Digestion 3 Flashcards
What do we want to absorb?
From proteins - amino acids
From lipids/fats - fatty acids/glycerol
From carbohydrates - simple sugars
Micronutrients - Vitamins, Trace elements
Degradation of complex molecules (catabolism)
Contributes to carbon and energy pools
Where does absorption take place?
The small intestine= aa,fats,vits,complex carbohydrates and some trace elements.
The large intestine=Water, Salts & Ions (electrolytes)
fats are absorbed into the lacteals
How are molecules absorbed?
*Water
*Ions
*Vitamins-Water-soluble
Fat-soluble Vits
Vit B12
*Amino acids
*Fatty acids and glycerol
*Simple sugars
*Water- nearly all that is ingested is reabsorbed via osmosis
*Ions- absorbed via diffusion, cotransport and active transport
*Vitamins-Water-soluble Vits absorbed by diffusion
Fat-soluble Vits absorbed as part of micelles
Vit B12 requires intrinsic factor
*Amino acids – absorbed by active transport
*Fatty acids and glycerol – Diffusion: micelle/chylomicrons
*Simple sugars – both active transport & facilitated diffusion
What Are the types of vitamins?
waters soluble and fat soluble
fat soluble=DEAK
water soluble=CA (ascorbic acid is vitamin C)
fat soluble vitamins may be absorbed with fat on the small intestine
Absorptive process of the small intestine
nutrients is in the lumen we want it to go to the lacteals or blood capillaries, it needs to be transported across apical barrier outside membrane of epithelial cells, it might have to be processed but first goes through basal lateral surface of epithelial cells to gain entry to lacteal or capillaries
The movement of ions and organic molecules from the
intestinal lumen through the gut wall to the blood or lymphatics
Process occurs in 3 stages:
Transport from lumen of the intestine into the epithelial cells
Metabolisation of nutrient within cell
Removal of processed material from cell to blood stream or lymphatics
Describe the types of transport
Absorption of nutrients from lumen occurs by:
Passive transport – simple diffusion with a concentration gradient
Active transport – involving specific carriers eg. Sugars,
amino acids. Carrier has 2 specific binding sites 1st nutrient
2nd Na+ (ionic transport shuttle). Against conc gradient
Pinocytosis – physical engulfment of particles, large molecules in contact with cell membrane e.g responsible
for absorption of intact proteins such as Igs (immunoglobulins)
Describe simple Diffusion / Passive Transport
Does not proceed against electrochemical gradients
Does not require energy
Based on processes of Diffusion and Osmosis
Diffusion: water, chloride, ascorbic acid, pyridoxine
and riboflavin
Facilitated diffusion: channel proteins transport
molecules down concentration/electrochem. gradients
Describe active Transport
Against electrochemical gradient
Requires energy
Proceeds at high rate
decreased by low temperature
Subject to saturation
Inhibited by metabolic inhibitors
Competitive inhibition by related materials
What nutrients are absorbed by active Transport?
Most nutrients are absorbed by active transport (Sugars, fats, amino acids, bile acids, vitamin B12, thiamine and calcium)
Active transport assisted by “trapping action.”
Membrane Carrier System – carrier/substrate complex allows translocation across membranes
Pinocytosis – incorporation of particles into cells by enveloping with membrane-derived vesicles
Facilitated Diffusion – features of both diffusion and active transport.
CARBOHYDRATES
What are the end products of carbohydrate digestion?
How are these sugars absorbed?
End products of CHO digestion: glucose and small amounts of galactose and fructose (simple sugars)
Starch –>Glucose
Sucrose –>Glucose and Fructose
Lactose –>Glucose and Galactose
Simple sugars absorbed into:
Portal Blood –> Liver –>organs via systemic blood
Used as energy sources & glycogen storage (muscle/liver)
if there is an excess they can be re-converted and stored for energy conversion later in the form of glycogen in the muscle and the liver.
Glucose and amino acid transport: active transport & facilitated diffusion
GLUCOSE
2. 1. Apical Surface - Lumen Side:
In the lumen of the small intestine, glucose is primarily present in the form of disaccharides.
Enzymes located on the brush border of the apical membrane of the intestinal epithelial cells (enterocytes) break down these disaccharides and oligosaccharides into individual glucose molecules through hydrolysis.
- Active Transport at the Apical Surface:
At the apical surface, glucose transport into the enterocytes is primarily accomplished through active transport.
The sodium-glucose co-transporter 1 (SGLT1) is located on the apical membrane.
SGLT1 simultaneously transports both glucose and 2 sodium ions (Na+) into the enterocyte against their respective concentration gradients. Sodium ions are actively pumped out of the cell by the sodium-potassium pump and ATP(Na+/K+ pump), creating a sodium concentration gradient. 3NA+ out and 2K+ in
This co-transport of glucose with sodium ions is an energy-dependent process and allows glucose to be transported into the enterocyte. - Glucose Diffusion to the Basolateral Surface:
Once glucose is transported into the enterocyte, it must then be transported across the cell to the basolateral side where it can enter the bloodstream.
Glucose is transported across the enterocyte’s cytoplasm through facilitated diffusion. This diffusion is facilitated by glucose transporter proteins known as GLUT2.
GLUT2 is present on the basolateral membrane of the enterocyte.
Glucose moves down its concentration gradient from the high concentration in the enterocyte to the lower concentration in the blood. This is a passive process.
AMINO ACIDS
Active Transport:
Amino acids are actively transported across cell membranes against their concentration gradient by specific amino acid transporters, such as amino acid symporters or antiporters.
Facilitated Diffusion:
Transporter: Amino acid transporters, facilitate the movement of amino acids across the membrane, allowing them to move from areas of higher concentration to areas of lower concentration.
PROTEIN
Digestion results in aas and small peptides from portal blood to enter liver where aa’s can be stored in an aa pool
Either for
Protein synthesis to occurs in liver and exported
or
aas pass to systemic circulation and join aa pool from tissue catabolism
Excess aas - returned to liver
Deamination (de-amino-grouping) to NH3 and keto-acids
Keto acids allowing for new de novo aa synthesis or
catabolised for energy
Some NH3 used for amination, the rest are converted to urea and excreted
LIPID
Triglycerides hydrolysed to fatty acids and glycerol
Free fa’s – catabolised for energy production
- metabolised for triglyceride synthesis
Triglycerides – re-enter blood stream to organs/tissues
for energy production, triglyceride storage (adipose tissue)
and fa synthesis (essential fas) – phospholipid synthesis
Hydrolysis of triglycerides (except direct absorption in the
liver) is a pre-requisite for absorption
Enter lacteals as chylomicrons, absorbed by liver and
venous blood via thoracic duct (500nm diam. within lipoprotein coat)
lipids to fatty acids and glycerides
lipids are broken down to components, bile salts process (emulsify) the fat to a form that is easily transportable across an apical membrane.
lipids= polar head and water insoluble fatty acid chain, cell membrane has polar heads on the outside and insoluble fatty acids on the inside. These are packaged into small vesicle-like structures called a micelle that is easily diffusible.
long chain Fas +monoglycerides (bile salts)= micelle
these are then repackaged inside to form a chylomicrons which can then exocytose out into lacteals of the villi
Regulation of Digestive Activities
digestion and absorption
They are controlled by processes either;
1. Neural
2. Hormonal
Control of the digestive motility
Movement of materials along the digestive tract is controlled by:
*Neural mechanisms
Parasympathetic and local reflexes
*Hormonal mechanisms
Enhance or inhibit smooth muscle contraction
*Local mechanisms
Coordinate response to changes in pH or chemical stimuli
Neural control
This consists of:
Neurons INTRINSIC to:
- salivary glands
- pancreas
- gall bladder
- digestive tract
Cell bodies located in ganglia of submucosal and myenteric plexus
INTRINSIC: CO-ORDINATE LOCAL ACTIVITIES OF DIGESTIVE TRACT
EXTRINSIC neurons which connect intrinsic to the CNS (large reflexes)
Regulation of motility and secretion
Enteric intrinsic nervous system
Submucosal (Meissner’s) plexus [Secretion & motility]
-regulates local motlily and secretion
-there are glands that are then controlled by the submucosal plexus
Myenteric (Auerbach’s) plexus [Motility]
Extrinsic innervation:
-control muscles for motility
Gastrointestinal Tract (GIT) nerves from autonomic NS (sympathetic and Parasympathetic)
parasympathetic=activatory in the GIT
sympathetic=negative regulatory
Extrinsic innervation – CNS involvement
Autonomic neural innervation of the GIT
main innervation vagus nerve but also include the facial and splanchnic nerves, these 3 nerve together coordinate responses from the salivary glands to the accessory organs lower down to the action of the intestinal and gastrointestinal tract
sympathetic innervation is provided through the Superior
Cervical ganglion ,Greater splanchnic, Lesser splanchnic and the Lumbar splanchnic. All of these go to different regions that negatively regulate the secretion in the salivary glands, action of accessory organs or specific action of motility and secretion within the intestines. ultimately we get a coordinated response that involves both local intrinsic and non-local extrinsic neural control mechanism.
Parasympathetic innervation
(Extrinsic, Primarily via Vagus)
Stimulation is excitatory to digestive system
Increases salivary, gastric, pancreatic and Biliary secretion
GIT Receptors to transduce innervations
Receptors of afferent neurons:
Chemoreceptors
Sense changes in chemical composition and pH of luminal fluid
Mechanoreceptors
Sense changes in stretch/tension of gut wall (distension)
Osmoreceptors
Sense changes in osmotic composition of luminal fluid
Coordination: secretion & absorption
Whatare the reflexes that control and coordinate stomach and intestinal secretion and absorption.
Neural and hormonal mechanisms coordinate secretion from glands
GI activity stimulated by parasympathetic innervation
-Inhibited by sympathetic innervation
Enterogastric, gastroenteric and gastroileal reflexes to coordinate stomach and intestinal secretion and absorption.
Salivary glands
Saliva secretion from gland controlled by sensory & motor nerve endings associated with SYMPATHETIC & PARASYMPATHETIC autonomic nervous system
salivary glands are entirely under neural control (no hormonal control)
Stimuli that control secretion of salivary glands are;
mechanical
thermal
chemical
psychic
olfactory
Hormones
(research the rest!!)
make a table like in next slide
Gastrin
Cholecystokinin (CCK)
Secretin (endocrine cells in duodenal mucosa)
Gastric inhibitory peptide (GIP)
Vasoactive intestinal peptide (VIP)
Enteroglucagon
Enkephalin
Somatostatin
Describe with examples positive and negative regulators of the gastrointestinal tract
gastrin can increase motility and secretion in the stomach but secretin and cholecystokinin can negatively regulate motility and secretion in the stomach so they are negative regulators. However in a different area of the gastrointestinal tract they are positive regulators they can activate bile secretion for the emulsification and processing of fat across the villi.
Describe the stomach and parasympathetic system involved
The innervation to the stomach is predominated by the parasympathetic system which is about signals received across neurons that trigger the neurotransmitter acetylcholine, this signals transduction of the parasympathetic stimulation (Ach NT) that induces - Secretion of pepsinogen, HCl and Gastrin.
Vagal activity stimulates motility and parasympathetic stimulation also increases Increasing gastric volume which stimulates motility (mixing)
HCL acts as a regulator it can inactivate salivary amylase whilst activating pepsinogen so it is both a negative and positive regulator
Slowing of gastric activities
(Negative regulation)
Name some negative regulators
Enterogastric reflex
Enterogastrones
Secretin
Cholecystokinin (CCK)
High [H+] directly inhibits gastrin release
Fat in duodenum-inhibition of motility
Cephalic phase
Neural: Long reflex – vegus (parasympathetic)
Hormonal: start of Gastrin release
Gastric phase
Neural: short reflex – intrinsic innervation
Hormonal: Gastrin release & +ve feedback
Intestinal phase
Neural: short reflex (intrinsic plexi involved)– duodenum –ve to myenteric intrinsic
Hormonal: Negative feedback on gastric secretion
Regulation: Pancreas
Pancreas: need to prevent auto-digestion
Inactive ZYMOGENS
zymogens are protected from the pancreas by compartmentalised in membrane-bound granules
pancreas can also produces protease inhibitors pancreatic trypsin inhibitor.
Digestion in duodenum requires coordinated effort in the production, secretion and activation of pancreatic enzymes.
Control of pancreatic secretion
Positive regulation
CCK stimulates release of enzymes
CCK stimulates contraction of gall-bladder
Secretin stimulates release of bicarbonate in response to acid in duodenum (to buffer digesta from stomach that goes into the duodenum)
defecation
the defecation is a neuronal reflex and utilizes both short and long reflex (parasympathetic innervation)
Compaction of digesta induces distention of rectum detected by stretch receptors which signal both locally and non-locally
-local (short reflex=stimulation of myenteric plexus in the sigmoid colon and rectum, thus positively induces peristalsis.
-stretch receptors can also signal via long reflex
Long reflex=stimulate parasympathetic motor neurons which feedback to spinal cord, 2 effects;
1. stimulation of motor neurons in sacral spinal cord increases peristalsis throughout the large intestine so intrinsic and extrinsic contributing to peristalsis
- stimulation of somatic neurons through CNS, this feeds back to allow contraction of the external anal sphincter at the same time parasympathetic motor neurons through pelvic nerves give a negative regulation resulting in relaxation of internal anal sphincter.
