Transcript Digestion of Fats

The Digestion of Fats
Aghdas, Keith, Kevin, Laura, and
Maria
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Outline
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Lipid and Cholesterol Background
Digestion in Mouth, Esophagus, and Stomach
Digestion in the Small Intestine
Absorption in the Small Intestine
The Fate of Dietary and Endogenous Fats in
Circulation
• Fat Utilization and Storage by Body’s cells
• Health Concerns
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Lipid Background Information
• Major source of energy in the body
• Along with carbohydrates, fats account for most of the
calories consumed in food
• Primarily consist of hydrocarbon chains and rings
• Nonpolar, organic molecules; insoluble in polar solvents (i.e.
water); hydrophobic
• Types:
– Triglycerides (Fats & Oils)
– Steroids (cholesterol: steroid hormone parent molecule)
– Ketone bodies (derivatives of free fatty acids)
– Phospholipids
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Triglyceride (Fats & Oils)
• 1 glycerol molecule (3-carbon)
+ 3 fatty acids
• Hydroxyl group (glycerol) &
carboxyl group (fatty acid)
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Fatty Acids
Short chain fatty acids
• Less than 8 carbons
• Broken off from triglycerides; do
not require bile acids
• Short-chain fatty acids  portal
vein  liver (without
chylomicrons)
Long chain fatty acids
• 16+ carbons
• Digestion starts in small intestine;
require bile acids & lipases
• Absorption and Transport
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Cholesterol Structure and
Functions
• Four fused rings as the
core, shared by all
steroids.
• Membrane component
• Precursor to
– Bile acids
– Vitamin D
– Steroid hormones
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CHOLESTEROL: Synthesis
• The liver manufactures most of the cholesterol
in our bodies
• The intestine and all cells contribute a small
amount
• Overall, the body produces about 2.0 g per day
• Serum cholesterol levels are homeostatically
controlled
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Digestion in the Mouth
• Little to no
digestion in the
mouth for adults
• The salivary glands
of newborn babies
produce lipase
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Cholesterol Synthesis Pathway
• Cholesterol is created from
acetyl-CoA
• The rate-limiting and
irreversible step in the
pathway is the conversion of
HMG-CoA to Mevalonate
• HMG-CoA reducatase is the
enzyme responsible for this
step
• Drugs targeting high plasma
cholesterol targets this step
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Digestion in the Esophagus/Stomach
• No digestion in the
esophagus
• Only the peristaltic
movement of the food
bolus
• Little to no digestion in
stomach
• The stomach’s acidic
environment produces
chyme
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Digestion in the Small Intestine
• This is where digestion
of fats begins
• Fat absorption primarily
occurs in the duodenum
and jejunum
• Key Players
– Bile
– Pancreatic Lipase
– Pancreatic Colipase
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Bile
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Produced by the liver and stored in the
gallbladder
Cholecytokinin (CCK) is released in SI
due when fat in chyme reaches
duodenum; Stimulates gallbladder to
release bile
Consists of bile salts, bilirubin,
phospholipids, cholesterol and inorganic
ions
Bile salts: bile acids such as cholic acid
or chenodeoxycholic acid conjugated
with glycine or taurine
Bile salts are mainly responsible for the
emulsification of the fats by creating the
micelles
The micelles increase the exposed
surface area of the fats for lipase to do
its work
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Pancreatic Lipase/Colipase
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CCK also stimulates the
release of Lipase from the
pancreatic duct into the
duodenum.
As bile is emulsifying fat
droplets, lipase is
chemically digesting the fat
The hydrolysis reaction
results in 2 Free fatty acid
chains and a monoglyceride
These products enter the
micelles and now they are
called mixed micelles
Colipase coats
emulsifaction droplets and
anchors lipase to these
droplets
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Absorption in Small Intestine
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The Mixed Micelle is absorbed by
the intestinal epithelium which has
increased surface area due to villi
and microvilli
The free fatty acids and
monoglcyerides resynthesize to
become triglycerides within the
epithelium cell
The fats combine with cholesterol,
phospholipids and proteins to form
a chylomicron
The chylomicron is then transported
into the central lacteals just deep to
the epitheliumlymphatic
systemvenous flow via thoracic
duct and into circulation
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Dietary Fats in Circulation
• Once the chylomicron enters the
blood, an apolilpoprotein (ApoE)
complexes with it
• Now the chylomicron-ApoE
complex binds onto the ApoE
receptors on the plasma
membrane of capillary endothelial
cells in muscle and adipose tissue
• Lipoprotein lipase digests the
triglycerides
• The remnant chylomicron
containing cholesterol is
eventually taken up by the liver
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The Role of the Liver
• Produces endogenous
triglycerides and cholesterol and
combines them with ApoE to
form VLDLs (very-low density
lipoproteins)
• VLDLs deliver triglycerides to the
body’s cells and subsequently
become low-density lipoproteins
(LDL’s)
• LDL’s now deliver cholesterol to
the body’s cells
• Excess cholesterol and
phospholipids bond and return to
the liver as cholesterol esters via
high-density lipoproteins (HDLs)
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Fat Utilization by the Body’s Cells
• The body’s tissues store fats in
adipose cells and utilize them
after the depletion of the glucose
supply
• Beta-oxidation: enzymes remove
two carbon acetic acid from the
acid end of fatty acid chain
resulting in 1 acetyl-CoA (12 ATP
for one cycle through Kreb’s +
1NADH + 1FADH2)
• Example: 16 carbon long fatty
acid 96 ATP + 3 ATP + 2 ATP
• 101 ATP!!!!
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Lipogenesis: Fat Synthesis/Storage
• The formation of fat when
blood glucose levels are high
• Occurs in Adipose tissue and
in the liver
1. Glucose
 3-phosphoglyceraldehyde
 glycerol
2. Acetyl-CoA
 fatty acid chains
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Lipogenesis (From Amino Acids)
• Proteins can be converted to
fats by deamination
• Isoleucine, Leucine, and
tryptophan can be converted
to Acetyl-CoA which can
be transformed into fatty
acid chains
• Alanine, Cysteine, Glycine,
Serine, and Trytophan can
be converted to pyruvate
which can be indirectly
converted into glycerol
FATTY
ACID
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Health Concerns
• Atherosclorosis /High
Cholesterol/Statins
• Saturated fats
• Unsaturated fats
• Polyunsaturated fats
• Omega-3 fats
• Omega-6 fats
• Ketone Bodies
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Lipoproteins, Cholesterol, &
Atherosclerosis
• Atherosclerosis: plaques (cholesterol, lipids, smooth muscle cells) protrude
into artery lumen & reduce blood flow
• Risk: high blood cholesterol (diet)
• LDLs (carrying cholesterol to organs & blood vessels) contribute to
development of atherosclerosis
• HDLs (carrying excess cholesterol from organs & blood vessels to liver)
help protect against development of atherosclerosis
• High LDL cholesterol treatment: Statins: inhibit enzyme HMG-coenzyme
A reductase (catalyze cholesterol synthesis); reduce liver’s ability to
produce cholesterol; decreased intracellular cholesterol promotes
production of LDL receptors (increase in liver uptake of LDL cholesterol)
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Degree of Saturation of Fats
Saturated: A fatty acid with a carbon
chain containing all the hydrogens
that it can hold
-elevates LDL cholesterol
Monounsaturated:A fatty acid with a
carbon chain that contains one
double bond
-can lower LDL cholesterol levels
Polyunsaturated:A fatty acid that
contains two or more double
bonds
-can help lower blood cholesterol
levels
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Ketone Bodies
• In times of fasting or when
immediate energy is needed, the
liver can convert free fatty acids
into acetyl-CoA then into ketone
bodies (Ketogenesis)
• Large amounts of ketone bodies
are released into the blood to
supply the body’s cells
• However, in a low-carbohydrate
diet or diabetes mellitus, the rapid
triglyceride breakdown can lead
to Ketosis
• Then if the excess ketone bodies
lowers the blood pH then its
called Ketoacidosis
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Omega-3 and Omega-6 Fatty Acids
• Polyunsaturated,
essential fatty acids
• Omega-3 acid (linolenic
acid)
• Omega-6 fatty acid
(alpha-linolenic acid):
increased ratio of
omega-6 to omega-3 is
associated with heart
disease and increased
allergies and asthma
incidence.
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Summary
Ingestion of
lipids in the
form of
triglycerides
and
cholesterol
Fats are
propelled
into the
esophagus
and then
into the
stomach
Bile salts
and
pancreatic
lipase
breakdown
fats in the S.
I.
Dietary and
Endogenous
Fats in
Circulation
Fat
metabolism
Health
concerns
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THE END
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