Digestion and Absorption of Lipids

Digestion and absorption of lipids
Lipids:
• Heterogeneous group of organic compounds: Containing
carbon, hydrogen, oxygen, and sometimes phosphorus,
nitrogen, and sulfur.
• Esters of fatty acids with alcohol: Insoluble in water but
soluble in organic solvents.
Source of lipids
Exogenous sources: Lipids obtained through diet.
• Animal source: Animal meats and seafood with its byproducts.
• Vegetable sources: Oils from various oil seeds like groundnut,
sunflower, flaxseed, chia seeds, and also avocado, coconut,
etc.
Endogenous source: Lipids synthesized in the body: Fatty acids, TAG,
Cholesterol, Cholesterol esters, Phospholipids.
Exogenous sources of Lipids:

• Triacylglycerols (TAGs): 90% of dietary lipids.
• Phospholipids & Cholesterol, Cholesterol esters, Free fatty
acids, and Fat soluble vitamins: 10% of dietary lipids.
Physiological role of lipids:

• Energetic role: Fuel molecules.
• Structural role: Components of cell membranes.
• Hormonal role: Precursors for many hormones (steroids).
• Signal molecules: Prostaglandins.
• Protective role: Lipids surround important organs.
• Enzyme cofactors: Vitamin K.
• Electron carriers: Ubiquinone.
• Insulation: Against temperature extremes.
TRIACYLGLYCEROLS
• Highly concentrated energy stores: More efficient than
glycogen due to their anhydrous form and reduced fatty acids.
• Provide more than six times the energy per gram: Compared
to glycogen.
• Glycerol and fatty acids are directly used as fuel: By
mammalian organisms.
What is digestion?
• Complex lipid food molecules are converted to simple and
absorbable forms.
Difficulty:
• Hydrophobic molecules in a hydrophilic environment.
Solution:
• Emulsification increases surface area.
Requirements:
• Sites of digestion: Mouth, stomach, and small intestine.
• Emulsifiers: Bile, Phospholipids.
• Enzymes: Lipases.
DIGESTION OF DIETARY LIPIDS:

• Lipids in diet: Triacylglycerols, phospholipids, and cholesterol.
Digestion in Mouth:
• Mechanical digestion: Mixing with
saliva.
• Limited enzymatic digestion: By
lingual lipase, important in pediatric
groups, directly absorbed into the
bloodstream.
Digestion in the stomach:

• Mixing/churning: Brings
emulsification.
• Limited enzymatic digestion: By
gastric lipase, less important in
adults.
• Action of lingual lipase continued:
Hydrolyzing triacylglycerols with medium-chain fatty acids.
Digestion in the small intestine:

• Emulsification: By bile salts.
• Enzymatic digestion: By
pancreatic lipases.
• Micelles: Help with absorption.
Enterohepatic Circulation of Bile Salts:

• Liver: Uptake, synthesis, and recycling.
• Portal vein: Secretion into bile and intestine.
• Delivery to the liver: Ileum >>> Colon.
• Absorption: ~95%.
• Gut: Emulsification and metabolization.
• Faeces: Clearance (~5%).
Functions of bile salts:
• Emulsification: Breaking down large fat droplets into smaller
droplets.
• Stabilizes the emulsion: Preventing the smaller droplets from
coalescing.
• Provides alkaline medium: For optimal enzyme activity.
• Helps in absorption: Of digested lipids.
• Produces surfactants: To aid in digestion and absorption.
• Potent choleretics: Stimulating bile production.
• Excretes the waste products: From the liver.
• Solubilizes the cholesterol: For absorption.
Digestion in the small intestine:

• Enzyme: Pancreatic lipase.
• Catalyzes hydrolysis: At the C1 and C3 positions of TGs,
producing free fatty acids and 2-monoacylglycerol.
Colipase:
• Protein: Present in the intestine.
• Helps bind the water-soluble lipase: To the lipid substrates.
• Activates lipase: Increasing its activity.
Bile salts:
• Synthesized in the liver: From cholesterol.
• Taurocholate and glycocholate: The most abundant bile salts.
• Amphipathic: Hydrophilic (blue) and hydrophobic (black).
TGs:
• Water insoluble: Require bile salts for emulsification.
• Lipase is water soluble: Digestion of TGs takes place at lipid-
water interfaces.
• Rate of digestion depends on the surface area of the
interface: Bile salts increase this surface area.
Bile salts:
• Act as detergent: Emulsifying the lipid drops.
• Activates the lipase: Increasing its activity.
• Inadequate production of bile salts: Results in steatorrhea.
Dietary phospholipids are degraded by phospholipases:
• Phospholipases: Synthesized in the pancreas.
• Major phospholipase: Phospholipase A2.
• Catalyzes the hydrolysis of ester bond: At C2 of
glycerophospholipids, forming lysophosphoglycerides.
Phospholipases
• Lysophosphoglycerides: Can act as detergent and disrupt
cellular membranes in high concentrations.
• Normally present in low concentrations: In cells.
• Snake venom contains phospholipase A2: Causing the lysis of
erythrocytes membranes.
Dietary cholesterol:
• Most dietary cholesterol is unesterified.
• Cholesteryl esters are hydrolyzed: In the intestine by an
intestinal esterase (cholesterol ester hydrolase).
• Free cholesterol is solubilized: By bile-salt micelles for
absorption.
• After absorption in the intestinal cells: Cholesterol reacts
with acyl-CoA to form cholesteryl ester.
ABSORPTION OF DIETARY LIPIDS:
• 2-monoacylglycerols, fatty acids,
lysophosphoglycerides, free
cholesterol form micelles with bile
salts.
• Lipid absorption: Passive diffusion process.
• Micelles migrate to the microvilli: And
lipids diffuse into the cells.
• Bile acids are actively absorbed: And
transferred to the liver via the portal
vein.
Normal Absorption in the Small Intestine:

• Short-chain and medium-chain fatty acids: Absorbed into the
blood via capillary.
• Long-chain fatty acids and monoglycerides: Form into
triglycerides and are transported in chylomicrons into lymph
vessels.
TRANSPORT FORMS OF LIPIDS:
• Lipoproteins: Spherical particles
formed by lipids assembling with
phospholipids and apoproteins
(apolipoproteins).
Structure:
• Hydrophobic core: Triacylglycerols,
cholesteryl esters.
• Hydrophilic surfaces: Cholesterol, phospholipids,
apolipoproteins.
The Classes of Lipoproteins:
• Chylomicrons: Largest lipoproteins, synthesized in intestinal

cells, main transport form of dietary triacylglycerols.
• Very low-density lipoproteins (VLDL): Formed in the liver,
main transport form of triacylglycerols synthesized in the
organism.
• Intermediate-density lipoproteins (IDL): Formed from VLDL

remnants.
• Low-density lipoproteins (LDL): Formed from IDL, major
carrier of cholesterol.
LDL uptake by the receptor-mediated endocytosis
• High-density lipoproteins (HDL): Formed in the liver and small

intestine, pick up cholesterol from peripheral tissues.
Lipoproteinlipase:
• Enzyme: Located within capillaries of muscles and adipose
tissue.
• Function: Hydrolyses of TGs of chylomicrons and VLDL.
• Formed free fatty acids and glycerol: Pass into the cells.
LDL:
• Formed in the blood from IDL: And in liver from IDL (enzyme
– liver lipase).
• Enriched in cholesterol and cholesteryl esters: Contain about
50% of cholesterol.
• Protein component: Apo B-100.
• Major carrier of cholesterol: Transport cholesterol to
peripheral tissue.
HDL:
• Formed in the liver and partially in small intestine.
• Contain the great amount of proteins: About 40%.
• Pick up the cholesterol: From peripheral tissue, chylomicrons
and VLDL.
• Enzyme acyltransferase in HDL esterifies cholesterols:
Convert it to cholesterol esters and transport to the liver.
LDL/HDL Ratio:
• Ratio of cholesterol in the form of LDL to that in the form of
HDL: Can be used to evaluate susceptibility to the
development of atherosclerosis.
• For a healthy person: The LDL/HDL ratio is 3.5.
• Ideal: Under 2.0.
• Good: Under 5.0.
• Bad: Over 5.0.
Storage and Mobilization of Fatty Acids (FA):

• TGs are delivered to adipose tissue: In the form of
chylomicrons and VLDL, hydrolyzed by lipoprotein lipase into
fatty acids and glycerol, which are taken up by adipocytes.
• Fatty acids are reesterified to TGs: And stored in adipocytes.
• To supply energy demands: Fatty acids and glycerol are
released – mobilization of TGs.
CLINICAL ASPECTS:
Steatorrhea:
• Clinical condition: Presence of excess fat in feces.
Causes:
• Bile duct obstruction: Gallstones blocking bile flow.
• Pancreatic disease: Pancreatitis, tumor, or pancreatectomy.
• Celiac disease: Damage to the small intestine lining.
Causes of steatorrhea:
• Chronic pancreatitis:
Inflammation of the pancreas.
• Celiac Disease: Autoimmune
condition that damages the
small intestine lining.
• Post-gastrectomy: Removal of the stomach.
• Cholestasis: Reduced bile flow.
• Giardiasis: Infection with Giardia parasites.
• Crohn's Disease: Inflammatory bowel disease.
Celiac Disease:
• Autoimmune condition: Damages the lining of the small
intestine.
• Caused by a reaction to eating gluten: Found in wheat, rye,
barley, and possibly oats.
Chyluria:
• Abnormal connection: Between lymphatics
and urinary tract.
• Milky urine: Due to the presence of lipids.
Chylothrorax:
• Rare but serious condition: Abnormal connection between
pleural cavity and thoracic duct.
• Leakage of lipid in the pleural fluid: Causing a buildup of fluid
in the chest cavity.
Prevention of Fat Absorption and Obesity:
Olestra:
• Commercial lipid: Produced by esterification of natural fatty
acids with sucrose instead of glycerol.
• 6 to 8 fatty acids are covalently coupled with sucrose: Not
hydrolyzed and excreted.
• Tastes like lipid: But not absorbed.
Orlistat:
• Non-hydrolysable analog of triacylglycerol: Powerful inhibitor
of pancreatic lipase.
• Blocks lipid absorption: Resulting in lipid excretion.
Oral Fat Tolerance Test (OFTT):

• Measures the body's ability to absorb fat: By measuring the
amount of fat excreted in the feces.
Deficiency of lipoprotein lipase:
• Leads to accumulation of triacylglycerols in the blood: Due to
the inability to break down TGs in chylomicrons and VLDL.

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Digestion and Absorption of Lipids

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Digestion and absorption of lipids

Exogenous sources of Lipids:

Physiological role of lipids:

DIGESTION OF DIETARY LIPIDS:

Digestion in the stomach:

Digestion in the small intestine:

Enterohepatic Circulation of Bile Salts:

Digestion in the small intestine:

Normal Absorption in the Small Intestine:

The Classes of Lipoproteins:

• Chylomicrons: Largest lipoproteins, synthesized in intestinal

• Intermediate-density lipoproteins (IDL): Formed from VLDL

LDL uptake by the receptor-mediated endocytosis

• High-density lipoproteins (HDL): Formed in the liver and small

Storage and Mobilization of Fatty Acids (FA):

Oral Fat Tolerance Test (OFTT):

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