MODULE – I

COMPARATIVE PHYSIOLOGY OF DIGESTION

MODULE 1: Comparative physiology of digestion:

Introduction

Principle of digestion

Digestive juices – composition, phases of secretion, regulations and functions

Absorption of digestive nutrients

Egestion of undigested food

Role of gut micro flora in digestion

Movements of GI tract – control and functions and reflexes.

Introduction
Definition

Digestion: Mechanical and chemical process in which food is broken down in the GI
tract, releasing many nutrients in forms the body can use.

Digestion: Basic Principles

1. Principle of change

-- The body cannot use food as it is eaten.

-- Food must be changed into simpler substances to be absorbed and then
used by cells to sustain life.

2. Principle of wholeness

-- The parts of the digestive process comprise a continuous whole.

-- Food components travel through the gastrointestinal (GI) system until they
are delivered to cells or excreted.

3. Digestion involves : Mechanical + Chemical Process

 http://www.biologydiscussion.com/human-physiology/digestive-system/small-intestine-
and-large-intestine-with-diagram/62584
https://study.com/academy/lesson/movement-through-the-small-intestine-peristalsis-
segmentation-pendular-movement.html
 http://www.biologydiscussion.com/human-physiology/digestive-system/small-intestine-
and-large-intestine-with-diagram/62584
https://study.com/academy/lesson/movement-through-the-small-intestine-peristalsis-
segmentation-pendular-movement.html
 The human intestine contains a large variety of microorganisms, this community
consists of at least 1014 bacterial cells and up to 500–1000 different species.

 As a whole this represents overall more than 100 times the human genome, and
is called the ‘‘metagenome’’. Thus, the intestinal flora can be considered as
an ‘‘exteriorized organ’’ which contributes to our homeostasis with multiple
functions largely diversified.

 The biological functions controlled by the intestinal flora are related to the
effectiveness of energy harvest, by the bacteria, of the energy ingested but not
digested by the host.

 Among the dietary compound escaping to the digestion occurring in the upper
part of the human gastro intestinal tract, the polysaccharides constitute the
major source of nutrient for the bacteria.

 Part of these polysaccharides could be transformed into digestible substances

such as sugars, or short chain carboxylic acids, providing energy substrates
which can be used by the bacteria or the host.
The animal/human gut is the natural habitat for a large and dynamic
bacterial community and the relevance and effect of resident bacteria
on a host’s physiology and pathology has been well documented.

Major functions of the gut microflora include metabolic activities that

result :

1. in salvage of energy and absorbable nutrients,

2. important trophic effects on intestinal epithelia and on immune

structure and function, and

3. protection of the colonised host against invasion by alien microbes.

Gut flora might also be an essential factor in certain pathological

disorders, including multisystem organ failure, colon cancer, and
inflammatory bowel diseases. Nevertheless, bacteria are also useful
in promotion of human health. Probiotics and prebiotics are known
to have a role in prevention or treatment of some diseases.
http://www.beeculture.com/honey-bee-gut-microbia/
http://thepowerofpoop.com/about/about-fecal-transplant/
 The gut flora controls pathogens, regulates immunity, regulates inflammation, synthesizes
vitamins, synthesizes enzymes, increases mineral bioavailability, synthesizes
neurotransmitters, regulates hormones metabolism, regulates blood sugar, regulates
appetite, and contributes to liver health.

 A healthy intestinal flora provides a barrier between the epithelial cells of the colon and
pathogenic bacteria, known as colonization resistance. In other words, these probiotics
colonize the entire colon wall effectively reducing space for pathogenic bacteria to take hold
or even break through the intestinal wall.

 These bacteria also synthesize certain vitamins, like B7, biotin, B12, folic acid and vitamin K.
In addition, the gut flora produces enzymes that are secreted into the epithelial cells of the
colon, allowing various bodily functions to take place.

 The healthy bacteria within the intestines also create molecules for the brain, otherwise
known as metabolites. This contributes to healthy brain function, as healthy bacteria have an
effect on neurological function.

 The intestinal flora receives its nutrients from mucin, a glycoprotein that is excreted by the
mucous membranes.

 Bacteria also ferment indigestible carbohydrates, otherwise known as dietary fiber, like
pectin, cellulose and hemicellulose into short chain fatty acids. These fatty acids are a great
source of energy for the body and contribute to healthy epithelial cell proliferation.

 Bacterial – Brain Connection: The gut flora also makes neurotransmitters like serotonin and
dopamine. It can therefore communicate with the brain and controls a large number of
processes within its realm. The gut has been considered the second brain, as it has more
neuron cells than the spinal cord. With that said, the next time you have a “gut feeling”, go
with it.
http://thescienceofeating.com/2017/06/28/gut-flora-holds-key-good-health-heres-keeps-
whole-body-healthy/
https://drjockers.com/6-steps-to-rebuild-gut-
flora-metabolism/
https://www.integrativepsychiatry.net/gut_bra
in_dysfunction.html
Metabolic functions

 A major metabolic function of colonic microflora is the fermentation of non-digestible dietary

residue and endogenous mucus produced by the epithelia.
 Fermentation of carbohydrates is a major source of energy in the colon. Non-digestible
carbohydrates include large polysaccharides (resistant starches, cellulose, hemicellulose,
pectins, and gums), some oligosaccharides that escape digestion, and unabsorbed sugars and
alcohols. The metabolic endpoint is generation of short-chain fatty acids.

 Colonic microoganisms also play a part in vitamin synthesis and in absorption of calcium,
magnesium, and iron.

 Absorption of ions in the caecum is improved by carbohydrate fermentation and production of

short-chain fatty acids, especially acetate, propionate, and butyrate. All of these fatty acids
have important functions in host physiology.

 Butyrate is almost completely consumed by the colonic epithelium, and it is a major source of
energy for colonocytes.

 Acetate and propionate are found in portal blood and are eventually metabolised by the liver
(propionate) or peripheral tissues, particularly muscle (acetate).

 Acetate and propionate might also have a role as modulators of glucose metabolism:
absorption of these short-chain fatty acids would result in lower glycaemic responses to oral
glucose or standard meal—a response consistent with an ameliorated sensitivity to insulin.
 In fact, foods with high proportion of non-digestible carbohydrates all have a low glycaemic
index. However, results of one study showed no effect of colonic fermentation of
carbohydrates on insulin resistance.
Trophic functions

 Epithelial cell growth and differentiation—intraluminal bacteria affect cell proliferation in

the colon. Differentiation of epithelial cells is greatly affected by interaction with resident
microorganisms.

 All three major short-chain fatty acids stimulate epithelial cell proliferation and
differentiation.

 However, butyrate inhibits cell proliferation and stimulates cell differentiation in epithelial
cell

 Moreover, butyrate promotes reversion of cells from neoplastic to non-neoplastic

phenotypes.
Interactions between gut bacteria and host immunity—

 The intestinal mucosa is the main interface between the immune system and the
external environment. Thus, that gut-associated lymphoid tissues contain the largest
pool of immunocompetent cells in the human body is not surprising.

 The dialogue between host and bacteria at the mucosal interface seems to play a
part in development of a competent immune system.

 Many and diverse interactions between microbes, epithelium and gut-associated

lymphoid tissue are involved in modelling the memory mechanisms of systemic
immunity.

Protective functions: the barrier effect

 Resident bacteria are a crucial line of resistance to colonisation by exogenous

microbes and, therefore, are highly relevant in prevention of invasion of tissues by
pathogens
https://phys.org/news/2016-03-gut-
microbiome-remarkably-stable.html
https://phys.org/news/2016-03-gut-
microbiome-remarkably-stable.html
The mouth, stomach and duodenum deal with the initial process of
mixing ingested food and initiating digestion.

In the duodenum, bile and pancreatic secretions enter through the

common bile duct.

The small intestine is the main digestive area: in the jejunum

digestive processes continue and absorption is initiated; it continues
in the ileum.

The large intestine (cecum, colon and rectum; primarily the colon)
is involved in the absorption and secretion of electrolytes and water.

Water and electrolyte handling in the gastrointestinal tract

Handling of electrolytes and water by the GI tract is one of
its main functions

Handling of electrolytes and water by the GI tract is one of its main

functions, and includes not only their absorption and secretion but
also cell volume maintenance, and affects cell proliferation and
differentiation, as well as apoptosis and carcinogenesis.

Large volume of fluid is secreted and reabsorbed by the GI

tract
In a 24 h period, around 10.0 L of fluid enter and leave the GI tract.
One liter of saliva is secreted per day; it contains electrolytes,
protein and mucus. Intestinal secretions total about 7.0 liters every
day, over and above an average water intake of about 2.0 liters.
Most of this fluid is reabsorbed by the small intestine. The colon is
particularly active in reabsorption: it absorbs around 90% of the
fluid that passes through it, and only about 150–250 mL of water
are normally contained in the stool.

Electrolytes are secreted by the salivary glands, stomach

and the pancreas
Several secretory processes take place in the GI tract. Salivary
glands, stomach and pancreas secrete digestive enzymes in the
form of inactive zymogens. There is the hydrogen ion secretion in
the stomach. Secretion of the bicarbonate ion takes place
throughout the GI tract, with particularly large amounts being
secreted in the pancreatic juice. Potassium secretion occurs
predominantly in the colon and is regulated by aldosterone.
Mechanisms of water and electrolyte transport in the intestine
Sodium-potassium ATPase is the driving force for transport processes in the enterocytes

Enterocytes possess an array of transporters and ion channels . The sodium-potassium ATPase, is located on the basolateral membrane (the
‘blood side’) and transports the sodium ion outside the cell in exchange for the potassium (3Na+ to every 2K+ ions). This creates a sodium
concentration gradient, and hyperpolarizes the membrane, increasing the intracellular negative potential and driving the passive transport
systems (and thus transcellular ion transport). Moreover, transport of sodium (and chloride) is accompanied by passive transport of water, which
is both paracellular (through the tight junctions) and transcellular (by membrane water transporters, the aquaporins).
Sodium co-transporters are a common mode of intestinal transport
Sodium co-transporters transport the sodium ion together with another molecule (Fig. 10.2A). For instance, glucose is absorbed
together with sodium by the sodium-glucose co-transporter present in the luminal membrane, known as SGLT-1 (Sodium/Glucose
Linked Transport-1). Glucose is subsequently extruded into plasma at the basolateral membrane by theGLUT2 transporter (Fig.
10.7 below). The discovery of the link between intestinal transport of sodium and glucose had enormous clinical consequences. It was
during a cholera epidemic in Manila, in the late 1960s, that researchers observed that patients who had been dehydrated because of
diarrhea did not absorb oral sodium chloride well during attempts at oral rehydration. However, they started to do so when glucose
was also provided. This observation led to the formulation of the WHO oral rehydration solution, which subsequently saved the lives
of millions of children affected by severe diarrhea worldwide.
Other modes of sodium transport are the electroneutral (Fig. 10.2B) and electrogenic transport
The electroneutral sodium transport is through sodium/hydrogen exchanger (NHE), usually combined with chloride transport via the
chloride/bicarbonate exchanger known as AE exchanger (Fig. 10.2C). The exchangers are present on both luminal and basolateral
membranes. This type of transport is responsible for most of the sodium chloride reabsorption in the colon. In the distal colon the NHE
exchanger is upregulated by glucocorticoids.
The electrogenic absorption of sodium occurs through the epithelial sodium channels (ENaCs, also known as amiloride-sensitive
sodium channels), which are present on the luminal side of the epithelium (Fig. 10.2D). ENaCs are regulated by steroids (aldosterone)
and are important particularly in the distal colon. Absorption of Na+ is accompanied by Cl− following through a chloride channel (which
could be the CFTR – see below). Aldosterone also upregulates the Na+/K+-ATPase.
Chloride transport: the cystic fibrosis transmembrane conductance regulator (CFTR)
Luminal secretion of chloride occurs via the cystic fibrosis transmembrane conductance regulator (CFTR; Fig. 10.2B). The CFTR is a
single-polypeptide membrane ion channel. It is also present in the epithelia of the lung and sweat glands. Its function is controlled by
the G-protein–cAMP-protein kinase A (PKA) signaling cascade (Chapter 40). Because the CFTR is activated by cAMP, prostaglandin
E2 (PGE2), serotonin, as well as the cholera toxin and the E. coli heat-stable enterotoxin, all activate chloride secretion. On the other
hand, the loss-of-function mutations of CFTR are the cause of cystic fibrosis, where the chloride transport is impaired or inhibited.
CFTR also has regulatory function: its phosphorylation inhibits the NHE exchanger, thus decreasing Na+ absorption. Interestingly CFTR is
also able to transport chloride in the opposite direction, aiding chloride reabsorption (above).
The basolateral C1− uptake occurs through the Na+ K+ C1− co-transporter (known as NKCC1) and through chloride/bicarbonate
exchangers.
Cystic fibrosis

Cystic fibrosis, a monogenic autosomal recessive disorder, involves inhibition of chloride

transport due to the absence of the CFTR. Different mutations of the CFTR gene lead to
either complete absence of the transporter or impair its functionality.
The prevalence of CF is 1 : 3000 live births in the USA and northern Europe. In the USA,
cystic fibrosis is the No. 1 cause of malabsorption. It manifests itself predominantly in
childhood. The main problems are usually respiratory. Chloride secretion is decreased
and the Na+ reabsorption is accelerated. This results in decreased hydration of epithelial
secretions. In the respiratory tract there is decreased hydration of the airway mucus and
thus failure of its clearance, with ensuing bacterial infections. Gastrointestinal problems
include meconium ileus and intestinal obstruction. The absence of the CFTR also affects
functioning of the Cl−/HCO3− exchanger (and thus the passive secretion of Na+) – this
impairs pancreatic enzyme secretion. Thickened biliary secretions may be a cause of
focal biliary cirrhosis and chronic cholelithiasis. There also is impairment of mucus
secretion in the colonic crypts, with enhanced Na+ reabsorption through Na+ channels
and Na+/H+ transporters.
CARBOHYDRATE DIGESTION
How, where and with what enzymes are starch and glycogen digested?

Salivary amylase and pancreatic amylase digest starch and glycogen in the mouth and
intestine.

How, where and with what enzyme are disaccharides digested? Be specific with what
enzyme breaks down which dissarcharide/linkage.

Disaccharides are digested by membrane-bound enzymes on apical side of the brush

border of mucosal cells in the upper jejunum/intestine. They are broken down into
monosaccharides that are released to the portal system of the liver. Maltase breaks down
1-4 linkages of maltose -> 2 glucose. Lactase (B-galatosidase) breaks Beta 1-4 linkage of
lactose -> glucose, galatose. Sucrase breaks 1-2 in sucrose into fructose and glucose.
Isomaltase breaks 1-6 in isomaltose.x

Where is salivary amylase active? Inactive? Why?

Active in mouth because bicarbonate buffers keep alkaline environments/optimum pH

for salivary amylase. Inactive in stomach because stomach HCl stops salivary amylase
activity. THERE IS NO CARB DIGESTION IN THE STOMACH!
What is chyme? How is it neutralized?

Chyme is the acidic mixture in the stomach which is neutralized in the intestine by
bicarbonate secreted by the pancreas.

What kind of enzymes are amylases? What are the end products of amylase digestion?
What do amylases not degrade?

Endoglycosidases. They break only alpha 1-4 linkages in the middle of the chain at random
intervals, they never degrade at the end of the chain. Results in a mixture of short,
branched alpha 1-6 and unbranched oligosacchrides with limited dextrins. (dextins,
trisaccharaides, isomatloses, maltose). Amylases do not digest dissarchades into
monosaccharides, alpha 1-6 linkages, or cellulose (B1-4).

How much salivary amylase and pancreatic amylase do we make in one day? How are
they secreted?

1L and 1.5L. Into the mouth and mixed with food during mastication. And into the
duodenum via the pancreatic duct after chyme from stomach has been neutralized by
bicarbonate.
Where are most carbohydrates absorbed? Where do they go after?

BEFORE they enter the large intestine. Mostly in the duodenum and upper jejunum. They
are then transported to the portal system--> to the liver.

What are the main transporters for glucose absorption? Where are they found?

SGLT-1 and SGLT2 in the intestine and kidney. SGLT1 for all of intestinal glucose absorption.
SGLT2 for 90% of renal glucose reabsorption (in proximal convoluted tubule) and SGLT1 for
other 10% (in proximal straight tubule).
What are the main transporters for tranport of glucose into/out of tissue to blood? How do
they work?

GLUT transporters. Facilitated diffusion with gradient/no ATP used. Transport changes
conformation to bind sugar and then release sugar.

Mechanism for SGLT tranporters

1. Primary active transport. Low concentration of Na in the cell maintained by Na/K ATPase
(Need ATP!). 2. Secondary active transport. Na/Glucose Symport (Na with gradient; glucose
against gradient to move glucose into the cell) on the apical side of the epithelium
 SGLT2 inhibitors
Flozins (canagliflozin/dapaliflozin), are second-line or third line diabetes treatment (type
2) because they reduce renal tubular glucose reabsorption/ reduce blood glucose without
stimulating insulin release. Also weight loss, reduce bp, and increase high density
lipoproteins.

What is the sweetest sugar? Fructose

What beta linkage can we not break?

A beta linkage between glucose and glucose (cellulose)

What are the 5 different types of GLUT transporters? Where are they found/whats
their function? Which is insulin independent?

Glut1=RBC, Brain, fetal tissue; Basal uptake of glucose in tissues to sustain respiration
of cell.

Glut2 = Transports glucose in/out of liver, kidney, and b-pancreatic cells. sends Glucose,
Galactose, Fructose to the portal system to be absorbed by t Glut3.

Glut3 = transports glucose into neurons.

Glut4= Most abundant in adipose and muscle glucose uptake/out of blood into tissue.
insulin sensitive/increased with insulin present!!! all others are not.

GLUT-5= Fructose absorption into intestinal cells.

Abnormal digestion of dissarchides leads to?

Osmotically active carbons in the large intestine which

1. draw water into the intestine and cause diarrhea.

2. lead to bacterial fermentation that creates Co2, H2 (which can be measured in

breath), lactic acid (acidity that can be measured in stool of infants) and leads to
cramps, diarrhea and flatulence

What can cause digestive enzyme deficiencies? (5)

1. Heredity (i.e. Lactase deficiency (b-galactosidase)=most common type of enyme

deficiency)
2. Intestinal diseases (i.e. Colitis= inflammation of the colon, gastroenteritis, cystic
fibrosis)
3. Malnutrition (Kwashiorkor)
4. Drugs/antibiotics destroy intestinal flora
5. Acquired (i.e. severe diarrhea can lead to loss of enzymes in intestine)
 Primary and secondary lactose intolerance

Due to lactase deficiency. Presents with diarrhea, bloating, cramps bc bacteria in large
intestine = H2, CO2, diarrhea. Some subpopulations and older people have it more
commonly. Secondary is because of injury; first to be lost and last to recover.
PROTEIN DIGESTION
Endopeptidases
Absorption of Amino Acids
Transport of Amino Acids into Cells
LIPID DIGESTION
What digestion of triacylglycerides occurs before the intestines? Describe what conducts
this process. Does any absorption occur in this area?

Acid lipases start the digestion,

there is lingual lipase in the mouth
and gastric lipase in the stomach.

They have an optimum pH of 4-6,

and act on TAG with short and
medium chain FA. Significant in
infants and in adult cystic fibrosis
patients with pancreatic
insufficiency.

SCFA and MCFA are directly

absorbed into the bloodstream from
the stomach.

Where does digestion of long chain fatty acids occur? What molecule mediates this?

Digestion of TAG with LCFA occurs in the duodenum by pancreatic lipase.

 What is Emulsification of fat and where does it occur ?

Emulsification is achieved with the help

of bile salts (detergent property) and
peristalsis (mechanical mixing). Dietary
lipid particles become smaller, stable,
and are prevented from coalescing.

It occurs in the duodenum, increases

the surface area of lipids.

Pancreatic lipase - what does it do? What are the products? What other components are
required? What drug inhibits pancreatic lipase?

Pancreatic lipase hydrolyzes the TAG in the

duodenum at positions 1 and 3. Products
are 2-monoacylglycerol and two LCFA
(absorbed in ileum).

Pancreatic colipase is secreted as a

zymogen (activated by trypsin), stabilizes
the binding of lipase to its substrate.

Orlistat is an inhibitor of pancreatic lipase

Digestion of phospholipids - what enzymes are used? What does each one do?

Have a glycerol backbone with 2 FA groups and a phosphate group. Phospholipids are
mainly digested by pancreatic phospholipase A2 (activated by trypsin/bile salts).

PLA2 takes away FA on position 2. PLA2 takes away P1, PLC hydrolyzes bond between
phosphate and glycerol.

PLD breaks bond between phosphate and head group. End result is lysophospholipid and 2
FA.

Add choline to the lysoPL to create lysoPC, absorbed from ileum in micelles
Digestion of cholesterol esters - what enzyme? What is the process and what receptors
are involved?

Free cholesterol is absorbed in the duodenum and jejunum with the aid of NPC1-L1
transporter protein. Cholesterol esters need to be broken down by pancreatic cholesterol
esterase to cholesterol + FA. Ezetimibe inhibits absorption of cholesterol by interfering
with NPC1-L1 receptors.

What makes up the majority of bile? What is the difference between gallbladder bile
and liver bile?

Bile is made in the liver, it mostly water. Organic comounds in bile include lecithin
(phosphatidyl choline), cholesterol, bile salts, and bilirubin). Majority of bile is stored in
gallbladder for times of need, can be recirculated 5-6 times times each day. Gallbladder
bile is a little more concentrated than liver bile, most of the organic components are
concentrated there. Released from gallbladder in response to CCK (produced from lower
duodenum and jejunum)
What is the purpose of bile salts? How do they achieve this? What other roles do they
have? How are they excreted?

Have detergent properties, which help emulsify fats during digestion in intestines to form
mixed micelles (many components). They also keep cholesterol from precipitating in the
gallbladder, activate pancreatic lipase, phospholipase A2, and cholesterol esterase, and are
needed for absorption and transport of fat-soluble vitamins (A, D, E, K). 5% of bile salts are
excreted in faeces, they are the only significant way for cholesterol to be removed from the
body.
Where is free cholesterol absorbed? Where are individual FA absorbed? What about 2-
MAG? Lysophospholipids? How are bile salts reabsorbed?

Micelles themselves are not absorbed.

Free cholesterol is absorbed via NPC1-L1

protein in duodenum and jejunum.

Lipids such as FA, 2-monoacylglycerol, and

lysophospholipids are absorbed in proximal
2/3 of ileum.

Bile salts are deconjugated by gut bacteria

and absorbed via ileal bile acid transporter
in the distal ileum.

Bile salts are transported to liver where

they are reconjugated and recirculated.

What enzymes enter the digestive tract

from the pancreas that are involved in TAG
digestion? What do they do?
 Produced by the I-cells in the duodenum
Cholecystokinin and jejunum. Acts on the gall bladder and
exocrine cells of the pancreas, stimulates
bile release.

Produced by duodenal S cells in response to

Secretin chyme acidicity. Stimulates bicarb secretion by
the pancreas
What happens to lipids once they have been taken in from the lumen by enterocytes?

2-MAG is converted back to a TAG by the readdition of 2 FAs. Fatty acids have CoA
added. Cholesterol is esterified again. All three of these are packaged into chylomicrons,
then sent into lymphatic circulation.
What are some examples of pancreatic insufficiencies? What is cholestasis? What are
some inflammatory bowel diseases? Lipid malabsorption affects what other nutrient
absorption?

Cystic fibrosis and pancreatic cancer are pancreatic insufficiencies.

Cholestasis is decreased bile flow, often by gall stones.

Inflammatory bowel diseases include celiac sprue (gluten sensitivity), Crohn disease
(autoimmune), and bowel resections.

Lipid malabsorption interferes with absorption of fat-soluble vitamins (A, D, E, K).

Orlistat

Anti-obesity drug that inhibits pancreatic and gastric lipase. Prevents TAGs from being
digested to MAGs, so cannot be absorbed

Olestra

6-8 FA attached to sucrose, it is non-digestible. Wear dark pants, cause you will leave stains

Steatorrhea

Increased fecal excretion of TAG when dietary

lipids are not absorbed. Causes foul smelling,
loose, fatty stools, and fecal incontinence
https://www.memorangapp.com/flashcards/151609/digestive+and+excretory+systems/

http://www.dnatube.com/video/6151/The-Digestive-System

http://slideplayer.com/slide/3383047/

https://www.slideshare.net/enamifat/introduction-to-digestion-and-absorption-local-hormones-of-git-different-digestive-juices

http://www.authorstream.com/Presentation/drraghu74-1526731-control-gastric-secretions/

https://doctorlib.info/anatomy/ross-wilson-anatomy-physiology-health-illness/12.html

https://doctorlib.info/medical/biochemistry/12.html

http://www.tankonyvtar.hu/en/tartalom/tamop425/0010_1A_Book_angol_05_termeleselettan/ch06.html

http://download.nos.org/srsec314newE/PDFBIO.EL13.pdf

http://www.austincc.edu/sziser/Biol%202404/2404LecNotes/2404LNExV/m.Digestive%20System.pdf

https://www.integrativepsychiatry.net/gut_brain_dysfunction.html

http://thepowerofpoop.com/about/about-fecal-transplant/

http://thescienceofeating.com/2017/06/28/gut-flora-holds-key-good-health-heres-keeps-whole-body-healthy/

http://www.uofmhealth.org/news/archive/201611/high-fiber-diet-keeps-gut-microbes-eating-colon%E2%80%99s-lining

http://www.uofmhealth.org/news/archive/201611/high-fiber-diet-keeps-gut-microbes-eating-colon%E2%80%99s-lining

http://www.gutmicrobiotaforhealth.com/en/bacteria-celiac-patients-influence-glutens-digestion-ability-provoke-immune-response/

http://schaechter.asmblog.org/schaechter/2013/06/fine-reading-the-gut-microbiota-of-insects-diversity-in-structure-and-function.html

https://phys.org/news/2016-03-gut-microbiome-remarkably-stable.html