PROVIDE INFORMATION ON NUTRITIONAL SUPPLEMENT

DEPARTMENT OF PHARMACY

DATE˸ 21/5/2016 PREPERD BY SHAMSA I

TIME˸ 8˸30-12˸00
NAME OF STUDENTS ID NO
•SHAMSUDEN EBRAHIM 097

•HABTAMU ABABU O44

•AMIN ABDULAHI 011
•HUSEN ABUBAKAR 048
•MAHIRET JAMAL 075

•ENDRIYAS MOHAMED 032

•SHOLAYE DABALA 096
•JAMILA AYYUB 050
•AYINALEM SALAMON 016
•BURTUKAN DIBABA 115
Contents
1. Carbohydrate digestion
1.1. Carbohydrate absorption
2. Lipid digestion/fat
2.1 Lipid absorption
3. Protein digestion
3.1 Protein absorption
4. What is lactose intolerance
4.1. What is the cause of lactose intolerance
4.2. Symptoms of lactose intolerance
 CARBOHYDRET DIGESTION

The major source of carbohydrates is found in plants

Glucose is the universal fuel for human cells
The glucose concentration in the body are maintained with in limits by various metabolic
processes
The principal sites of carbohydrate digestion are the mouth and small intestine the dietary
carbohydrate consists of
•Polysaccharides ˸starch, glycogen and cellulose
•disaccharides˸ sucrose, maltose and lactose
•monosaccharide , mainly glucose, glactose and fructose
monosaccharides need to digestion prior to absorption where as disaccharides and
polysaccharides must be hydrokyzed to sinple sugar before their absorption

DIGESTION IN MOUTH
The mechanical and chemical digestion of carbohydrates begins in the mouth chewing also
known as mastication ,crumples the carbohydrate foods in to smaller and smaller pieces.
Salivary glands secrete alpha amylase (ptylin) which initiates the hydrolysis of a starch
Salivary amylase enzyme breaks the bonds b/n the monomeric sugar units of disaccharides,
oligosach aride and stanches .the salivary amylase breaks down amylase and amlaspection
in to smaller chain of glucose called dextrins and maltose
During mastication ,salivary alpha amylase acts briefly on dietary starch in random manner
breaking some alpha 1-4 bonds ,alpha amylase hydrolyzes stanch in to dextins
Salivary glands secrete salivary amylase ,which begin the chemical break down of
carbohydrate by breaking the body b/n monomeric sugar units
 DIGESTION IN SMALL INTESTINE
Further digestion of carbohydrate occur in the small intestine pancreatic enzymes there are
two phases of intestinal digestion
•Digestion due to pancreatic alpha amylase
•Digestion due to intestinal enzymes ,sucrose ,maltose ,lactose and isomaltose
1.digestion due to pancreatic alpha- amylase
The fuction of pancreatic alpha –amylase is to degrade dextrins further in to a mixture of
maltose ,iso maltose and alpha limit dextrin
The alpha-limit dextrins are smaller oligo saccharides containing 3to 5 glucose units
2.digestion due to intestinal enzymes
Enzymes responsible for the final phase of carbohydrate digestion are located in the brush
border member
Sucrose breaks sucrose in to glucose and fructose
Maltose breaks the bond b/n glucose and glucose
Lactose breaks lactose in to glucose and galactose
Isomaltose breaks isomaltose in to glucose and glucose
The end products of carbohydrate digestion are glucose ,fructose and galactose which are
readily absorbed through the intestinal mucosal cells in to the blood steam

CARBOHYDRATE ABSORPTION
Carbohydrates are absorbed as monosaccharide from the intestinal lumen
Two mechanisms are responsible for the absorption of monosaccharide’s
 1.Active transport against a concentration gradient ,I.e. from a low glucose concentration to a higher
concentration
2.focilitative transport with concentration gradient i.e.from a higher concentration to a lower one
1. ACTIVE TRANSPORT

The transport glucose and galactose across the brush border membrane of mucosal cells occur by an active
transport
Active transport is an energy requiring process that requires a specific transport protein and the presence of
sodium ions
A sodium dependent glucose transport (SGLT-1) binds both glucose and sodium at separate sites and
transport them both through the plasma membrane of the intestinal cell
The free energy required for this active transport is obtained from the hydrolysis of ATP links so a sodium
pump expels nat from the cell in exchange of K

2.FACILITATIVE TRANSPORT

Fructose and mannose are transpoted across the brush border by Na ion independent facilitative diffusion
process requiring specific glucose transporter GLUT-5
The same transport can also be used by glucose and galactose if the concentration gradient is favorable
 Digestion and absorption of lipids
. Lipid digestion/fat
The average daily intake of lipids by adults is about 81 g, of which more than 90% is normally triacylglycerol. The
remainder of the dietary lipids consists primarily of cholesterol, cholesteryl esters, phospholipids, and
unesterified fatty acids.

Dietary lipids intake is ~81 g/day Triacylglycerol is >90% The

remainder includes: • Cholesterol • Cholesterol ester •
Phospholipids • Glycolipids • Free fatty acids

Stomach • Lingual lipase • Gastric lipase Small intestine • Lipase / C0-lipase •

Cholesterol esterase • Phospholipase A2 • Lysophospholipase

Lipids digestion in the stomach

Catalyzed by an acid-stable lipase (lingual lipase)
Triacyglycerols (TAGs) are hydrolyzed by the lipases
secreted:  Under the tongue and gastric mucosa
Acid lipases are important for lipid (milk fat) digestion in
neonates and patients with pancreatic insufficiency

The digestion of lipids begins in the stomach, catalyzed by an acid stable lipase that originates
from glands at the back of the tongue (lingual lipase). TAG molecules are primary target of this
enzyme. These same TAGs are also degraded by a gastric lipase, secreted by gastric mucosa.
Both enzymes are acid stable, with pH optimums of pH 4 to pH 6. These acid lipases play a
particularly important role in lipid digestion in neonates, for whom milk fat is the primary source
of calories. They are also important digestive enzymes in individuals with pancreatic
insufficiency, such as those with cystic fibrosis. Lingual and gastric lipases aid these patients in
 Lipid digestion in the small intestine
Emulsification: Occurs in the duodenum Increases surface
area of lipid droplets To maximize the effect of digestive
enzymes Two mechanisms: 1. Detergent properties of bile
salts in the bile Bile salts emulsify dietary lipid particles 2.
Mechanical mixing by peristalsis

The critical process of emulsification of dietary lipids occurs in the duodenum. Emulsification increases the
surface area of the hydrophobic lipid droplets so that the digestive enzymes, which work at the interface of
the droplet and the surrounding aqueous solution, can act effectively. Emulsification is accomplished by to
complementary mechanisms, use the detergent mechanism of bile salts, and mechanical mixing due to
peristalsis.
Degradation of dietary lipids by pancreatic enzymes
The dietary TAG, cholesteryl ester, and phospholipids are enzymatically degraded by pancreatic enzymes, whose
secretion is hormonally controlled.
1/ TAG degradation: TAG molecules are too large to be taken up efficiently by the mucosal cells of the intestinal
villi. They are therefore, acted upon by a pancreatic lipase, which preferentially removes the fatty acids at carbon
1 and 3. The primary products of hydrolysis are thus a mixture of 2-monoacylglycerol and free fatty acids.

2/ Cholesteryl ester degradation: Most dietary cholesterol is present in the free form, with 10-
15% present in the esterified form. Cholesteryl esters are hydrolyzed by pancreatic cholesteryl
ester hydrolase, which produces cholesterol plus free fatty acids.
3/ Phospholipid degradation
Pancreatic juice is rich in phospholipase which removes one fatty acid from carbon 2 of
phospholipid, leaving a lysophospholipid. For example, phosphatidylcholine ( the predominant
 Lipid absorption
Free fatty acids, free cholesterol, and 2-monacylglycerol are the primary products of
lipid digestion in the jejunum. These, plus bile salts and fat soluble vitamins, form
mixed micelles-disk-shaped clusters of amphipathic lipids that coalesce with their
hydrophobic groups on the outside. Mixed micelles, are therefore, soluble in aqueous
environment of the intestinal lumen. These particles approach the primary site of lipid
absorption, the brush border membrane of the enterocytes (mucosal cells). This
membrane is separated from the liquid contents of the intestinal lumen by an
unstirred water layer that mixes poorly with the bulk fluid. The hydrophilic surface of
the micelles facilitates the transport of the hydrophobic lipids through the unstirred
water layer to the brush border membrane where they are absorbed

Note: Relative to other dietary lipids, cholesterol is only poorly absorbed by the enterocytes.

Protein Digestion and Absorption

Protein Digestion
What is Protein?
• Proteins are sequences of amino acids • There are 20 amino acids – 9 are essential amino acids •
phenylalanine, valine, threonine, tryptophan, isoleucine, methionine, histidine, leucine, lysine
 Amino Acids: Structure
• Consist of a central carbon atom bonded to: a hydrogen, a carboxylic acid, an amino group, and an additional
side group that is unique to each amino acid • The side group creates unique characteristics for each amino acid so
they differ in: shape, size, composition, electrical charge, and pH H H N H C R
C OH
O
Amino Group
Side Group
Carboxyl Grou

• Amino acids (AA) are linked to form proteins

• Amino acids are joined by
PEPTIDE bonds – Dipeptide
– 2 amino acids – Tripeptide
– 3 amino acids – Oligopeptides
– 4-10 amino acids – Polypeptide – more than
10 amino acids • Most proteins in the body and
diet are long polypeptides (100s of AA)
 Protein Digestion - Mouth
• No digestion occurs in the oral cavity or esophagus

Protein Digestion - Stomach

• Gastric phase
– Gastrin released from G cells
• Stretch receptors stimulate release
• AA in stomach stimulate release
– Parietal cells secrete HCl
• Gastrin stimulates Parietal cells to secrete
HCl
• HCl denatures proteins - 40, 30, and 20
• Converts pepsinogen to pepsin

– Chief cells secrete Pepsinogen

• Stimulated by cephalic vagal input
• Secretion enhanced
– Acetylcholine, CCK and gastrin
– Pepsinogen is auto-activated at pH <4 to
Pepsin
– Cleavage of an N-terminal peptide –
Pepsin can break down collagen
– Pepsin cleaves proteins at large aliphatic
or aromatic side group
 Protein Digestion - Intestines

• Intestinal phase Overview –

Majority of proteolysis occurs in
the intestines
• 70% of proteins are converted to
oligopeptides
– Still require terminal action at
enterocyte membrane
Protein Digestion – Small Intestine

• Majority of protein digestion occurs within the intestine due to the action of
pancreatic proteases.
– Proteases break down polypeptides into smaller peptides and AA
• Two main forms of pancreatic enzymes
– Endopeptidase – cleaves internal bonds
– Ectopeptidase – cleaves AA at C-terminus
 Protein Absorption
• Most protein absorption takes place in the duodenum and jejunum
– Tripeptides, Dipeptides and AA are absorbed
– There is minimal absorption of peptides longer than three amino acids
• Most AA are absorbed into the bloodstream, but some remain in the enterocytes
and are used to support the cells
• >99% of protein enters the bloodstream as amino acids

• Essentially no absorption of peptides

longer than three amino acids
• Di- and tri-peptides are more rapidly
absorbed than free amino acids due to
PEPT1
– Active transporter – PEPT1
• Coupled to sodium-hydrogen exchanger
(NHE3)
• Accommodates various sizes and charges
• Di- and tri-peptides are digested into
amino acids by cytoplasmic peptidases
Groff
 Lactose Intolerance
What is lactose?
Lactose* is a sugar found in milk and milk products.
The small intestine produces lactase, an enzyme that breaks down lactose.

What is lactose intolerance?

Lactose intolerance means you have symptoms such as bloating, diarrhea, and
gas after you have milk or milk products. If your small intestine does not produce
much lactase, you cannot break down much lactose. Lactose that does not break
down goes to your colon. The colon is an organ that absorbs water from stool and
changes it from a liquid to a solid form. In your colon, bacteria that normally live
in the colon break down the lactose and create fluid and gas, causing you to have
symptoms.

The causes of low lactase intolerance

 The causes of low lactase intolerance

● In some people, the small intestine makes less lactase starting at about age 2,
which may lead to symptoms of lactose intolerance. Other people start to have
symptoms later, when they are teenagers or adults.
● Infection, disease, or other problems that harm the small intestine can cause low
lactase levels. Low lactase levels can cause you to become lactose intolerant until
your small intestine heals.
● Being born early may cause babies to be lactose intolerant for a short time after
they are born.
● In a rare form of lactose intolerance, the small intestine produces little or no
lactase enzyme from birth.
The
 What are the symptoms of lactose
intolerance?

Common symptoms of lactose intolerance include

● bloating, a feeling of fullness or swelling, in your belly

● pain in your belly

● diarrhea

● gas

● nausea

You may feel symptoms 30 minutes to 2 hours after you have milk or milk
products. You may have mild or severe symptoms.