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The Digestion of Fats
Aghdas, Keith, Kevin, Laura, and Maria
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Outline
• 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 Concerns2
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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• 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• 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• 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 epitheliumlymphatic systemvenous 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
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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
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THE END
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