LI.
excretion: 0.1L feces
total output = 9L

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26
Q

Fluid secretions makeup 7L of total input into body. What are they?
GI1

A
  1. water: ions transported from ECF to lumen makes osmotic gradient
  2. digestive enzymes: exocrine glands (salivary, pancreas), epithelial cells (stomach and SI)
  3. mucus: viscous glycoproteins secretions that protect GI cells and lube contents (mucus cells in stomach, salivary glands, goblet cells in intestine)
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27
Q

Digestive enzymes are usually released (secreted) as their inactive form _____.
GI1

A

Zymogens

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28
Q

Fluids facilitate _____ (3).

GI2

A
  • digestion, motility and protection
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29
Q

Where does secretion and absorption usually occur?

GI2

A

secretion: stomach and LI
absorption: mostly SI, some LI

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30
Q

Purposes of motility? Where in the GI tract is skeletal muscle? Smooth muscle?
GI2

A
  • move food from mouth to anus and mix food to break them down and expose them to digestive enzymes
  • *needs to be small since absorption largely depends on transporters which can only pick up small particles

top of esophagus is skeletal, rest of GI is smooth

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31
Q

Steps leading to smooth muscle contraction? *motility

“GI motility is determined by properties of smooth muscle contraction and is modified by _____.”
GI2

A
  • Ca+2 enters ICF from ECF via channel
  • ICF Ca+ increase, causing sarcoplasmic reticulum to release Ca+2
  • inc Ca+2 binds to calmodulin
  • Ca-CaM causes activation of myosin light chain kinase
  • active MLCK phosphorylates the light chains in myosin heads using ATP and also inc myosin ATPase activity
  • active myosin forms cross bridges w actin (cocked position)
  • myosin slides along the actin and creates muscle tension

“modified by chemical input from nerves, hormones, paracrines, stomach distension, osmolarity changes” i.e. these are stimuli

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32
Q

Single-unit smooth muscle cells connected by ____.

GI2

A

gap junctions

  • cells contract as a single unit
  • neurotransmitters released from autonomic neurons in SI bind to receptors in smooth muscle cells in SI wall, cause contraction
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33
Q

Types of GI contraction *motility

GI2

A
  • slow waves (spontaneous depolarization in smooth muscle cells; APs fire when slow wave potentials exceed threshold, propagate via gap junctions)
  • tonic smooth muscle (always contracted; sphincters: only relax to let chyme pass)
  • phasic smooth muscle (cycles b/n contraction and relaxation; posterior stomach and SI/LI; driven by pacemaker cells creating slow waves)
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34
Q

interstitial cells of cajal *motility

GI2

A
  • origin of spontaneous slow waves
  • modified smooth muscle cells serving as pacemaker for slow wave activity
  • electrically coupled to adjacent cells
  • different regions controlled by different ICC groups
  • stomach: 3 slow waves/min
  • duodenum (SI): 12 waves/min
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35
Q

Phasic contraction *motility

GI2

A

3 patterns of contraction creating diff types of movement

  • migrating motor complex *no food
  • peristaltic contractions *during or following a meal
  • segmental contractions *during or following a meal
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36
Q

migrating motor complex

GI2

A
  • motilin (hormone) thought to drive this contraction in response to SI being empty
  • occurs b/n meals, begins in stomach and ends in ilium: sweeps food remnants and bacteria out of upper GI and into LI ***this is what your stomach growling is
  • takes 90-120 min: first 45-60 min is inactive, then 20-30min of infrequent peristaltic contractions, then 5-15 min of rapid forceful contractions
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37
Q

Why do some medications need to be taken with a meal?

GI2

A

Other reasons too, but 1 is that if there’s no food, the MMC will sweep it out of upper GI tract and prevent its absorption in SI.

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38
Q

Motility occurring during or following a meal?

GI2

A

Peristaltic – esophagus and stomach; progressive waves of contraction of CIRCULAR muscle behind a bolus of food, pushes it FORWARD (2-25 cm/s) *in front of bolus, muscle relaxes

Segmental – SI and LI; small segments alternatively contracting and relaxing the CIRCULAR and LONGITUDINAL muscle to MIX bolus/food. Also exposes food to digestive enzymes

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39
Q

Regulation of GI functions

GI2

A

–motility and secretion regulated *digestion and absorption depend on motility and secretion so not controlled

Neural regulation: enteric nervous system
GI peptide regulation: cell-signalling substances (hormones, neuropeptides, cytokines/paracrines/autocrines)

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40
Q

ENS – motility/secretion regulation

GI2

A

“the little brain”

  • submucosal and myenteric plexus
  • 100-150 million neurons
  • synapse with other neurons, smooth muscle, glands and epithelial cells to modify them
  • short reflexes entirely integrated w/n ENs in GI wall
  • long reflexes integrated w CNS
  • myenteric plexus: controls motility
  • submucosal plexus: controls secretions from GI secretory cells
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41
Q

ENS similarities w/n CNS

GI2

A
  • intrinsic neurons in ENS like interneurons in CNS: get input from sensory neurons to modify afferent neurons
  • neurotransmitters in ENS (serotonin, ACh, VIP, NO) identical to CNS – serve to modulate motility and secretion
  • glial support cells in ENS similar to astrocytes in brain stem
  • diffusion barrier in ENS like blood brain barrier (protection)
  • function autonomously
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42
Q

ENS short reflex

GI2

A
  • originate in ENS and are carried out entirely w/n gut wall
  • local stimuli: distension of stomach, osmolarity changes, acid secretion
  • local stimuli sensed by receptors –> interneurons –> enteric neurons in ENS
  • enteric neurons and local stimuli signal stomach/SI secretory cells
  • secretory cells trigger GI peptide release: signals brain for hunger/satiety cues and pancreas for (endocrines) insulin/glucagon
  • enteric neurons and GI peptides also trigger smooth muscle and exocrine cells to release bile and pancreatic secretions, enzymes, acid and bicarbonate synthesis/release, as well as GI motility changes
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43
Q

ENS long reflex

GI2

A
  • originate in CNS/integrated in CNS
  • works with the short reflex
  • if it begins in brain, is a cephalic reflex (feedforward bc of sight/smell/thought of food). Sends info to sensory receptors which signals cephalic brain, which sends into to ENS via autonomic neurons: inc in parasympathetic input enhances GI function (rest and digest), sympathetic inhibits
  • same result as short reflex
  • sensory info also sent to cephalic brain
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44
Q

GI peptides - motility/secretion regulation

GI2

A
  • hormones/paracrines excite or inhibit motility/secretion
  • secreted into lumen to act on apical membrane receptors, or ECF to act on adjacent cells
  • some act outside GI tract like brian ex, ghrelin (hunger cue) and cholecystokinin (satiety)
  • > 30 peptides have been identified from GI mucosa, only some considered hormones (work in entire body)
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45
Q

Hormone families

GI3

A
  • based on receptors
  • Gastrin family: gastrin (influences acid secretion), cholecystokinin (influences release of digestive enzyme from pancreas)
  • Secretin family: secretin (bicarbonate release from pancreas), vasoactive intestinal peptide (MMC), gastric inhibitory peptide (inhibits acid secretion into stomach if levels high, however main job is feedforward insulin secretion *glucose-dependent insulinotropic peptide)
  • other: motilin
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46
Q

Integrated function w/n digestive system described in 3 phases:
GI3

A

cephalic/oral phase: digestive processes occuring before food enters stomach
gastric phase: in stomach
intestinal phase: SI and LI

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47
Q

Cephalic phase of digestion

GI3

A

digestive processes can start before food enters mouth, reinforced once food enters GI (mouth)

  • long reflex: initiated by smell, sight or thought of food
  • once in mouth, mechanical receptors inc saliva flood and secretions into stomach via inc parasympathetic input from medulla to salivary glands via facial and glossopharyngeal nerve, and to the ENS via vagus nerve (nagal reflex)
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48
Q

Chemical and mechanical digestion begins in the ___.
Functions of saliva? (4)
GI3

A

Mouth
-mastication (chewing): teeth
-lips and tongue help manipulate food
-joined by flood of saliva from 3 pairs of salivary glands
saliva functions:
-soften/moisten food
-digestion of CHOs (salivary amylase for complex CHOs)
-dissolving foods (taste)
-defense (contains lysozymes, immunoglobulins)

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49
Q

Saliva is an ____ secretion. What is within saliva (solutes)? Where does each component come from?
GI3

A

exocrine: non-hormonal, comes from duct
- 1.5L/day, 99.5% of which is water *hypoosmotic; solutes secreted and reabsorbed regularly
- contains low [Na+] and [Cl-], high [K+], [HCO3-] and [PO4-]
- contains amylase, lysozymes, mucus (allows food to slide down esophagus), immunogl. A

  • acini = clusters of secretory cells w/n duct
  • parotid gland: watery sol w amylase
  • submandibular: watery, amylase, mucus
  • sublingual: mucus mainly
  • primarily under parasympathetic control
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50
Q

Jobs of:
serous cells, myoepithelial cells, mucous cells
GI3

A

Serous: produces thinner liquid component (water, digestive enzymes)
Myoepithelial: contracts to squeeze saliva out of acini lumen into duct and into mouth
Mucous: produces mucus

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51
Q

Deglutition reflex

GI3

A
  • moves food from mouth to stomach (swallowing)
  • once you start, push food into back of mouth and reflex takes over so you can’t stop swallowing
  • pressure against soft palate and back of mouth activates sensory neurons going to medulla: sends somatic motor outputs to pharynx and upper esophagus (sphincter relaxes and opens), and autonomic outputs to lower esophagus (sphincter tension relaxes)
  • soft palate closes off nasopharynx so food doesn’t go up
  • peristaltic waves push bolus down, move larynx up and forward and epiglottis closes trachea (breathing is inhibited as bolus passes closed airway)
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52
Q

Do you need gravity to swallow?

GI3

A

food moves downward into esophagus aided by gravity, but is PROPELLED by peristaltic waves
so, NO – think abt keg stands

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53
Q

Gastroesophageal reflux disease (GERD)

GI3

A

Heartburn

  • lower esophageal sphincter not a true anatomical sphincter (no thickening of muscle, just has high contractibility unless swallowing)
  • weak LES, or churning of stomach, can cause backflow into esophagus which burns it
  • “heart” cause its right next to heart so it feels like its there
  • pressure in stomach is negative during inspiration, can cause esophagus to EXPAND drawing gastric acid/pepsin up from stomach
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54
Q

Gastric phase of digestion

GI3

A

*stomach: 3.5L of food, drink and saliva (1.5L) enter /day
-little absorption, mechanical and chemical digestion occurs
3 functions:
1. storage: stores food and regulates it passage into SI to prevent nutrient loss/diarrhea
2. digestion: chemical/mechanical digestion of food into chyme, proteins mainly chemically digested
3. defense: destroys pathogens in food, and the trapped ones in mucus pepsin

once food enters stomach, motility and secretion initiated in cephalic phase is reinforced; driven by stomach distension and reflexes

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55
Q

Receptive relaxation and how it relates to Propulsion and Retropulsion.
GI3

A

upon swallowing, parasympathetic neurons send info to ENS, causes fundus of stomach to relax and make room for food

  • distension enhances motility: weak peristaltic waves inc in force, moves chyme towards pyloric sphincter (propulsion) to let small amounts of chyme through
  • larger molecules moved back bc pylorus doesn’t let big food through and contractions squeezes it backwards (retropulsion)
  • moving propulsion –> retropulsion mixes food w acid/digestive enzymes
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56
Q

Gastric acid secretion: Gastrin and G-cells

GI3

A

protect and digest

  • main stimulus is inc ENS activity (parasympathetic input in cephalic phase)
  • G cells release gastrin in response to AA, peptides, ACh and distension short reflex of ENS, as well as cephalic phase stimulates ENS in long reflex
  • G cells indirectly stimulates histamine release from enterochromaffin-like cells (ECL) which stimulates parietal cells
  • G cells directly stimulate gastric acid secretion right from parietal cells
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57
Q

Parietal cells

GI3

A
  • produce 1-3L of gastric acid (HCl) daily: activates pepsin and kills bacteria
  • stimulated by ACh from ENS neurons via long and short reflexes, gastrin from G cells, histamine from ECLs
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58
Q

Gastric acid functions (HCl; 6)

GI3

A
  • stimulates release of pepsinogen from chief cells
  • cleaves pepsinogen to pepsin so it can digest proteins
  • denatures proteins making it easier for pepsin
  • kills bacteria/microorganisms
  • inactivates amylase from saliva bc pH too low
  • stimulates D cells to release somatostatin (inhibitor of further acid secretion once pH drops enough)
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59
Q

Process of acid secretion in the stomach (parietal cells) primary and secondary process
GI3

A
  • apical memb lining lumen of stomach has Cl- and K+ leak, and H+/K+ ATPase
  • baso memb lining interstitial fluid (ECF) has Cl-/HCO3- channel
  • free H+ actively transported across apical into stomach lumen
  • WATER dissociates into H and OH- in parietal cell, free up more H+ to be actively transported out to lumen, bring in a K
  • OH- combines with CO2 via carbonic anhydrase, to make HCO3-
  • HCO3- goes down electrochem. gradient into interstitium, exchanged with Cl- at basolateral memb
  • Cl- diffuses all the way across into lumen via leak channels bc of electrochem. gradient
  • Cl- combines with H+ produces HCl in lumen of stomach!

secondary process is CA converts CO2 and H2O right into H2CO3, a H+ is removed and sent across into lumen, HCO3- goes down gradient into ECF.

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60
Q

“alkaline wave” after a meal is because of?

GI3

A
  • all the HCO3- entering interstitium of blood during acid secretion
61
Q

Stimuli for acid secretion

GI4

A

histamine from ECLs, gastrin from G cells, ACh from ENS cells

  • *somatostatin inhibits acid secretion (D cells): once food enters intestine, somatostatin signals parietal cells to stop acid secretion
  • causes exocytosis and insertion of apical transporters (P+ pump, Cl and K leak channels)
62
Q

Treatment for heartburn

GI4

A

H2 receptor antagonist or p+ pump inhibitor

63
Q

Gastric digestive enzyme secretion (pepsin)

GI4

A
  • stimulated by acid secretion via short reflex
  • chief cells stimulated to secrete pepsinogen
  • Gastric lipase (HCl) cleaves pepsinogen into pepsin so it can cleave proteins into smaller peptides
  • Pepsin also can cleave more pepsinogens as well
64
Q

Paracrine secretions involved in pepsin secretion. What happens when enough pepsin has been release?
GI4

A

ECL: histamine activates H2 receptors on parietal cells to stimulate HCl secretion

  • *Parietal cells also make intrinsic factor that forms complex with vitamin B12 so it can be absorbed
  • stimulates pepsinogen release from chief cells
  • activated by HCl to pepsin

when there is enough HCl/pepsin and pH drops: D cells make somatostatin to inhibit acid secretion (G cells, parietal cells and ECL cells), and pepsinogen release (chief cells)

65
Q

Mucus secretion

GI4

A

from mucous cells

  • mucus with HCO3- secretion stimulated by parasympathetic input and irritation in stomach
  • lines stomach to prevent acid/pepsin from getting to stomach wall epithelial cells
  • if it did get to stomach wall, would digest those cells
  • the HCO3- in the mucus buffers the acid
  • so even though stomach pH is ~2, the lining of the stomach is ~7
66
Q

Peptic ulcers. Causes?

GI4

A
  • sore or break in lining of stomach/duodenum caused by breakdown of HCO3-mucus layer. Acid starts to digest the exposed epithelial cells within walls
  • can be caused by excessive acid production in parietal cells
  • gastrin secreting tumours
  • nonsteroidal anti-inflammatory drugs like aspirin, causes less mucus production because cells are irritated by the drug
  • bacteria Helicobacter pylori can be responsible as well
67
Q

How does Helicobacter pylori cause peptic ulcers?

GI4

A
  • to create livable environment, go to wall of stomach to be surrounded by HCO3-
  • bacteria is surrounded by ammonia, eventually breaks down the layer
  • causes inflammatory response
68
Q

Intestinal phase of digestion

GI4

A
  1. 5L of food, fluid and secretions enter SI, along w 3.5L added from hepatic, pancreatic and intestinal input
    - motility regulated to ensure proper absorption: promoted by parasympathetic input, gastrin and cholecystokinin. Inhibited by sympathetic input
    - most chemical digestion occurs in SI
    - segmental and peristaltic contractions mix chyme with enzymes, expose digested nutrients to mucosal epithelium for absorption: 7.5L absorbed in duodenum and jejunum
69
Q

___ and ___ inc SA in SI

GI4

A

plicae and villi

  • large SA in SI to facilitate absorption *similar folds in stomach
  • villi also secrete mucus, and most nutrients are absorbed via capillaries in the villi
  • enterocytes have microvilli as well (called brush border)
70
Q

Crypts

GI4

A

contain hormones, fluid secretory cells and stem cells within mucosa layer

71
Q

Once nutrients are absorbed through capillaries in villi, where do they go?
GI4

A

fats: lacteals of lymphatic system

water-soluble items: hepatic portal system (blood)

72
Q

Hepatic portal system. Why do drugs given orally commonly have a higher dosage than IV?
GI4

A
  • heads to LIVER for filtering: contains enzymes that metabolize drugs and xenobiotics and clear them from blood before it can enter systemic circulation
  • drugs given orally have to go to liver first where enzymes will break down some of the drug, and IV bypasses the liver
73
Q

What is the makeup of the 3.5L of secretions entering SI lumen?
GI4

A
  • digestive enzymes (brush border enzymes and pancreas releases)
  • bile
  • bicarbonate
  • mucus (goblet cells: mucus cells in mouth and stomach is same thing; found in walls of intestines to prevent digestion of it via acid)
  • isotonic saline (crypt cells: lubricates gut contents and contains dissolved enzymes so everything moves)
74
Q

w/o enough saline _____.
Cystic Fibrosis?
What drives saline creation?
GI4

A
  • clogs some ducts
  • *cystic fibrosis: alters pancreatic secretions which clogs ducts and results in pancreatitis since pancreas cannot secrete enzymes
  • mainly Cl- drives creation, brought into lumen via 2 Cl/1 K/ 1 Na .. K and Na pumped back out after brought into intestinal cell
  • creates gradient for water to follow Cl into lumen of intestine
75
Q

Pancreas

GI4

A
  • contains endocrine secretory epithelium (α and ß islet) that secretes insulin and glucagon
  • contains exocrine secretory epithelium (acinar and duct cells) which secrete digestive enzymes and HCO3- (respectively)

stimuli for exocrines: distension of SI, neural signals, CCK

76
Q

Pancreatic enzymes

GI4

A

released as zymogens
-trypsin activates (cleaves) ALL of them, trypsinogen is activated to trypsin by brush border enteropeptidase

Zymogens released: chymotrypsinogen, procarboxypeptidase, procolipase, prophospholipase

77
Q

Bicarbonate release from pancreas

GI4

A
  • neutralizes acid entering SI duodenum from stomach
  • secreted/made via duct cells
  • in a pancreatic duct cell or duodenal cell, there is high levels of CA converting H2O and CO2
  • apical memb (lines lumen of pancreas or intestine) contains HCO3/Cl exchanger and Cl- channel (CFTR)
  • basolateral memb contains Na/K/2 Cl channel , Na/K ATPase. K+ channel, Na/H exchanger
  • Cl- enters cell by active transporters on basolateral memb, leaves through apical memb by CFTR channel
  • Cl renters cell in exchange for HCO3- going out
  • HCO3- will bind H+ secreted from parietal cells
  • water follows ion movement via paracellular movement
78
Q

Gastric acid not considered to be a _____.

GI5

A

digestive enzyme

79
Q

In the liver… the common bile duct takes ____. The hepatic artery brings ____. The sphincter of Oddi controls ____.
GI5

A
  • Common bile ducts takes bile from gallbladder, water, ions etc to lumen of SI. the common hepatic duct takes bile made in liver to gallbladder
  • Hepatic artery brings oxygenated blood containing metabolites from peripheral tissues to the liver. hepatic vein goes liver products to periphery – this is not the same thing as hepatic portal vein
  • Sphincter of Oddi controls release of bile and pancreatic secretions into the duodenum
80
Q

Liver basic jobs?

GI5

A 
glucose and fat metabolism
protein synthesis
hormone synthesis
urea production
detoxification
storage
81
Q

Structures in the liver and how they produce bile?

GI5

A
  • cells arranged in hepatic lobules (hexagons) containing hepatocytes
  • outside of lobule contains 2 branches: hepatic artery (bringing O2 blood to hepatocytes) and hepatic portal vein (bringing blood from digestive tract through the liver)
  • blood is detoxified when passing hepatocytes
  • detoxified blood goes outside of lobule into central vein to proceed back into systemic circuit

-bile canaliculi run opposite (hepatocytes to outer portion of lobules) and produce bile as a detoxification/waste byproduct (xenobiotics/drugs)

82
Q

What is the makeup of bile?

GI5

A
  • non-enzymatic solution produced by canaliculi, secreted from hepatocytes
  • made of: bile salts (bile acid/AA), bile pigments (bilirubin, gives bile/urine yellow color), cholesterol
83
Q

Fat digestion includes which molecules?

GI5

A
  • triglycerides (90%)
  • cholesterol
  • phospholipids
  • long chain fatty acids
  • fat soluble vitamins
  • bile is needed to help the digestion of fats*
84
Q

Fats are not very ___ soluble which complicates its digestion. What is needed for fat digestion? What is a micelle?
GI5

A

not very water soluble

  • enzymes unable to chemically digest fats so bile salts needed to coat (coarse emulsion) the large fat droplets into smaller, stable particles
  • an emulsion has fats inside and is coated by bile salts facing outwards so its water-soluble
  • after emulsion has occurred, enzymes come and digest fats
85
Q

Lipase and Colipase (fat digestion in detail)?

GI5

A
  • In small intestine
  • lipase: breaks apart TGs into mono and 2 fa
  • colipase: allows lipase to cross bile-salt layer of fat droplet and get into centre where lipids are

after lipase does its job: mono and diglycerides, bile salts, phospholipids, fatty acids and cholesterol form a small disk (MICELLE)

86
Q

Fat absorption?

GI5

A
  • micelles move towards and come into contact with brush border (SI)
  • fa and monoglycerides diffuse through enterocyte membrane, comes into cytoplasm of SI cell
  • cholesterol is transported into the same cell
  • fats reform into TG’s via ER
  • absorbed fats combine with cholesterol and proteins in cell and form chylomicron
  • chylomicrons packaged in golgi, exocytosed out of cell, enters lacteal (lymphatic system) then blood, and goes to adipose
87
Q

Gallstones?

GI5

A

hardened deposits in gallbladder due to excess cholesterol or bilirubin that are pushed out of the liver and cause clogging of common bile duct or cystic duct

  • causes: obesity or excess RBC breakdown
  • symptoms: upper right abdominal pain and jaundice
  • treatment: remove gallbladder since don’t actually need it
88
Q

Carbohydrate digestion?
-amylase, disaccharidase’s
GI5

A

-starch, sucrose, glycogen, cellulose, disaccharides (lactose and maltose), monosaccharides (gluc, fruc)

Amylase breaks down glucose polymers (glycogen, starch) into disaccharides.
Each disaccharide has brush border enzyme called disaccharidases (maltose has maltase, sucrose has sucrase) to break them into monosaccharides:
-Maltase breaks maltose into 2 glucoses.
-Sucrase breaks sucrose into 1 glucose 1 fructose.
-Lactase breaks lactose into 1 glucose 1 galactose.

89
Q

Why is lactase considered an “ancestral allele”?

GI5

A

stops in adults since most ancestors did not drink milk past breastmilk
-now seeing it last longer

90
Q

Carbohydrate absorption in SI?

GI5

A

apical (lines lumen of intestine and mucosa layer of intestine) transporters:

  • glucose/galactose in along with Na+
  • other once brings fructose in via GLUT5

on basolateral membrane:

  • GLUT2 to bring in fructose/glucose/galactose
  • ATPase bringing Na+ into capillary in exchange K+

upon entering mucosa layer, glucose passively goes into capillary since [ ] gradient

91
Q

Protein digestion and enzymes involved?

GI5

A

~50% is ingested, 30-60% is dead cells/turned over proteins

  • endopeptidases (pepsin, trypsin, chymotrypsin): digest internal peptide bonds; cleave larger proteins into smaller peptides
  • exopeptidases cleave off single AA from peptide: aminopeptidases and carboxypeptidases
92
Q

Types of aminopeptidases and carboxypeptidases?

GI5

A

amino: cleave AA from amino-terminal end, made by entero-cell themselves (brush border enzyme)
carboxy: cleave AA from carboxy-terminal end, pancreatic A1, A2, B

all use H2O to cleave these peptide bonds

93
Q

Protein digested primarily results in ____.

GI5

A

results in free AAs, dipeptides and tripeptides

94
Q

Protein absorption for single AAs, dipeptides and tripeptides?
GI5

A
  • di and tripeptides cotransported into cell (apical) with H+ transporter, exchanged with H+ on basolateral memb
  • *most di’s and tri’s tho broken by peptidases into AA’s
  • AAs: Na+ cotransporters (apical) and Na+ exchangers (basolateral)

sent to liver via hepatic portal system (blood)

95
Q

Protein absorption for oligopeptides over 3 AA?

GI5

A
  • transported via transcytosis after binding a receptor on apical memb *endocytosis
  • exocytosed on basolateral membrane and send to liver via hepatic portal vein

Issue: can act as antigen stimulating antibody production cause an allergic rxn to that peptide, especially in infants since peptide absorption is high when an infant (villi are small) may play a role in food intolerances or allergies

96
Q

vitamin and mineral absorption?

GI5

A
  • Fat soluble vitamins (ADEK) absorbed with fats, same process
  • water soluble vitamins (CB’s) absorbed by mediated transport: B12 absorbed in ileum after forming complex with parietal cell intrinsic factor
  • mineral absorption is active transport, direct or indirect: Fe and Ca+2 are regulated (uncommon)
97
Q

Ca+2 and Fe+2 (mineral) absorption?

GI5

A

Ca+2: when Ca+2 levels drop, kidneys produce vitamin D to cause TRPV6 (Ca+2 channel on apical), Ca+2 exchanger and ATPase transporters (basolateral)
Fe+2: if too high, hepcidin (hormone), binds the ferroportin transporter on basolateral memb, causes removal of it to dec amnt of Fe+2 in the body

98
Q

Ion and water absorption?

GI5

A

Na+ enters intestinal cell (apical, from lumen) by…
leak channel, Na+ and Cl- transporter, Na+ and H+ exchanger, Na+ and organic solute transporter.

apical memb: HCO3- and Cl- exchanger brings Cl- into cell

this amnt of solute moving causes osmotic gradient for water to paracellularly across into ECF, creates electrochemical gradient for K+ to do same

basolateral memb has Cl- leak channel, K+ channel and K+/Na+ exchanger (Na going out)

99
Q

regulation of the intestinal phase?

GI5

A
  • long reflexes: CNS increases sympathetic output, causes dec gastric emptying in stomach
  • short reflexes: inc acidity, fat, amino acids, distension, and hypertonicity in the duodenum causes.. secretion of enterogastrones (inc plasma enterogastrones dec stomach gastric emptying) AND stimulates neural receptors (dec stomach gastric emptying and activates the long reflex)
100
Q 
GI peptides (enterogastrones) involved in motility regulation?
GI5
A

primarily regulated by ENS, initiated by long reflexes:

  • Mo cell: motilin causing MMC when fasting
  • S cell: secretin
  • I cell: cholecystokinin
  • K cell: glucose-dependent insulinotropic peptide (GIP)
  • L cell: glucagon-like peptide 1 (GLP-1)

all enteroendocrine cells (secrete hormones, found in crypts) play some role in digestion of intestinal phase

101
Q

Fed state motility is stimulated by?

GI6

A

(segmental contractions)

  • slow waves brought to threshold in pacemaker cells, pacemaker stimuli:
  • distension of stomach
  • distension of small intestine
  • inc parasympathetic input (long reflexes)
102
Q

Pancreatic secretions beginning in cephalic phase and continuing into gastric phases STIMULI?
GI6

A
  • sight/smell/thought/taste of food
  • distension of stomach (inc parasympathetic output to pancreas)
  • gastrin in stomach (G cells inc secretion)
  • enteropancreatic reflexes: ACh inc binding to M3 receptor of G cells, causes release of gastrin and also enzyme release (and water and bicarbonate) into SI
103
Q

S cells: Secretin Jobs (2) and stimuli?

GI6

A

-stimulated by acid entering duodenum from stomach

  • primary role in pH regulation
  • causes inc pancreas secretions of bicarbonate and inhibits gastric acid secretion so there is less gastric motility and less emptying into SI (gives it time to breakdown what is entering)

some involvement in bile secretion

104
Q

I cells: Cholecystokinin (CCK) jobs (2) and stimuli?

GI6

A

-stimulated by presence of fa and AA in SI

  • pancreatic enzyme secretion: inc enzyme secretions from acini cells entering SI
  • bile secretion: causes gallbladder contraction/relaxation of sphincter of Oddi (more bile flowing into common bile duct and out into duodenum)

some inhibition of gastric acid production/emptying by inhibiting G cells, parietal cells, motility of stomach

105
Q

Which phase of pancreatic secretions take up which % of maximum enzyme secretion?
25%, 10-20% and 50-80%
GI6

A 
Cephalic phase (regulated by vagal pathway) - 25%
Gastric phase (vagal-cholinergic pathway) - 10-20%
Intestinal phase (cholecystokinin, secretin, enteropancreatic reflexes) - 50-80%
106
Q

K cells: GIP jobs and stimuli?
L cells: GLP-1 jobs and stimuli?
GI6

A

Both are the same

  • stimulated by presence of carbohydrates in SI lumen
  • primary endocrine function is glucose homeostasis
  • promotes insulin secretion: acts on ß islet cells of pancreas to inc insulin secretion
  • indirectly helps to dec glucose in blood as inc insulin causes dec plasma glucose which negatively feedbacks to α-cells of pancreas (which secrete glucagon to inc glucose in blood)
  • inhibit gastric acid secretion and motility
107
Q

Entero =

GI6

A

intestinal

108
Q

Large intestine Jobs?

A
  • store and concentrate fecal matter: ~1.5L of chyme comes in through ileocecal valve (relaxes as contraction goes through ilium caused by food in stomach = gastroileal reflex)
  • *NO VILLI HERE! but there are crypts to make mucus

by end, ions and water are reabsorbed so only 0.1L leave body

109
Q

Appendix possible jobs?

GI6

A

immune functions

- reservoir for good bacteria so if ever severe diarrhea removes existing microbiome, have bacteria to repopulate the LI

110
Q

Secretions and digestion in LI

GI6

A

-minimal secretions consisting of mucus from goblet cells
-initially thought 0 digestion occurs here, but indigestible complex carbohydrates (fiber), fats, and proteins, broken down by microbiome bacteria through fermentation
-produces lactate, propionate, butyrate, used by the colonocytes for energy production
-microbiome can also facilitate absorbable vitamins (K, some Bs)
-gas is a side product of fermentation
~100 trillion bacteria is in colon

111
Q

LI motility

GI6

A

Food last in here 18-24 hours

  1. slow/infrequent segmental contractions (don’t reach threshold often)
  2. Haustral rolling/churning (thickened bands of longitudinal muscle layer = taenia coli, which is tonically sem-contracted causing formation of haustra=pouches which inc ions exposure to wall for absorption)
  3. mass peristalsis (gastrocolic reflex can stimulate defecation reflex as the food moves rapidly down to prepare more space for next meal)
112
Q

Defecation reflex

GI6

A

Short/long reflex initiated by distension of rectum walls

Short reflex: myenteric plexus stimulated in later portion of sigmoidal and rectal portion of colon causes local peristaltic waves to push food into rectum, which causes more local peristalsis, causing involuntary relaxation of internal sphincter as rectum distends and contraction of external sphincter

Long reflex: info sent to sacral region of spine stimulates to parasympathetic motor neurons in spine, causes relaxation of internal sphincter and more forceful peristaltic contractions. *As well somatic motor neurons cause involuntary contraction of external sphincter

To defecate, must voluntarily relax the external sphincter skeletal muscle Aided by abdominal contractions as well

113
Q

Diarrhea: causes? Types?

GI6

A

-inc secretion, dec absorption, inc motility (combo)

  • osmotic: inc solute so less water absorption, ex, Lactose intolerance
  • secretory: infection, ex. E.coli and cholera
  • inflammatory: intestinal wall damage causes dec absorption, inc secretion
  • motility induced ex. nervousness
114
Q

Cholera causing diarrhea

GI6

A

cholera toxin causes adenylate cyclase pathway to activate inside intestinal wall: inc cAMP causes the CFTR channel to inc amnt of Cl- leaving cell, which inc amnt of Na and water following paracellularly.
= inc secretions
= more water and ions leaving
= dec absorption

115
Q

Vomiting: How does it occur? Stimuli? Responses from vomiting centre in medulla?
GI7

A
  • contents of stomach/SI forcefully expelled via mouth; linked with nausea
  • drugs/metabolites in blood stimulate chemo-receptive neurons that activate vomiting centre
  • abnormal vestibular input stimulate chemo-receptive neurons
  • abnormal subs in stomach/SI/LI stimulate chemoreceptors
  • smell or emotional shock

responses: retrograde contractions in stomach/SI; contraction of abdominal/inspiratory muscles (diaph.) to compress stomach and inc gastric pressure; relaxation of esophageal sphincters

116
Q

GI tract immune functions

GI7

A
  • 80% of all lymphocytes in gut wall (GALT)
  • Microfold cells: constantly sample lumen of stomach
  • M cells will phagocytose sampled antigens, carry them into epithelial cells where macrophages, lymphocytes and dendritic cells are waiting, present them for immune response and will release cytokines to attract more immune cells (cytokines can trigger Cl- secretion i.e. diarrhea, to flush out pathogens)
117
Q

The GI system does not regulate intake of food/water so we rely on ____.
GI7

A

behavioural mechanisms

  • feeding state: full intestines indirectly cause insulin release causing anabolism (glucose uptake into tissues)
  • fasting state: empty intestines indirectly cause glucagon release causing catabolism (glycogen released from liver)
118
Q

If dietary intake is = or > or < energy expenditure,what happens to body?
GI7

A

= stable weight (healthy)
> obesity
< starvation

119
Q

Behavioural mechanisms regulate food/water intake, but what drives the desire to eat/drink? original structures vs. now
GI7

A

ORIGINALLY: Lateral hypothalamus is the hunger centre, and ventromedial hypothalamus is the “satiety centre” (linked together though)

  • if animals have lateral hypo. burned, will not eat as much
  • if ventromedial hypo. burned, won’t stop eating

NOW: arcuate nucleus (responds to leptin), PVN (paraventricular nucleus; satiety), lateral hypothalamus, NTS (nucleus tractus solitarii; satiety)

120
Q

Theories of what triggers the hunger and satiety centres of brain?
GI7

A

mechanisms to keep weight stable

  • glucostatic theory: short term glucose metabolism in hypothalamus regulates food intake, stimulated by amnt of glycogen being used vs amnt of glucose being stored
  • lipostatic theory: long term signals from the body’s fat stores regulate food intake
121
Q

Lipostatic theory evidence? Protein identified?

GI7

A

1960s: ID of ob/ob mice: mutation in ob gene causes continuous eating (lack ability to signal brain abt fat stores)
- gene prob encodes a pro that tells brain fat stores are good
- evidence: when you link 1 ob and 1 normal mouse together, the normal’s ob gene goes into abnormal mouse and it loses weight
- this mutation can occur in people. if given artificial leptin, will lose weight!

1994: protein identified as LEPTIN (curbs hunger when fat stores are adequate)

122
Q

Leptin

GI7

A
  • released from adipocytes in response to adequate fat storage (energy excess)
  • regulates body mass by acting on neurons in hypothalamus to DEC APPETITE AND INC ENERGY EXPENDITURE (metabolism; gets rid of excess)
123
Q

Why does metabolism increase during/right after a meal?

GI7

A

Release of leptin signals increased energy expenditure to use excess energy

124
Q

Response to elevated leptin? Which peptide is involved?

GI7

A

activation of α-MSH and CART neurons act on arcuate nucleus to inhibit lateral hypothalamus (feeding/hunger centre) and activate PVN (inc energy expenditure)

activated PVN causes…

  1. humoural response: inc release of TSH (thyrotropin; thyroid stimulating hormone) and ACTH (adrenocorticotropic hormone) from pituitary to increase metabolism
  2. visceromotor response: increased sympathetic output to inc body temperature

PEPTIDE: ANORECTIC PEPTIDES

125
Q

Response to decreased leptin?

GI7

A
  1. dec activity of α-MSH and CART so dec humoural response: less PVN activation = less TSH, ACTH, sympathetic output = metabolism decreases
    - activation of parasympathetic output
  2. activation of NPY and AgRP containing neurons which stimulate lateral hypo (eat) and further inhibition of PVN
    - lateral hypothalamus releases MCH and Orexin *OREXIGENIC PEPTIDES release MCH (melanin concentrating hormone) to prolong consumption
126
Q

α-MSH and CART neurons specific jobs?

GI7

A

α-MSH (when elevated leptin): causes inhibition of NPY and AgRP neuron activity

CART (when elevated leptin): stimulates TSH and ACTH release

127
Q

Why did leptin supplementation fail to treat obesity?

GI7

A

likely high amnts of leptin all the time = dec sensitivity to leptin
-leptin could have less ability to cross BBB or less receptor expression

128
Q

Short term regulation of feeding behaviours? Factors that affect it?
GI7

A

depends on how long its been since last meal, and how much we consumed then

  • if fasting, orexigenic signals will increase (less satiety) i.e. ghrelin
  • factors: ghrelin (hunger hormone direct), gastric distension, CCK (I cells), inulin/gluc concen
129
Q

Ghrelin stimuli, response to it and evidence of its job?

GI7

A
  • inc release of ghrelin by cells in stomach in response to emptying. Once stretching of stomach occurs (eating), will decrease ghrelin release
  • if less stretch: ghrelin stimulates NPY/AGRP neurons in arcuate nucleus in hypothalamus.

Evidence:
Mice lacking these neurons will not respond to ghrelin injections
Even if just eaten, ghrelin injections will cause you to eat

130
Q

Gastric distension and CCK are ____.

GI7

A

Satiety signals

  • gastric distension sensed by mechanosensory neurons, info sent to NTS which connects to PVN and ARC to activate α-MSH and CART
  • CCK released by I cells in response to fats and AA entering SI (if injected, inhibits meal frequency and size)

Both act on NTS to stimulate satiety

131
Q

Insulin and blood glucose levels related how?

GI7

A

during cephalic and gastric phase, inc insulin = drop in blood glucose = drive hunger more via NPY/AgRP activation in ARC

-feedforward fashion of endocrine cell stimulation and ß-eyelet cells to secrete insulin

during intestinal phase, inc blood glucose = insulin secretion inc = acts as satiety signal via α-MSH and CART neuron activation in arcuate nucleus

132
Q

Marijuana and the munchies: chronic disease use?

GI7

A

prescribed as a means to stimulate appetite in patients with reduced appetite bc of chronic disease

  • research points to enhanced sense of smell
  • evidence for indirect activation of NPY/AgRP neurons in ARC **CB1 receptor in lateral hypothalamus
133
Q

Energy input and output?

GI8

A

goal is to maintain mass balance by having input = output

input: diet
output: heat (50%), work (50%)

134
Q

Types of energy output?
i.e. Energy output =
GI8

A

= heat + work
heat - regulated and unregulated (chemical regulation in body)
work - active transport across membranes, mechanical work (movement), chemical work (synthesis for growth and maintenance, energy storage via high-energy phosphate bonds like ATP and phosphocreatine, and chemical bonds like glycogen and fat)

135
Q

Measuring energy input and output: Bomb Calorimetry?

GI8

A

measures input: find it via heat released from BURNED FOOD

  • how much energy is within something we eat (Kcal)
  • one kcal is amnt of heat needed to raise the temp of 1L of water by 1ºC

slight over-estimate because we don’t completely digest/absorb some food ingested (cellulose - fiber)

to measure input, use atwater factors from nutrition (1g fat gives 9 kcal etc)

136
Q

Measuring energy input and output: Direct Calorimetry?

GI8

A

most accurate
measure how much heat is lost during EXERCISE (work)
know how much you are bringing in, difference b/n brought in and let out = energy used to produce work

  • heavily control O2 supply
  • have person doing nothing to get BMR and then doing activity to see how much energy is used only for that activity
137
Q

Measuring energy input and output: Indirect Calorimetry?

GI8

A

used more often

  • O2 consumption or CO2 production
  • estimate how much energy is being used since most is made during aerobic metabolism
138
Q

Basal metabolic rate: factors affecting overall metabolic rate?
GI8

A

persons lowest metabolic rate: most accurate when sleeping, measured as RMR since that’s more practical
Factors:
-age and sex (men burn 1 kcal/hr/kg mass, females 0.9)
-amnt of lean muscle mass
-activity level
-diet (induced thermogenesis, takes more energy to digest/store proteins vs fats)
-hormones (thyroid hormone considered single most important BMR determinant since they influence O2 consumption, heat production and CHO/lipid metabolism)
-genetics

139
Q

How is everything used (i.e. what makes up metabolism)?

GI8

A

Sum of all chemical reactions in body fall into 1 of these..

  • extract E from nutrients
  • use E for work: transport /mechanical, synthesis
  • store excess E for later use
140
Q

After absorbed in the SI, where does glucose, fa’s, AA’s go? fed state anabolism
GI8

A

glucose is main use for most cells energy production

glucose - to liver and muscle for glycogen production (glycogenesis), most body cells for energy, some goes to liver and adipose to be turned into glycerol

fa - to liver and adipose where 3 are combined with glycerol to make triglycerides (lipogenesis)

AA’s - to liver to be converted to fa for ^^ or go to muscle and some cells to be made into protein (peptide chain)

141
Q

Skeletal muscle, liver and adipose tissue use/store which % of glucose, fa, AA during anabolism (fed state)?
GI8

A

muscle - 71% of glucose stored here, 98% of AA here for protein turn over, unless starving then used as energy

liver - 24% glucose stored here, any excess converted to fa, uses 2% AA for fa production or converted to ketones

adipocytes - uses/stores 99% TGs, ~5% glucose taken up

brain has last <1% glucose

glycogen and protein storage limited, fat storage is unlimited as any excess AA and CHO converted to fat for adipocytes

142
Q

Overall energy reserve is majority ___.

GI8

A

TGs: 75-80%
proteins are 20-25% and glycogen is 1%

glycogen stores last ~few hrs
TGs last ~2 months
proteins can last long time, use can compromise cellular functions

143
Q

Fasted state energy use?

GI8

A

main role is maintaining glucose levels in blood, bc brain (neurons) and RBCs can only use glucose
-most other cells use TGs (fa’s) to spare glucose for CNS, this is called glucose sparing

144
Q

What happens to the stores in muscle, liver and adipose tissue, during fasted state?
GI8

A

muscle: converts glycogen back to glucose 6-P (glycogenolysis) for itself, forms pyruvate and lactate for liver, protein degradation to AA if extreme starvation
liver: glycogen back to glucose, put into blood for CNS, uses pyruvate, lactate, glycerol (and AA) for glucose (gluconeogenesis), converts fa’s to ketone bodies (ketogenesis) if starving
adipocytes: lipolysis occurs to produce energy (major*): TG’s converted to fa’s for use and glycerol for the liver. fa’s also sent around body for all non-nervous tissue

145
Q

Regulation of fed and fasted states? High insulin promotes ___.
GI8

A

insulin (ß islet cells) and glucagon (α islet cells) - both rely on blood gluc concen

high insulin (fed state) promotes anabolism: inc plasma glucose sensed by ß-cells, GIP and GLP-1 hormones also stimulate insulin release from ß-cells as well

146
Q

ß-cell production of insulin (mechanism)?

GI8

A
  • GLUT2 transporter on ß-cell membrane: facilitated glucose diffusion into cell if [blood glucose] is high
  • glucose goes through glycolysis/OP to make ATP
  • ATP gated K+ channels close as ATP increases (so low glucose = low ATP = open K channels = stable memb)
  • less K leaks out
  • cell depolarizes
  • volt. gated Ca channels open
  • Ca mediated exocytosis of insulin
147
Q

How does insulin signal for glucose uptake into tissues (mechanism)?
GI8

A
  • insulin binds to tyrosine kinase receptor
  • receptor linked to enzyme tyrosine kinase
  • tyrosine kinase phosphorylates insulin receptor substrate (protein), activates 2ndary cell signalling pathways
  • causes insertion of glucose transporters (GLUT4) on membrane
  • changes metabolic enzyme activity (ones that breakdown glycogen are inhibited, stimulates activity of ones that build TGs and glycogen)
148
Q

In the fasted state, glucagon’s main target is ____.

GI8

A

LIVER
Acts on G-protein coupled receptor to activate adenylate cyclase pathway and change enzymatic activity so….
-glycogenolysis, gluconeogenesis, ketone synthesis, protein breakdown stimulated
-glycogen synthesis and protein synthesis inhibited

Glucagon is released in response to dec plasma glucose

PHSI 208 - Resp., Renal, Acid/Base, Blood, GI, Repro. (5 decks)

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