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📘 Lipids - Biochemistry and Metabolism (AV-7)

This is a biochemistry lecture on Lipids, authored by Vladimir Ilyukha (vladimir.ilyukha@abmu.edu.ge), covering 22 slides from lipid classification all the way to ketone body metabolism.

Slide 1 - Title

Course: Biochemistry and Metabolism (AV-7). The instructor's email is provided. Slide 2 contains a QR code (likely linking to course materials) alongside a photo of Lehninger's Principles of Biochemistry, 7th Edition (Nelson & Cox) - the primary textbook for the course.

Slide 5 - Digestion Overview (Context for Lipids)

Before diving into lipids specifically, the lecture reviews the full digestive process:

Site	What Happens
Oral cavity	Mechanical breakdown; amylase starts starch digestion
Esophagus	Transport of food bolus
Stomach	HCl + enzymes digest proteins; forms chyme
Small intestine	Main stage - pancreatic enzymes + bile break down proteins, fats, carbs; absorption into blood/lymph
Large intestine	Bacterial fiber breakdown, water/salt absorption, feces formation

The slide ends with a thought-provoking "What is missed?" - prompting students to think critically.

Slide 6 - Lipid Classification

Lipids are divided into four major classes:

Simple Lipids - Fatty acid (FA) + Alcohol only
- Triacylglycerols (TAG) - the main storage form of fat
- Waxes
Compound Lipids - FA + Alcohol + additional group
- Phospholipids - contain a phosphate group (key membrane components)
- Glycolipids - contain a sugar
- Lipoproteins - lipid-protein complexes for transport
Derived Lipids - Products of hydrolysis of simple/compound lipids
- Fatty acids
- Steroids (e.g., cholesterol)
- Eicosanoids (e.g., prostaglandins)
- Ketone bodies
Miscellaneous Lipids - Possess characteristics of lipids but don't fit other categories
- Squalene (cholesterol precursor)
- Carotenoids (vitamin A precursors)

Slide 7 - Fatty Acids Important for Human Health

This slide shows the structural formulas and nomenclature of the key fatty acids:

Common Name	Standard Nomenclature	Omega Family
Palmitic acid (PA)	16:0	- (saturated)
Stearic acid (SA)	18:0	- (saturated)
Oleic acid (OA)	18:1Δ⁹	ω-9 (monounsaturated)
Linoleic acid (LA)	18:2Δ⁹˒¹²	ω-6 (essential)
α-Linolenic acid (ALA)	18:3Δ⁹˒¹²˒¹⁵	ω-3 (essential)
Arachidonic acid (AA)	20:4Δ⁵˒⁸˒¹¹˒¹⁴	ω-6
Eicosapentaenoic acid (EPA)	20:5Δ⁵˒⁸˒¹¹˒¹⁴˒¹⁷	ω-3
Docosahexaenoic acid (DHA)	22:6Δ⁴˒⁷˒¹⁰˒¹³˒¹⁶˒¹⁹	ω-3

The notation "16:0" means 16 carbons, 0 double bonds. "Δ9" means a double bond at carbon 9 from the carboxyl (α) end. Omega notation counts from the methyl (ω) end.

Slide 8 - Phospholipid Structure

Slide 8 shows three key images:

Image 1: Structure of phosphatidylcholine - two fatty acid tails (one saturated, one unsaturated - yellow), a glycerol backbone, a phosphate group (green), and a choline head group (blue, positively charged). This is the classic membrane phospholipid.

Image 2: Structure of a sphingomyelin - instead of glycerol, it uses sphingosine as the backbone, with two fatty acid chains and a phosphocholine head.

Image 3: The four polar head groups that can attach to the phosphate:

Choline (forms phosphatidylcholine)
Serine (forms phosphatidylserine)
Ethanolamine (forms phosphatidylethanolamine)
Myoinositol (forms phosphatidylinositol)

Slide 9 - Digestion of Lipids

Title: Digestion of Lipids - Emulsification and Hydrolysis

Lipid digestion occurs in stages:

Oral cavity (E) - Emulsification begins (lingual lipase)
Stomach (E + minor H) - Further emulsification; minor hydrolysis (gastric lipase)
Small Intestine - The main site:
- Emulsification (E): Peristalsis + bile constituents break fat globules into tiny droplets (~0.5 μm)
- Hydrolysis (H):
  - Cholesterol esters → Cholesterol esterase
  - TAG → Pancreatic lipase
  - Phospholipids → Phospholipase A1, A2, C, D

Slide 10 - Phospholipase Cleavage Sites

This diagram shows exactly where each phospholipase cleaves the phospholipid molecule:

Phospholipase A₁ - cleaves the fatty acid at the sn-1 position (carbon 1 of glycerol)
Phospholipase A₂ - cleaves the fatty acid at the sn-2 position (carbon 2 - usually where the unsaturated FA is)
Phospholipase C - cleaves between glycerol and the phosphate group
Phospholipase D - cleaves between the phosphate group and the head group (e.g., choline)

A₂ is particularly important clinically - it releases arachidonic acid (the precursor to prostaglandins, leukotrienes).

Slide 11 - Absorption of Lipids

After digestion, the products are too large to be absorbed directly. Here's what happens:

Hydrolysis products (lysophospholipids, fatty acids, monoacylglycerols/MAG, cholesterol) + bile acids form micelles - tiny spherical structures with hydrophilic outsides and hydrophobic cores
Micelles diffuse to the intestinal brush border epithelium
Products are absorbed, mainly in the ileum
Inside enterocytes, they are re-esterified back into TAGs, packaged with proteins as chylomicrons, and secreted into lymph (lacteals)

Slide 12 - Transport of Lipids: Lipoprotein Structure

A lipoprotein is a spherical particle with:

Outer shell: Phospholipid monolayer + free cholesterol + apoproteins (proteins that determine function and receptor targeting)
Inner core: TAGs (triacylglycerols) + cholesterol esters (CS esters)

Slide 13 - Types of Lipoproteins

Lipoprotein	Primary Cargo	Function
Chylomicrons	TAG (dietary)	Transport dietary fat from intestine to tissues
VLDL (Very Low Density)	TAG + minor CS	Transport endogenous TAG from liver to tissues
IDL (Intermediate Density)	Remnant	Created as VLDL loses its fatty acids to tissues
LDL (Low Density)	Cholesterol	Transport endogenous cholesterol to peripheral tissues
HDL (High Density)	Cholesterol	Carry cholesterol back to the liver (reverse transport)

Clinical note: LDL is the "bad" cholesterol (deposits in artery walls); HDL is the "good" cholesterol (removes it).

Slide 14 - Lipid Digestion in Children (Pediatric Differences)

Children have distinct lipid digestion characteristics:

Lingual lipase is active and continues working in the stomach
Gastric lipase is more active than in adults because the infant stomach pH ~5.0 is less acidic
In infants, breast milk contains lipase that further aids digestion (cow's milk does not)
Because of these factors, 25-50% of all lipolysis in infants occurs in the stomach - far more than in adults
Pancreatic lipase is low until about age 7, limiting fat digestion; it doesn't reach peak activity until age 8-9 years

Slide 15 - Nutritional Composition Through Development

This graph (from rat studies, representative of mammalian development) shows the proportion of macronutrients at different developmental stages:

Fetus: Almost entirely proteins + carbohydrates, essentially no fat
Birth → Suckling period: Dramatic rise in FAT (up to ~50% of diet in breast milk)
Weaning onwards (day 16 → 30): Fat content in diet declines; carbohydrates increase This shift explains why pancreatic lipase develops progressively - the metabolic demand for fat digestion peaks during suckling.

Slide 16 - Beta-Oxidation of Fatty Acids: Activation Step

Before a fatty acid can be oxidized, it must be activated:

R-COOH + ATP + CoA-SH → (Mg²⁺) → R-CO~S-CoA + AMP + H₄P₂O₇

The fatty acid reacts with CoA (coenzyme A) using ATP
The product is Acyl-CoA (a fatty acyl-CoA thioester)
This reaction occurs on the outer mitochondrial membrane (catalyzed by acyl-CoA synthetase)
ATP is hydrolyzed to AMP + pyrophosphate (equivalent to using 2 ATP)

Slide 17 - Beta-Oxidation Steps (Cyclic Pathway)

The activated fatty acid enters the mitochondrial matrix via the carnitine-acylcarnitine transporter (carnitine shuttle). Then the cycle repeats:

Step	Reaction	Enzyme	Product
1	Fatty acid activation (outside mito)	Acyl-CoA synthetase	Acyl-CoA
2	Oxidation at α-β bond	Acyl-CoA dehydrogenase	Trans-enoyl-CoA + FADH₂
3	Hydration	Enoyl-CoA hydratase	L-3-Hydroxyacyl-CoA (+H₂O)
4	Oxidation	Hydroxyacyl-CoA dehydrogenase	3-ketoacyl-CoA + NADH+H⁺
5	Thiolysis (cleavage)	Thiolase (+CoASH)	Acyl-CoA (2C shorter) + Acetyl-CoA
6	Repeat	-	Continue until all carbons consumed

Each cycle yields: 1 FADH₂ + 1 NADH + 1 Acetyl-CoA, and the chain is shortened by 2 carbons.

Slide 18 - Oxidation of Unsaturated Fatty Acids

Using oleoyl-CoA (18:1, ω-9) as an example:

Normal β-oxidation runs for 3 cycles, producing 3 Acetyl-CoA
The remaining intermediate is cis-Δ³-dodecenoyl-CoA (double bond in the wrong position/geometry for β-oxidation)
An isomerase (Δ³,Δ²-enoyl-CoA isomerase) converts the cis-Δ³ bond to a trans-Δ² bond
Now normal β-oxidation resumes for 5 more cycles, yielding 6 Acetyl-CoA

Total: 9 Acetyl-CoA (one FADH₂ less than a fully saturated C18 acid, because the isomerase bypasses the first dehydrogenation step)

Slide 19 - Oxidation of "Odd-Chain" Fatty Acids

Odd-chain fatty acids (uncommon in humans but found in some foods) follow normal β-oxidation until the last 3-carbon unit - propionyl-CoA is produced instead of acetyl-CoA. Propionyl-CoA is then converted:

Propionyl-CoA → (propionyl-CoA carboxylase, requires biotin + CO₂) → Methylmalonyl-CoA
Methylmalonyl-CoA → (methylmalonyl-CoA mutase, requires vitamin B₁₂) → Succinyl-CoA
Succinyl-CoA enters the TCA cycle

Clinical link: Vitamin B₁₂ deficiency impairs this pathway, causing methylmalonic acidemia.

Slide 20 - Fatty Acid Synthesis

Fatty acid synthesis is essentially the reverse of β-oxidation, but uses different enzymes, occurs in the cytosol, and uses NADPH (not NADH/FADH₂):

Acetyl-CoA (2C primer) is loaded onto ACP (acyl carrier protein)
Malonyl-CoA (3C) is made from Acetyl-CoA by Acetyl-CoA Carboxylase (ACC) - the key regulatory enzyme - and loaded onto ACP
Condensation: β-ketoacyl-ACP synthase joins them, releasing CO₂ → β-ketobutyryl-ACP
Reduction 1: β-ketoacyl-ACP reductase (NADPH) → β-hydroxybutyryl-ACP
Dehydration: β-hydroxyacyl-ACP dehydratase (+H₂O) → Crotonyl-ACP
Reduction 2: Enoyl-ACP reductase (NADPH) → Butyryl-ACP
The cycle repeats, adding 2 carbons each time, until palmitoyl-CoA (16:0) is produced

All these reactions are catalyzed by a single multienzyme complex: Fatty Acid Synthase (FAS).

Slide 21 - Ketone Bodies

The three ketone bodies:

Acetone - volatile, lost in breath (fruity smell in ketoacidosis)
Acetoacetic acid (Acetoacetate) - the central ketone body
Beta-hydroxybutyric acid (Beta-hydroxybutyrate) - the most abundant in blood during ketosis

Why are ketone bodies made?

Fatty acid oxidation is energy-intensive and not all tissues can use it (neurons cannot oxidize FA directly)
The liver oxidizes fatty acids and re-packages the acetyl-CoA into ketone bodies that can travel in blood
Ketone bodies are made in: fasting, Type 1 diabetes, prolonged exercise
They also rise with alcohol poisoning and high-fat diets

Slide 22 - Ketogenesis and Ketone Body Oxidation

Ketogenesis (in liver mitochondria):

2 Acetyl-CoA → (mThiolase) → Acetoacetyl-CoA (AcAc-CoA)
AcAc-CoA + Acetyl-CoA → (HMG-CoA synthase) → HMG-CoA
HMG-CoA → (HMG-CoA lyase) → Acetoacetate (AcAc) + Acetyl-CoA
AcAc is either:
- Spontaneously decarboxylated → Acetone (+ CO₂)
- Reduced by BDH1 (NAD⁺/NADH) → β-Hydroxybutyrate

Ketone Body Oxidation (in peripheral tissues - brain, heart, muscle):

β-Hydroxybutyrate → (BDH1, NAD⁺) → Acetoacetate
Acetoacetate + Succinyl-CoA → (SCOT = Succinyl-CoA:3-oxoacid CoA transferase) → Acetoacetyl-CoA
Acetoacetyl-CoA + CoASH → (mThiolase) → 2 Acetyl-CoA
Acetyl-CoA → enters the Citric Acid Cycle (via Citrate Synthase)

The liver cannot use its own ketone bodies (it lacks SCOT), which is why it exports them.

Summary of Topics Covered

Section	Slides	Key Concept
Course intro & textbook	1-3	Lehninger biochemistry
Digestion overview	5	GI tract roles
Lipid classification	6	Simple, Compound, Derived, Misc.
Fatty acid nomenclature	7	Omega-3/6/9; essential FAs
Phospholipid structure	8	PC, sphingomyelin, head groups
Lipid digestion	9-10	Bile emulsification; phospholipases
Absorption & micelles	11	Micelle → chylomicron
Lipoprotein transport	12-13	HDL, LDL, VLDL, IDL, chylomicrons
Pediatric lipid metabolism	14-15	Lingual lipase, developmental shifts
β-Oxidation	16-17	Activation, carnitine shuttle, 4-step cycle
Unsaturated FA oxidation	18	Isomerase adjustment
Odd-chain FA oxidation	19	Propionyl-CoA → succinyl-CoA (B₁₂)
Fatty acid synthesis	20	FAS complex, ACP, ACC
Ketone bodies	21-22	Ketogenesis, SCOT, BDH1, TCA

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