digestion Flashcards
What is motility
the speed at which food moves through the digestive system
what is digestion and what three parts does it include
the chemical breakdown of food molecules by enzymes
-digestion
-absorption
-metabolism
steps of digestion (5)
1) mechanical breakdown
2) chemical breakdown
3) absorption
4) metabolism
5) egestion
What does mechanical breakdown include
1) prehension - movement of food into the oral cavity
2) mastication - chewing
3) motility - movement of food gradually through the digestive tract
What does chemical breakdown include
1) secretion
2) digestion
What is egestion
defaecation (getting rid of waste)
What is the difference between egestion and excretion
egestion is getting rid of waste products that haven’t been absorbed in the body whereas in excretion the waste products have been absorbed
What does saliva do
secretes amylase to breakdown starch and creates optimum environment for eznymes further down. Helps lubricate food going down oesophagus
What steps is the stomach involved with
motility and secretion
What is the liver/gall bladder/ pancreas involved in
secretion
What is the small intestine involved in
motility/digestion/absorption
What is the large intestine involved in
motility/fermentation/absorption/egestion
fermentation produces gases – farts
What salivary gland produces serous saliva
parotid
What glands produce mucous and serous saliva
mandibular/buccal/sublingual
What is the saliva like in simple stomached animals
mainly mucous to lubricate food passage
ph neutral for amylase action
What is the saliva like for complex stomached animals
mainly serous saliva for optimum conditions for fermentation
ph alkaline to buffer forrestomach for fermentation (carbonate)
large volme of salivary secretion
no amylase
What happens to digestive fluids released
most reabsorbed, if not causes diarrhea
How does saliva differ between herbivores and carnivores
carnivores don’t produce amylase
What components does saliva contain (8)
mucin (add water = mucus)
amylase (omnivores and horses, not ruminants or carnivores))
bicarbonate (to neutralise and buffer)
phosphate (in ruminants)
lysozymes+ antibodies (reduce infection)
protein binding tannins (digestion of cellulose_
urea (ruminants)
composition depends on species
What is the primary secretion of saliva
saliva that is first produced before it is released into the oral cavity so is still inside the gland
How does saliva osmotic effect change in non ruminants
primary secretion is isotonic with blood
at low flow rates (not eating) there is time for the minerals to be reabsorbed as it moves out of the gland so saliva becomes hypotonic
at high flow rate (eating) not enough time for minerals to diffuse so saliva is still isotonc
What happens to saliva composition for ruminants when digesting
ruminants digesting continuously so saliva is always isotonic
ruminant saliva needs to be buffered to keep rumen ph levels optimum for microbes
at low rates (not eating) PO4 is higher
at high rates (eating) HCO3 is higher
How is saliva secretion regulated
all under nervous syestem control
sympathetic causes reduction of production
parasympathetic causes increase for digestion
basal salivary secretion for oral hygeine
2 reflex pathways :
-congenital (innate)
-conditioned (learned)
What is the congenital reflex pathway of saliva
initiated by taste/smell of food in mouth
due to afferent nerves going to salivary centre in the brain and efferent nerves going to the salivary gland
(in ruminants also triggered by distension of cardia, rumino-reticular and reticulo-osmasal orficeses, swallowing and regurgitation)
What is the conditioned reflex pathway of saliva
iniated by repeated sensory stimuli associated with feeding so produces saliva in anticipation
(sight,smell noise)
iniated in cerebral cortex and then goes to salivary centre in medulla oblongata
where is the salivary centre
medulla oblongata
What are segmental contractions
breakdown and churning of food to mix it together, mechanical breakdown
What are peristaltic contractions
movement of food in aboral (away from mouth) direction at rate that allows enough time for digestion and absorption
What are anit-peristaltic contractions
movement of food in oral direction (back to mouth)
happens in some species to slow down moevment of food to allow sufficeint time to absorb
in ruminants occurs to allow rumination
also protective measure ( vomit)
What is mass movement (motiility)
exteneded peristaltic contraction used to empty sections of GI tract (happens in colon for defaecation)
How is motility regulated
before pharynx is voluntarily controlled by skeletal muscle (chewing + initial swallowing)
contractions of rest of gi tract (stomach + bowels) are involuntarily controlled by smooth muscle by nerves and hormones
final egestion stage is voluntarily controlled - not all species
What parts of the gi tract is chemical breakdown done by
salivary glands, liver, pancreas, glands in stomach and intestine wall
what is the ph in the stomach
2 for protein digestion
what is the ph in the small intestine
6-7 for enzyme
what enzymes breakdown carbohydrates
amylase, disaccharidases (produced in saliva, pancreas and intensitnal mucosal surfaces)
what enzymes breakdown proteins
pepsin,, trypsin and peptidases
produced in stomach glands, pancreas, intestinal mucosal surface
what enzyme breakdown fat
lipase and phospholipases
fat is not water soluble but blood is aqueous so breakdown and transportation needs emulisfcation by gall bladder?)
produced by pancreas and intestinal mucosal surface
How are food molecules absorbed
is selective process as most nutrients need specific transporter proteins
- actively transported if moving against conc. gradient (most by secondary active transport as requires indirect energy)
-passively transported either by tranporter protein or just diffuses down conc. gradient
what are three layers of the abdominal wall
skin
subcutaneous fascia
muscles
How does skin vary in species
can be very tough in species (e.g. ox used in leather)
variable cover in hair for insulation (dense in horse, ox, carnivores. minial hair in pigs, and wool in sheep)
what is the subcutaneous fascia
lowest layer that underlies skin - ( superficial fascia contains adipose (all over in pig)
contains cutaneous trunci muscle
- deep fascia in ox and horse
developed into tough fibro-elastic sheet
What are the muscles of the abdominal wall
external abdominal oblique
internal abdominal oblique
transverse abdominal
rectus abdominis
how is the abdomen laterally contained
by the external and internal abdominal obliques and the tranverse abdominal
how is abdomen ventrally contained
rectus abdominis (straight six-pack muscle)
what are the functions of the muscles in the abdominal wall
- enclose the abdominal cavity and its contents
- motor functions:
contraction causes increase in intra-abdominal pressure (vomiting, defaecation and micturtion)
if larynx closed, also causes increase in intra-thoracic pressure (via diaphragm) used in breathing, coughing and sneezing
where does the recuts abdominis originate
ventral surface of sternal ribs/sternum
Where does the rectus abdominis insert
on cranial border of pubis via pre- pubic tendon
what are the left and right sides of the rectus abdominis separated by
linea alba - in immature animals this is pierced by the umbilicus
what is the external oblique
outermost lateral abdominal wall muscle , is a flat muscle so tendon is massive flat tendon
where does the external oblique originate
lateral caudal surfaces of ribs 4+ and lumbodorsal fascia
where does the external oblique abdominal insert on
the line alba and prepubic tendonh
which ways do the muscle fibres run in the external oblique abdominal wall
obliquely from cranio dorsal to caudo ventral (left to bottom right)
what is the internal oblique
middle layer abdominal wall muscle
where does the internal oblique originate
coxal tuber and lumbodorsal fascia
where does the internal oblique insert
line alba, last rib and cartilages of caudal rib (by tendon)
what is aponeurosis
flattened tendon
which way do the fibre run in the internal oblique
caudo dorsal to cranio ventral (top left to bottom right )
what is the tranverse abdominal muscle
the innermost abdominal wall muscle
where does the transverse abdominal muscle originate
medial surfaces of ventral parts of caudal ribs and deep lumbodorsal fascia
where does the transverse abdominal muscle insert on
linea alba
which way does the transverse abdominal muscle fibres run
transvers (dorsal to ventral)
what is the sheath of the rectus abdominis muscle
formed from the tendons of the lateral abdominal wall muscles
they pass above and below the rectus abdominis to join in the midline
join = aponeurosis and forms the linea alba
in the cranial abdomen of the dog how the muscles arranged in respect to the rectus abdominus
transverse abdomen passess dorsally
internal obliques split and run both dorsally and ventrally
external obliques and the yellow abdominal tunic and the external obliques
all of the abdomen in the ox is set up like this
what is the yellow abdominal tunic
part of the deep fascia which is only present in horses and oxen
in the mid abdomen of the dog how are the muscles arranged in respect to the rectus abdominus
the transverse abdomen passes dorsally
the internal, external obliques and the yellow tunic passes ventrally
all of the horse abdomen is set up like this
in the caudal abdomen in the dog how are the muscles arranged in respect to the rectus abdominus
they all pass ventrally
which part of the dog abdomen is the strongest
cranial is strongest but the least flexible, caudal is the weakest but the most flexible
more movement means the section has weaker connections
how is the abdomen innervated
spinal nerves of last thoracic vertebra and L! - L5
dorsal roots innervate dorsal musculature
ventral roots split into 3 branches:
- medial (runs between transverse abdominal and internal abdominal obliques down to rectus abdominus)
- lateral (runs between IAO and EAO down to midway)
- lateral cutaneous (perforates EAO to innervate skin)
what is the inguinal canal
potential space between the deep inguinal ring and the superficial inguinal ring
the deep inguinal ring is the gap in the internal oblique muscle
the superficial inguinal ring is the slit in the external oblique muscle
what are the 14 parts of the adult gi tract
Mouth
Salivary Glands
Pharynx
Oesophagus
Stomach
Liver
Duodenum
Pancreas
Jejunum
Ileum
Caecum
Colon
Rectum
Anus
Where does the epithelium lining GI tract and associated exocrine glands arise from in the embryo
endoderm
where does the muscle and connective tissue arise from in the embryo
mdsoderm
describe the formation of the gut in the embryo
as embryo develops part of yolk sac taken into body
This goes on to form the gut
Midgut separated from foregut / hindgut by cranial / caudal intestinal portals
Foregut / hindgut end blindly at oral / cloacal plates
In later development these will perforate so gut is continuous with mouth and anus
what does the forgut differentiate to in the embryo
the pharynx, oesophagus, stomach and initital duodenum
what does the midgut differentiate to in the embryo
duodenum, jejunum, caecum and ascending / transverse colon
what does the hindgut differentiate to in the embryo
descending colon and rectum
describe the development of the foregut
Enlargement of caudal part of foregut identifies stomach
Oesophagus develops from gut tube between this and the pharynx
Rotation of stomach along its longitudinal axis brings dorsal aspect to the left
Becomes greater curvature
Dorsal mesogastrium is also pulled to the left
Becomes greater omentum
Rotation of stomach along a dorsoventral (vertical) axis pulls cranial extremity to left
Becomes cardia
This rotation also pulls caudal extremity to right
Becomes pyloric antrum
Short terminal portion of foregut becomes initial duodenum (as far as entrance of bile / pancreatic ducts
Part of stomach to left of cardia enlarges to form fundus
describe the development of liver
Endodermal diverticulum at junction of foregut and midgut becomes liver
Cranial branch becomes gland tissue and hepatic ducts
Caudal branch becomes gall bladder and cystic ducts
Liver then expands caudally into abdominal cavity
Pancreas arises from same endodermal diverticulum
Dorsal primordia becomes left lobe of pancreas with pancreatic duct
Ventral primordia becomes right lobe of pancreas with accessory pancreatic duct
Dorsal and ventral primordia eventually fuse
liver detoxifies the bllod so alot of damage so needs to be able to regenerate
develops very early on and then expans so not at alot of space for other things to develop
celiac artery resposnible for all foregut organs
which artery is resposnible for supplying blood to all foregut organs
celiac artery
how does the pancreas develop
starts with two separate organs that fuse together so there is two secretory ducts
how does the midgut develop
forms most of intestine from duodenum (after bile/pancreatic ducts) to end of transverse colon
not a lot of room to elongate due to liver
connection with yolk sac reduces to form vitelline duct (later is lost but remnant sometimes visible at Meckel’s diverticulum)
early growth rapid so it hangs in elongated loop along with mesentery with extensive blood supply
rapid expansion of liver pushes mid gut out of the abdominal cavity into the umbilical cord where it continues to develop (physiological herniation)
- cranial limb becomes ret of small intestine
- caudal limb becomes ascending/transverse colon
- diverticulum arises between these to become caecum
gut develops outside of animal and then comes back into abdomen and the umbilical closes to stop hole (comes back due to further enlargement of the abdominal cavities)
what is the mesentery
fold of peritoneum which attaches the stomach, small intestine, pancreas, spleen and other organs to the posterior wall of the abdomen
How does midgut rotate
cranial limb elongates rapidly to form small intestinge
- this rotates around its arterial axis ( caudal limb pulled cranially and to left side)
further rotation occurs (caudal limb pulled across abdomen to right side
caecum and ascending colon pulled with it to the right side
transverse colon ends up passing cranial to the cranial mesenteric artery
how does the hindgut develop
rotation of midgut means hindgut is on the left side of the abdomen
it differentiaties into descending colon and rectum
bud develops from ventral part to form the allantois – expands through the umbilical opening to form the allantoic sac
urorectal septum enlarges to meet cloacal membrane – divides gut into 2 separate tubes (dorsal continuous with colon and ventral part continuous with allantois which forms the lower urogenital tract)
need to separate unrinary tract and gi tract (rectum) by the urorectal septum
what is the blood supply to hindgut
branches of caudal mesenteric artery
what is the peritoneum
serous membrane that lines abdominal cavity and envelops abdominal organs
it is a single continuous sheet
contains the parietal peritoneum, the visceral peritoneumum and the connecting peritoneum
what is the parietal peritoneum
lines abdomen and goes through the inguinal canal
what is the visceral peritoneum
peritoneum that lines the organs surfaces
what is the connecting peritoneum
joins different organs, dictates where in abdomen and how movement different organs should have in the abdomen
- mesentery = connects bowel to body wall
- omentum = connects stomach to something
- fold = connects bowel to bowel
- ligament = connects non-bowel to something
what is the bowels
tubes = small + large intestine
how is the anatomy of the abdominal cavity defined
by peritoneal attachments to one another or body wall
aids or hinders surgical access
some organs are tightly/loosely attached which changes how easy to access
what is the abdominal cavity
contains everything includes peritoneum
defined by diaphragm cranially
abdominal wall contained laterally
what is the peritoneal cavity
potential space between parietal and visceral peritoneum
contains nothing but peritoneal fluid of abnormalities
what is peritonitis
peritoneal inflammation
what is the diaphragm
separates thorax from abdomen
attaches to body wall at level of last rib
extends into thorax to level of 5th intercostal space
what does aorta pass through
aortic hiatus between left and right crura
Where do hormones get released into and why in the gi system
hormones in the gut get released into the blood stream not the lumen as they are proteins so will be digesting
what are the digestive processes co-ordinated by
neural regulation and hormonal regulation
what is the enteric nervous system
the nervous system of the gi tract, entirely within the wall of the gi tract, no connection to the brain operates by itself
has sensory cell and motor cell
sensory - responds to content of lumen (lots of carbs) and degree of wall stretch
motor cells - cause smooth muscle to contract and epithelial cells to secrete digestive juices and hormones
what are the two reflex arcs of the digestion system
-short reflex arc (enteric nervous system, sensory and motor nerve cells with wall of GI tract that can operate by itself but can be affected by the CNS)
- long reflex arc which sypmathetic + parasympathetic nervous system working to regulate digestion, connects to central nervous system (stimuli from other parts of body e.g. vision, sight, smell
can effect salivary glands, liver, pancreas of smooth muscle and glands in the wall of the gi trat
what does a simple reflex arc consist of in the enteric nervous system
single sensory cell and a single motor nerve cell
what does a complex reflex arc in the enteric nervous system consist of
simple reflex arcs connected by interneurons so nerve impulse is propogated across a wider area
what do short reflex arcs in the enteric nervous system allow
allow gastrointestinal tract to have extensive control most reflexes are stimulatory, (contraction or secretion)
acetylcholine is main transmitter
can also be inhibitory neurotransmitter that usually act on sphincters to relax them to allow food to move through the gut
how does the parasympathetic nervous system affect digestion
-promotes digestion
- long pre-ganglionic fibres run in vagus
- cholinergic receptor, transmitter acetylcholine
- post-ganglionic fibres embedded in the wall of the GI tract and connect to the ENS to stimulate secretion and motility
how does the sympathetic nervous system affect digestion
- inhibits digestion
- pre-ganglionic fibres run in splanchnic nerves
- cholinergic receptors (transmitter= acetylcholine)
- post-ganglion fibres separate run along arteries to organ or in hypogastric nerves
- synapse with ENS or redduce acetylcholine release at parasympathetic pre-synapses
- post ganglionic hace adrenergic receptors that transmit noradrenaline to inhibit secretion and motility + decrease blood supply to the GI tract
what are the entero-enteric reflexes
reflexes that affect different parts of the gi tract to coordinate activity between different sections
e.g. mastication stimulates release of saliva, gastric juice, pancreatic uice and bile
- stretching of stomach relaxes ileo-colic sphincter to allow food to move out of SI to allow food to move in (gastro-colic reflex)
where is gastrin produced and what is it stimulated by
produced in the caudal stomach
stimulated by peptides and amino acids
and acetylcholine
causes HCL to be released and growth of gastric/intestinal mucosa
where is secretin produced and what is it stimulated by
mainly produeced by the duodenum
stimulated by Hcl
causes pancreatic HCO3 to be released
where is cholecysotkinin produced and what is it stimulated by
mainly produced in the duodenum
stimulated by fatty acids, monoglycerides, amino acids and peptides
causes pancreatic enzymes to be released and contracts gall bladder
where is gastric inhibitory peptide produced and what is it stimulated by
produced by the cranial small intestine
stimulated by fat, glucose and amino acids
inhibits Hcl release and stimulates insulin production
what are the phases of regulation
they relate to the site of stimulus
-cephalic phase = head (e.g. anticipation of food, emotion) ANS (stimulated by para)
-gastric phase = stomach (e.g. stomach distension, presence of peptides) ANS, ENS and hormones (gastrin)
- intestinal phase = intestines (e.g. intestinal distension/lumen contents)
co-ordinated by ANS, ENS and hormones (secretin, CCK and GIP)
how is appetite regulated
by the appetite centre and the satiety centre in the hypothalamus
where is the appetite centre found and what does it do
found in ventro lateral hypothalamus
causes food searching anf voracious eating
has direct effect on animals behaviour
where is the satiety centre and what does it do
ventro - medial hypothalamus
causes refusal of food and inhibits appetite centre, stops overeating as a protective function
theories of how appetite is regulated
-glucostat theory (glucose levels)
- CCK thory (levels of CCK)
- lipostat theory ( levels of fat)
how is motility regulated in the gi tract
by pacemaker cells
they produce continuous oscillation in membrane potential in groups of pacemaker cells called the interstital cells of the cajal
where are the interstitial cells of cajal found
they are pacemaker cells found between the circular and longitudinal muscles
synchronisation of smooth muscle contraction acheived by osciallations transferring via gap junctions
how do pacemaker cells in gi tract cause contraction
if stimulus absent depolarisation is not big enough to reach threshold
if stimulus (neural or hormonal) present then depolarisation is enough to cross threshold and causes action potential to contract smooth muscles due to opening of calcium channels
it is the frequency of the action potentials not the height that affects the strength of muscle contraction
what is deglutition
swallowing
the movement od food from oral cavity into oesophagus
how is food swallowed
1) food is molded into the bolus by tongue and moved upwards and backwards to pharynx – this is under voluntary control
2) soft palette is forced up to seal off nasal cavity
3) pressure sensitive sensory cells at back of throat are stimulated, sends impulses to swallowing centre in medulla
4) swallowing reflex is initiated under involuntary control
5) epiglottis closes trachea to prevent food going into the lungs
what can go wrong with swallowing
- failure of soft palette to close off nasal cavity
- failure of epiglottis to close off trachea
-pharyngeal paralysis = nerve/muscle injury
-myaesthesia gravis = antibodies form against acetycholine receptors - botulism - clostridial toxins block acetylcholine release
- anaesthesia often induce vomity but swallowing process is impaired
what are the four layers of the oesophagus
1) mucosal layer = stratified squamous epithelium
2) submucosal layer
3) muscular layer = inner circular, outer is longitudinal . smooth and striated muscle
4) serosal layer = not true serosa, is loose connective tissue in neck called adventita + slower healing. in thorax it becomes true serosa
how is food tranpsorted down the rest of the oesophagus once it has been swallowed
need to get food into the stomach
1) upper oesophageal sphincter closes behind food bolus (epiglottis reopens to allow respiration)
2) peristaltic contractions force food down oesophagus
3) lower oesophageal sphincter opens to allow passage of food into stomach
what does the lower oesophageal sphincter do
separates oesophagus from the stomach (also called the cardiac sphincter)
cannot easily see except in horses = physiological sphincter
always closed except during swallowing
how does the oesophagus enter the abdomen
enters at oblique angle so stomach exerts pressure on the diaphragm due to the higher pressure in the abdomen compared to the thorax so helps close the oesophagus to stop regurgitation of acidic stomach contents
How does vomiting occur
vomiting is a protective measure of stomach to get rid of bad substances
it is the active propulsion of stomach contents back into the oral cavity
1) deep inspiration with simultaneous closures of trachea/nasal cavity causes increased intrabdominal pressure via diaphragm extending
2) forceful contraction of abdominal muscles (not the gastric)
3) cardiac sphincter (lower oesophageal sphincter) opens
4) food is propelled up the oesophagus
5) upper oesophageal sphincter opens to allow food out
what is vomiting controlled by
vomiting centre in the medulla
stimulated by pharyngeal/gastric distension or irritation (fingers at back of pharynx)
what is emesis
vomiting
difference between vomiting and regurgitating
ruminants prefer to regurgitate
regurgitating is a passive process as it only involves slow contraction of stomach walls not the abdominal muscles
what is gastric torsion
occurs in horses and wide chested dogs
when the stomach rotates 90-360 which seals off the caridac sphincter which prevents vomiting
causes stomach to distend further due to trapped gas
rotation can stop blood supply to gastric tissue so can become hypoxic and die
stomach dilation can stop venous return to heart via caudal vena cava = causes circulatory shock = extreme emergency (need to restore blood volume first as in hypovolaemic shock)
occurs in wider chest as there can be more movement of stomach, stomach has loose connection to abdominal wall
what are the functions of the simple stomach
1) digestion = continuing hydroysable carbohydrates digestion and starting protein digestion
2) protection = acid secreted kills microbes ingested with food
3) storage = ensures food going to small intestine at a slow enough rate to allow optimum absorption
4) mechanical breakdown/mixing = breaks down food and mixes with enzymes and acid to form chyme
what are the anatomical regions of the stomach
1) cardia = entrance to stomach, physiological valve, where oesophagus enters
2) fundus = blind ending part of stomach
3) corpus = main body
4) pylorus = exit from stomach to the small intestine
greater curvature is the round edge facing the rest of the abdominal cavity
lesser curvature is the round edge facing the diaphragm
what are the embryological regions of the stomach
give rise to different mucosal linings of the stomach
1) oesophagul region = non-glandular, stratified squamous epithelium
2) cardiac region = secretes mucus only
3) fundic region = secretes mucus and gastric juices
4) pyloric region = secretes mucuos only and regulates stomach emptying
what are the different cell types of the stomach
consists of cylindrical glands
1)mucous (goblet) cells
2) parietal (oxyntic) cells
3) chief ( peptic) cells
4) entero-endocrine cells
what do mucous goblet cells do
secrete mucus to protect stomach from hcl
what do parietal cells do
secrete hcl to digest protein
what do chief cells do
secrete pepsinogen (active = pepsin) to digest proteins
what do entero-endocrine cells do
secrete hormones
what does motility in the stomach need to do
- relax to receive food
- mix and mechanically breakdown chyme
- empty contents into small intestine
- prevent regurgitation of contents into oesophagus
how does the stomach prepare for eating
relaxes smooth muscle = receptive relaxation
regulated by swallowing centre via the vagus nerve
transmitter is vasoactive intestinal peptide
what neurotransmitter causes the stomach to relax in preparation for eating
vasoactive intestinal peptide
how does emptying of stomach occur
by strength of smooth muscle contraction and opening/closing of the pyloric sphincter
how is emptying of the stomach stimulated
- neurally as expansion of the stomach walls increase strength of contraction
- hormonally as the release of gastrin increases strength of contraction and dilates pyloric sphincter
how is emptying of the stomach inhibited
factors in duodenum act = increased pressure in duodenal walls, lower ph, high fat/peptide conc, high osmolarity
- neurally via increased sympathetic activity and decreased para activity
- hormonally via secretin, cholecystokinin and gastric inhibitory peptide
what is digestion
enzymatic breakdown of nutrient macromolecules into smaller units can be absorbed
how is starch digested in stomach
by amylase at a ph greater than 6
amylase is produced by saliva in mouth
newly swallowed food is forced into stomach centre where acid is secreted so theere is gradual decline in ph from centre to edge so starch digestion continues for a while
how is protein digested
by pepsin in a low ph. gastric juice consists of Hcl and pepsinogen (inactive so it doesn’t digest own organs until in contact with foreign protein)
stomach mucosa is resistant to digestion to stop ulceration
what is the structure of starch
starch is a complex carbohydrate made up of glucose monosaccharides joined by alpha glyosidic bonds
2 glucose molecules = maltose
starch is made up of amylose (straight) and amylopectin (branched)
what is fibre
non-hydrolysable carbohydrate that cannot be digested by animal enzymes as it contains beta glyosidic links
Compare omnivore, herbivores and carnivores starch digestion
omnivores = high starch levels. Pig adapted stomach to allow starch digestion to continue for longer as fundus is made from cardia region so no acid is secreted.
herbivores has low levels of starch, more fibre. Working horses have increased level of starch to allow more energy so they have adapted their stomachs to allow starch digestion to continue for longer as aread of stomach made from oesoephagul region so no acid is secreted
carnivores = low levels of starch so saliva doesn’t contain amylase only digested in SI from pancreatic amylase
what are the functions of Hcl
converts pepsinogen into pepsin
provides acidic environment for pepsin to digest protein
prevents fermentation by killing micro-organisms (pigs and horse large part of sotmach doesn’t produce acid some fermentation of starch into VFAs by digested micro-organisms does occur)
degrades large chunks of connective and muscle tissue into smaller more digestible particles
how is hcl made
co2 out of blood cell joins with water in celll to form carbonic acid
which breaks down to produce H+ which is actively released into gland lumen which becomes acidic and blood flow becomes relatviely alkaline (alkaline flow)
duration + volume of HCL secretion depends on secretion
maximum secretion occurs 2-3 hours after a meal in dogs, pigs is almost continuous
where is HCL secreted from
parietal cells
why does urine ph increase after a meal
to correct the alkaline tide carbonate is secreted into the urine
due to delay between food passing from stomach to pancrease (pancreas neutralised ph of food passing into duodenum)
describe secretion of pepsinogen
made and stored in chief (peptic) cells
secreted as pepsinogen (inactive) which gets activated by HCL in stomach
pepsin degrades protein and collagen by breaking peptide links adjacent to amino acids (peptides produced cause further HCL secretion
pepsin also activates more pepsinogen to be released (auto-catalysis, positive feedback)
what is self perpetuation
when something can be digested by itself (pepsinogen gets digested by pepsin)
how is secretion of HCL stimulated in the stomach
- reflex arcs (long = vagus, short = locally)
acetylcholine + histamine, causes direct stimulation as they act directly on the cells, act on chief cells to produce pepsinogen, parietal to produce and mucin cells to produce mucin - gastrin stimulate endrochromaffin light cells to produce histamine
which then acts on parietal cell - these 3 substances amplify eachothers effects
what is the cephalic phase of digestion
caused by neural stimulation before food enters the stomach (sight, smell, taste, presence of food in mouth) which stimulates secretion directly via acetylcholine and indirectly via gastrin in blood
what is the gastric phase of digestion
caused by neural stimulation once food has entered the stomach
caused by:
-stomach expansion
- peptides in lumen
stimulate secretion :
- directly by acetylcholine
-indirectly by gastrin
what is the intestinal phase of digestion
after food has entered duodenum
stimulated by neural (cholinergic) or hormonal (gastrin,CCK)
either stimulation or inhibition depending on acidity of chyme and food components
CCK hormones have different roles can be a partial or strong agonist (different levels of H+ secreted) dogs are partial cats are strong
most intestinal response are inhibitory
what is chyme
food mixed with digestive juices
how does the hormonal stimulation occur in gastric digestion
mediated by gastrin primarily in response to peptides in stomach, reaches target cells via blood
how is secretion inhibited in the stomach
dudenal signals that inhibit stomach motility also inhibits gastric juices via neuronal (vagus) and hormonal (secretion,CCK and GIP)
stomach is localally inhibited
when - ph is less than 2 gastrin released to protect gastric mucosa from damae
- before food enters stomach H+ is low but not buffered so gastrin inhibited
- once food enters stomach with buffer (mainly protein) H+ reduces therefore gastrin released again
- more protein in diet = more gastrin released (protein is a buffer)
what is stomach mucosa protected by
- secretion of mucin by mucous layer
- epithelaial cell membrane and interconnecting tight junctions are impenetrable b yH+
- epitheiial cells are replaced every 2-3 days
what is pathophysiology ]
how normal physiology goes wrong
what happens to cause gastric and duodenal ulceration
duodenal ulcers caused by increased acid production
gastric ulcers caused by decreased protective function
hcl and pepsin damage epithelial cells and underlying tissue
damaged ccells produce histamine which stiumlates acid secretion + increases proble,
why does diarrhoea occur
occurs due to increased secretion and decreased absorption of gastric juices (so there is higher water content in lumen of gut)
villi damaged by acid
faeces appear dark red as blood gets partially digested
What abnormalities cause gastric and duodenal ulceration
Non-steroidal anti-inflammatory drugs (NSAIDs)
Inhibit prostaglandin synthesis (prostaglandins stimulate production of mucous & HCO3-)
Protective mechanisms reduced
Mast cell tumours / Mast cell leukaemia
Produce excess histamine
Increases HCl production
Gastrin-producing tumours
Produce excess gastrin
Increases HCl production
how to treat gastric ulceration
-inhibit proton pump into lumen of gut (gland cells)
antacids neutralise acid in gut to reduce damage
- MBA (mucosal binding agents bind to damaged ulcerated tissue and create protective layer
- anithistamines stop histamine
- proton pump inhibitors
where is the liver located
dome of diaphragm within the abdominal cavity
how many lobes does the liver have
4
left, quadrate, right and caudate
in dog,cats and pigs the left and right lobes are split into lateral and medial to allow movement of the liver due to the diaphragm pushing it
the caudate lobe has 2 parts - the caudate and papillary processes (except in horses)
in horse liver is displaced to the right due to enlargement of the colon so only the left lobe is split
in rumens live is displaced the whole way to the right due to the rumen so doesn’t make contact with the diaphragm so lobes don’t split
which species is the gall bladder present in
present in carnivores, ruminants, pigs and mice
absent in horses and rats
how to identify left and right lobes
left lobe is bigger and has a knotched edge
right side has a groove where the kidney normally sits
what does the histology of the liver look like
liver organ is surrounded by a capsule of connective tissue
this capsule extends into liver as septae (highly branched)
the septae delineate the structural units of the liver into hepatic lobules which are haxagonal in shape around a central vein
what is a hepatic lobule
histology - hexagonal structural unit of liver cells separated by septae
in centre is a vein
what are hepatocytes
main functional cells of the liver
absorb molecules from the space of disse across the sinusoidal membrane
create bile acids
what is the space of disse
gap between endothelium of liver and the liver cell
that contains blood plasma
what are bile canaliculus
dilated intercellular space between cells that collects bile secreted y hepatocyte cell
bile is secreted across the canalicular membrane
where is bile produced and secreted
produced in the liver
secreted and stored in the gall bladder
what is the biliary system
moves bile from liver to duodenal lumen or into gall bladder to be stored
1) bile is secreted across hepatocyte membranes into canaliculi
2) bile flows from canaliculi into smaller bile ducts called ductules
3) ductules anastomose into larger ducts
4) these coalesce to form hepatic bile ducts
5) hepatic bile ducts lead into common bile duct along with gall bladder duct (joins by cystic duct) and the pancreatic duct
6) common bile duct enters duodenum at sphincter of Oddi
good diagram in powerpoint slide 10
where does the common bile duct enter the duodenum
the sphincter of oddi
how does the bile move between the gall bladder and the bile duct
cystic duct
when animal is not eating what happens to the bile
bile enters the gall bladder and is stored and concentrated
horse has no gall bladder as it is continuously eating so no need to store bile
describe the blood supply of the liver
most of blood entering comes from the hepatic portal vein ( comes from gi tract so anything absorbed from the gi tract passes through the liver so liver can determine if substances are safe before they enter the body)
bit of blood enters from the hepatic artery which is a branch from aorta
the venous and arterial blood mix as they flow into sinusoids and then go into central veins
hepatic vein takes blood from liver back to heart via the caudal vena cava
fat bypasses liver as too big to enter the capillariess
what molecule from digestion skips the liver
fat (molecules too big to enter capillary bed)
describe hepatic lobules
-hexagonal in shape
- made of plates of hepatocytes which radiate outwards from a central vein
- at corners are portal tracts (triads) made up of bile duct, hepatic artery and hepatic portal vein that connect to the main vein by sinusoids
what is in a portal triad
bile duct
hepatic artery
hepatic portal vein
sometimes lymphatic vessels
connected by sinusoids to the centre vein by sinusoid (blood channel lined by hepatocytes)
what is the hapatic acinus
functional unit of liver that can be divided into zones
centred on line connecting two portal triads
has different zones that correspond to the distance from the arterial blood supply
zone 1 = cells closest to artery so have best oxygen supply
zone 3 = cells furthest away from artery supply so have worst blood supply
how does the hepatic acinus relate to the pattern of disease in the liver
cells in zone 3 (further away) tend to die first
death occurs from outside in
what are sinusoids
connecting vascular channels that are lined with fenestrated endothelial cells and behind that layers of hepatocytes
contain kupffer cells (macrophages of liver)
allows blood flow from portal bein and arteries to central vein
what are kupffer cells
macrophages of the liver found in the sinusoids
what are the main functions of the liver (8)
-detoxify of body waste, xenobiotics and drugs
- synthesis cholesterol and bile acids
- synthesise plasma proteins
- breakdown red blood cells and degrade haem
- metabolise carbohydrates, lipids and amino acids
- remove bacteria
- produce clotting factors
- store glycogen, iron, copper and vitamins
what does liver metabolise
carbohydrates:
-glycogenesis (build glycogen store)
-glycogenolysis (breakdown glycogen)
-gluconeogenesis (maintain blood glucose levels)
lipids:
-oxidise fatty acids, produce ketone bodies
-synthesise cholesterol, phospholipids and bile acids
proteins:
-deamination and transamination of amino acids
- synthesise non-essential amino acids
how does liver clear the bloodwh
major role in purification, transformation and clearance (as all substances absorbed from gi go through liver)
- converts substances (drugs/toxins) into less toxic compounds
- first general pathway is the cyochrome P450 pathway, as hepatocyte microsomes contain non-specific enzyme system
- further degradation occurs
- toxins are then conjugated with water soluble compounds and excreted in bile via the biliary system
what substances the liver detoxicfy and clear
- drugs (nearly all drugs are modified/degraded i the liver and conjugated or modified for excretion)
-toxins (liver is responsible form detoxicfying chemical agents + poisons, try to stop blood poisoning) - endogenous metabolites (ammonia is converted to urea by liver and excreted in urine by kidneys, hormones inactivated in liver and haem is broken down to stop it building up and excreted in bile)
in older animals liver function is reduced so need to have a smaller drug dose
what are the stages of detoxification
1) cytochrome P450 = liver microsomes
2) phase 1 = product (hydrogenation, hydroxylation and oxidation)
3) phase 2 = conjugation (transported and excreted by urinary or biliary system, e.g. glutathione, amino acids, sulfate and glucoronic acid
examples of plant toxins
- digitalis (used to be used to treat heart conditions as made heart beat quicker but has very low safe margin)
- aflatoxin = from fungal growth on damp grain/soybeans
- phylloerythrin = found in any green photosynthesising plant, made by metabolite of chlorophyll
how are red blood cells removed from the blood
removed by macrophages in spleen and liver as they have a finite life
how are bile pigments excreted
with bile in common bile duct into duodenum (biliary system)
play no part in digestion, purely a waste route for haem
in gut bilirubin can be acted on by intestinal bacteria which removes glucoronic acid, then bilirubin is oxidised to become brown = faeces colour
how is haem converted to bile pigments
1) haem first converted to biliverdin (green) in macrophage
2) still in macrophage biliverdin is transformed to bilirubin (yellow)
3) bilirubin transported to liver in blood bound to albumin
4) in liver bilirubin is conjugated with gluoronic acid and excreted as bile pigment in biliary system
bile pigments have nothing to do with digestion
what is urobilinogen
created when conjugated bilirubin is metabolised by bacteria in the small intestine
goes to kidney and then excreted in urine
gives urine its yellow colour
what does the small intestine do
major site of digestion and absorption in simple stomached mammals
absorption is a selective process happens via specific transported proteins
most absorption happens irrespectively of body requirements
most nutrients absorbed along all of small intestine
anything undigested passes onto large intestine for microbial fermentation
what ions are absorbed depending on body requirements
divalent ions and trace requirements as they can be toxic at too high a level so won’t be absorbed in body levels are too full
what nutrients are only absorbed in the ileum
vitamin B and bile salts
what are the 2 phases of digestion in the small intestine
- luminal (enzymes secreted by salivary glands and pancreas
- membranous (enzymes attached to epithelial surface of intestinal cells
what are the 3 parts of the small intestine + what percent are they
- duodenum (15%)
- jejunum (75%)
-ileum (10%)
what are the 4 layers of the small intestine
standard, same as rest of gi tract
-mucosa
-submucosa
-muscle (circular and longitudinal)
-serosa
how is surface area of the small intestine increased
mucosal folds
vili
microvili
what are the 4 types of the intestinal epithelial cell
goblet cells
enteroendocrine cells
paneth cells
enterocytes
what are goblet cells
secrete mucus for lubrication and protection of mucosa
secrete HCO3 for neutralisiation of stomach acid
what do enteroendocrine cells do
control digestive function via sensory mechanisms and release hormones
what do paneth cells do
not sure
might be involved in defence against microbial penetration
what do enterocytes do
majority of cells that are responsible for absorption via transporter proteins
-contain many brush border enzymes for digestion
- enzymes not secreted but remain attached to epithelial membrane
what is the continuous turnover of cells in the small intestine
cells migrate from cryptus up to the villus
then cut off from villus tip
and get digested by enzymes
migtation takes 2-5 days (so if change diet need to do it gadually as cells have to mature to be able to cope with diet)
what does small intestine motility do
- mixes luminal contents by segmental contractions
- propel contents down at appropiate rate to allow max digestion + absorption by peristaltic contractions
-emptying as circular muscle at ileo-colic junction is well developed and acts as a physiological valve (sphincter)
how do segmental contractions mix food in the small intestine
segmental contractions during eating
circular contractions occur along distended intestine that causes the intestinal contents to be divided into small segments
new contractions occur in centre of segment
this is repeated repeated many times to mix contents with digestive juices and to move contents towards mucosal surface for digestion and absorption
weak peristaltic contractions occur too to move food down
how does segmental contractions stop
when chyme reaches distal small intestine feedback mechanism inhibits proximal small intestine
this is mediated by neural and hormonal mechanisms
this major mechanism for co-ordinating small intestinal transit to allow maximal digestion and absorption to occur
small intestinal transit in about 3-4 hours in most species
how do peristaltic contractions in small intestines work
main type of contraction when digestion/absorption complete (inter-digestive)
-irregular moderate peristaltic activity propagates a short distance before dying out
-regular strong peristaltic activity that moves food a long distance
each new contraction starts a little further down the small intestine
when contractions reach ileum a new one starts in duodenum
- contractions strart in the migrating myo-electric complex
takes 1-2 hours to move down the small intestine these contractions prevent backflow from colo
-anit-peristalsis die out very quickly in small intestine
what starts peristalsis contractions in the small intestine
most motor neurons of enteric nervous system release acetyl choline
that stimulates inhitory transmitters are released
distension of segment causes stimulation and inhibition
(longitudianal muscle relaxes while circular muscle contracts behind chyme
longitudinal muscle contract and circular muscle relaxes infront of chyme)
how is motility regulated in the small intestine
controlled by interstitial cells of cajal (same as stomach) which are pacemaker cells
-spontaneous oscillations are always present independent of neural and hormonal influencees
highest frequence in duodenuom lowest in ileum
duodenum can inhibit stomach emptying if chyme causes too much distension
- if depolarised enough multiple action potential spikes occur to cause smooth muscle contractions
- these go cell to cell via gap junctions
primarily regulated by ENS
-presecnce of chyme in duodenum stimulates short reflex arcs dependent on degree of distension
strength of contraction increased by para / decreased by sympathetic
(ANS is to co-ordinate motility in different parts of GI via long reflex arcs
what is the function of carbohydrates
provide most of energy in herbivores and omnivores
what are polysaccharides + examples
repeated disaccharide units
alpha glycosisdic bonds are digestible by mammalian enzymes
starch (amylose)
amlyopectin
glycogen
beta glycosidic bonds = indigestible
cellulose requires microbial fermentation
what are 3 most common disaccharides + what are their monosaccharides
Maltose (glucose + glucose)
Sucrose (glucose + fructose)
Lactose (glucose + galactose)
what is the luminal digestive phase for carbohydrates
break down of starch into maltose
salivary amlase continues digestion in stomach until acid inhibits or destroys it
then amylase digestion continues in small intestine with pancreatic amylase
what is the membranous digestive stage
maltase sucrase and lactase are produced by enterocytes on the brush border to digest the disaccharides as only monosaccharides can be absorbed
how does disaccharide digestion compare
digestion of maltose and sucrose is very quick with the limiting factor being the rate of absorption
lactose digestion is much slower and the rate of digestion is the limiting factor
how does disaccharidase enzyme levels change with age
-neonate = high lactase (milk) low maltase
adults = low lactase and high maltase
ruminants have no sucrase
How is glucose and galactose absorbed in the small intestine
by the sodium-glucose co-transported called SGLT!
this is secondary active transport as energy released from sodium going down concentration is used to bring the glucose in
1) Na and glucose bind to transporter (luminal side)
2) conformational change in transported moves NA and glucose into cells and releases them into cytosol , Na moves from lumen into enterocyte down its concentration gradient
3) high levels of Na in digestive juice maintians luminal conc of Na high, Na gradient maintained by NA/K pump whhich maintains net negative charge in cell and requires energy
3) concentration fo glucose in cytosol now high so diffuses down concentration gradient into the blood stream vi a facilitative transporter GLUT2 (passive)
what does GLUT2 do
passively transports glucose, fructose and galactose out of cytosol into the blood stream
how is fructose absorbed into the small intestine
fructose is absorbed down the concentration gradient by GLUT%
this is passive transport
then diffuses out of cytosol down concentration gradient passsively into blood stream by GLUT2
what happens once monosaccharides are in the blood stream
transferred to live via hepatic portal vein
and stored as glycogen or continue in circulation to be metabolised for energy
how are omnivores adapted to their diet
omnivores have high hydrolysable carbohydrates
SGLT1 levels remain high (expressed high throughout small intestine)
How are ruminants adapted to their diet
in lambs SGLT1 expression as high as more galactosse and glucose reaching the small intestine
as rumen develop less hCHO pass into small intestine = declines to negibile amounts in adult grazers
maintained in intermediates as some hCHO bypasses fermentation and passes into the small intestine
how are horses adapted to their diet
in wild horses on grass the SGLT1 highest proximally declining distally
- race horses needs a ot of food to produce energy so diet has massively increased levels of hCHO and so adapts by increasing SGLT1 expression overall but especially proximally (2-5 days to deal with diet)
what happens during for lactose intolerance
lactase activity high in neonate but programmed to decline as animal is weaned (in adults very low lactase)
1) in absence of lactase, lactose accumulates in gut lumen
2) osmotic forces increases so there are decreased water absorption
3) more water stays in gut lumen (diarrhoea)
4) once reaches large intestine ferments lactose into lactic acid
4) lactic acid causes pH to decline upsetting microbial balance
5) lactate is poorly absorbed compared to VFAs which increases osmotic effect further which further decreases water absorption
6) gas products cause distension results in pain and discomfort
Where does protein digestion occur
in the sotmach and continues in the small intestine by pancreatic proteases (luminal phase of digestion)
what are the end products of protein digestion and how are they transported
di/tri-peptides and amino acids
most absorbed as di/tri-peptides
amino acids transported into enterocytes via Na co-transport (similar to monosaccharide) this is secondary active transport
di/tri-peptides transported into enterocytes via H+ co-transport
then get transported out of enterocytes down their concentration gradient via facilitative transporters (passive transport)
enzymatic digestion very fast therefore rate limiting step is absorption
compare protein and carbohydrate digestion
-carbohydrate occurs in the final stage of digestion at membranous phase whereas protein digestion occurs in the final stage of digestion at the luminal phase of digestion
- carbohydrates only monomers can be absorbed, whereas in protein monomers,dimers and trimers can be absorbed
-for carbohydrates only small number of enzymes required as complex CHO only 3 types of monomers whereas large numbers of enzymes required for protein digestion as proteins are compared of 20 different monomets
what do cells use absorbed nutrients for
source of energy and for protein synthesis
what are excess cho, fat and protein stored as
lipids and glycogen
fat is not as efficient as glycogen in converting back to glucose, but excess glycogen also goes into fat
in carnivores and omnivores how are carbohydrates absorbed
cho absorbed as monosaccharides
galactose and fructose are converted to glucose in the liver
in herbivores how are carbohydrates absorbed
cho are fermented to vfas
what should blood glucose levels be
5 mmol/l
what happens to glucose during the absorptive stage
glucose is removed (mainly by the hpetatic portal vein) and is stored and metabolised
what happens to glucose in the post absorptive stage
glucose stores released
what happens to glucose when taken up by the liver
glucose taken up ad stored as glycogen, continues until glycogen is 5% of total liver mass
glucose remaining is converted to tri- glycerides (some stored in liver but most exported to blood as VLDL)
what happens to glucose in the skeletal muscle
stoered as glycogen until used for respiration
what happens to glucose taken up by adipose tissue
glucose is taken up and converted to glycerol for synthesis of try-glycerides
if in excess some converted to FFA
adipose is a secondary store of energy
how are lipids made water soluble
FFA bound to albumin
other lipids are bound to apoprotein (complex of lipids bound with apoprotein = lipoprotien)
what are the 4 types of lipoprotein
-chylomicrons
-very low density lipoproteins
- low density lipoproteins
-high density lipoproteins
How are lipids metabolised
chylomicrons absorb fat from the liver
VLDL made in liver transport tri-glycerides lipids from the liver
transport it to lipoprotein lipase in capillary wall to be converted to FFA
FFA are taken up by adipose tissue (stored as triglycerides) or muscle (oxidised for energy)
chylomicron remnants and some VLDL remnants converted to LDL (IDL) taken up by liver and metabolised
- remaining VLDL remnants converted to LDL and transfer cholesterol to other cells (LDL= bad)
- HDL is synthesised in the liver and transfers apoproteins to chylomicrons and VLDL to improve lipid uptake
- removes cholesterol from other cells and tranfers it to liver to be broken down
- cholesterol rich HDL is degraded and releases cholesterol which is converted to bile salts or excreted i bile
What is cholesterol used for un the liver
converted to bile salts or excreted in bile
What happens to amino acids when digested
liver keeps level of amino acids constant
most are taken up by liver by the hepatic portal vein and used for:
-protein synthesis to make: albumin, fibrinogen, enzymes, coagulation factors, globulins…
- converted to keto acids to provide energy for liver cells, converted to glucose and glycogen, fatty acids (for lipid synthesis)
- used to synthesise non-essential amino acids
25% bypasses liver and enters systemic circulation :
-used for protein synthesis
-used for energy if glucose levels are low
- converted to fat or glycogen for storage
what happens when amino acids are degraded
degradation of amino acids for energy leads to NH3 produced
this is converted to urea by liver and excreted by kidneys
except in herbivores:
-urea is transferred to fore-stomach / large intestine via diffusion across epithelium or secreted in saliva if it is a ruminant
- to be used for microbial protein synthesis
and excess urea is excreted by the kidneys
what is the post-absorptive state
once digestion has occurred there is nothing being absorbed (after eating) so normal bodily functions have to be maintained by stores
How does the liver maintain plasma glucose levels in the post-absorptive state
-mobilising glycogen stores
-producing glucose from other sources for gluconeogenesis
in carnivores and omnivores this comes from proteins
in herbivores this comes from propionic acid
in the post-absorptive state what is the use of glucose reserved for
brain, erythrocytes and kidneys
and if anaerobic conditions then skeletal muscle (can ony metabolism fat in aerobic conditions)
other tissues derive energy from lipids (glucose- sparing tissues)
in pregnant/lactating animals glucose in essential for foetal growth and lactose synthesis so maintaining blood glucose levels
how does liver respond to no glucose being absorbed in the post-absorptive state and therefore less glucose in the blood
- reduces its anabolic activites
-mobilising glycogen stores to release glucose into the blood
glycogen stores are quite small (only maintain glucose levels for a few hours)
where is gluconeogenesis performed
liver and kidneys
what is the substrate used for gluconeogenesis and what is it formed from
pyruvate
formed from lactate, glycerol or amino acids
why do only omnivores absorb sufficient glucose in their diet
carnivores main component is protein = low on hCHO so gluconeogenesis occurs from digested fat and protein
herbivores - hCHOs fermented to VFAs not glucose
only propionic acid can serve as glucose pre-cursor in gluconeogenesis
during starvation glucose pre-cursor is animals skeletal muscle
What is the role of skeletal muscle in metabolism
skeletal muscle has glycogen stores
in post-aborptive state skeletal muscle also starts glycogenolysis
but can’t dephosphorylate glucose phosphate so it can’t exit muscle cell = free glucose can’t be transported in the blood stream
instead glucose is oxidised to pyruvate/lactate and then can exit
pyruvate/lactate is then converted to glucose by liver and then enters bloodstream
this is cor cycle
when glycogen stores depleted amino acids from protein = precursor
what is cori cycle
skeletal muscle starts glycogenolysis in post-absorptive state but can’t dephosphorylate glucose phosphate so can’t exit muscle cell so no glucose can enter blood stream
instead glucose is oxidised into pyruvate or lactate
and then transported in blood stream to liver where it is then converted into glucose and released back into the blood stream
what are VLDLs synthesised from in the absorptive stage and post-absorptive stage
excess glucose in the liver absorptive stage
synthesised from plasma FFA in the post - absorptive stage
How are FFA normally transported in the blood
bound to albumin so they can dissolve in aqueous solution
albumin amount limits transport of FFA
FFA transport increased by VLDL synthesis
Why are VLDL important in mobilisation of tri-glycerides from adipose tissues
FFA in fat stores converted to VLDLs to distribute energy round the body in post-absorptive stage as no chylomicrons coming in from capillaries with fat
- tri-glycerides are broken down by hormone - dependant lipase and glycerol is used in gluconeogenesis , FFA oxidised for energy production in glucose-sparing tissues
in mono-gastric animals where are ketone bodies synthesised
only by liver
low levels in pigs and horses as most FFAs are re-erterified into tri-glycerides
brain can switch to ketone bodies as energy source = proteins can last longer
In ruminants where are ketone bodies synthesised from/where
llver
and butyrate in ruminal epithelial cells (they are a VFA) important to convert to ketone bodies as butyrate inhibits gluconeogenesis from pyruvate
how and why are ketone bodies synthesised
FFA taken up by liver and converted to acetly coa which is used as an energy source in the liver
most is excess so is converted ketone bodies
How is carbohydrate metabolism regulated
-insulin (absorptive state)
-glucagon (post absorptive state)
-adrenaline (exercise/stress)
-glucocorticoids (starvation)
How does insulin regulate carbohydrate metabolism
dominates in the absorptive state
causes increased uptake of glucose
stimulates glycogenesis/inhibits glycogenolysis
increases use of glucose for ATP production
and inhibits gluconeogensis
released from endocrine cells in the pancreased by the islet of langerhan
How does glucagon regulate carbohydrate metabolism
dominates in post-absorptive state
reduces uptake of glucose
stimulates glycogenolysis/ inhibits glycogenesis
decreased use of glucose for ATP production and stimulates gluconeogenesis
= increases glucose in plasma
released from endocrine cells in the pancreas (islets of langerhan)
how does adrenaline regulate carbohydrate metabolism
adrenaline is released during stress and exercise as a anticipation
stimulates glycogenolysis in the liver
and maintains plasma glucose despite increased glucose consumption by body
but if too stressed too much glucose is released so become hyperglycaemic (cats in vets are often hyperglycaemic so need to take into account when measuring blood glucose levels)
How does glucocorticoids regulate carbohydrate metabolism
released during starvation
increase gluconeogenesis but unsure how
how is protein metabolism regulated by insulin
during the absorptive state
causes increased amino acid uptake
and increased protein synthesis in liver and muscle (anabolysis)
how is protein metabolism regulated by glucagon
post-absorptive state
causes increased amino acid uptake in liver only (as amino acids are used as a pre-cursor for gluconeogenesis)
proteins degraded into amino acids for gluconeogenesis
= glucagon not opposite to insulin affects
how is fat metabolism regulated by insulin
absorptive state
causes triglycerides to be synthesised from glycerophosphates/FFA and then stored
causes inhibition of FFA released into blood
how is fat metabolism regulated by glucagon
glucagon released during post-absorptive state and during exercise
causes increased lipolysis in adipose
and mobilised triglycerides for ATP production
when does gluconeogenesis occur in ruminants
both absorptive and post-absorptive states as primary source of energy is VFAs
glucose is made from :
-propionic acids/amino acids in absorptive state
-amino acids/glycerol in post-absorptive state
