The Digestion of Fats Aghdas, Keith, Kevin, Laura, and Maria
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
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
Triglyceride (Fats & Oils) • 1 glycerol molecule (3-carbon) + 3 fatty acids • Hydroxyl group (glycerol) & carboxyl group (fatty acid)
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
Cholesterol Structure and Functions • Four fused rings as the core, shared by all steroids. • Membrane component • Precursor to • Bile acids • Vitamin D • Steroid hormones
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
Digestion in the Mouth • Little to no digestion in the mouth for adults • The salivary glands of newborn babies produce lipase
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
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
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
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
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
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
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 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)
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!!!!
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
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
Health Concerns • Atherosclorosis /High Cholesterol/Statins • Saturated fats • Unsaturated fats • Polyunsaturated fats • Omega-3 fats • Omega-6 fats • Ketone Bodies
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)
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
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
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.
Summary
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