1. Aghdas, Keith, Kevin, Laura, and Maria
The Digestion of Fats
Aghdas, Keith, Kevin, Laura, and Maria

2. 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 Concerns

3. 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

4. Triglyceride (Fats & Oils)
1 glycerol molecule (3-carbon) + 3 fatty acids
Hydroxyl group (glycerol) & carboxyl group (fatty acid)

5. 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

6. Cholesterol Structure and Functions
Four fused rings as the core, shared by all steroids.
Membrane component
Precursor to
Bile acids
Vitamin D
Steroid hormones

7. 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

8. Digestion in the Mouth Little to no digestion in the mouth for adults
The salivary glands of newborn babies produce lipase

9. 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

10. 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

11. 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

12. 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
Define bile salts (pg 631)
CCK

13. 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
Monoglycerides and free fatty acid

14. 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 epitheliumlymphatic systemvenous flow via thoracic duct and into circulation

15. 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
The liver can use free fatty acids, monoglycerides, and cholesterol received from HDL’s for energy purposes

16. 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)
Define VLDL, LDL, HDL????
Explain cholesterol esters

17. 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!!!!

18. 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

19. 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

20. Health Concerns Atherosclorosis /High Cholesterol/Statins
Saturated fats
Unsaturated fats
Polyunsaturated fats
Omega-3 fats
Omega-6 fats
Ketone Bodies

21. 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)

22. 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

23. 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
Ketosiselevated levels of ketone bodies in the blood

24. 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.

25. 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
Fats is placed into the mouth… salivary glands and stomach (of newborn) produce lipase (enzyme).. Little to no fat digestion occurs
From the mouth, it goes down to the esophagus to the stomach where HCl is present and makes it possible to produce chyme
Chyme arrives in the duodenum of S.I. where bile and pancreatic juice breakdown fats. Then, it is absorbed into the intestinal epithelial cells. Formed into triglycerides, phospholipids again… then triglyceride, phospolipid and cholesterol mix with protein to form vesicles called chylomicrons..
Transport of blood… dietary fat circuation/endogenous circulation
Fat can be used as stored energy when there’s no more glucose… used for ATP synthesis………..// excess fat is stored in fat depots (hips, abdomen, breasts)
Health concerns

26. THE END