The structural difference that determines fat's physical state
Saturated: all single C-C bonds, no kinks, pack tightly → solid at room temp (butter). Unsaturated: C=C double bonds → kinks → can't pack → liquid (olive oil). Trans fats: artificially hydrogenated, behave like saturated.
Cell Membrane Structure
Phospholipid bilayer: hydrophilic heads face water, hydrophobic tails face inward
Cell Membrane Structure
The self-organizing phospholipid bilayer
Each phospholipid: polar head (faces water) + two nonpolar fatty acid tails (face inward). Bilayers form spontaneously. Fluid mosaic model: proteins float in this bilayer.
Cholesterol in Membranes
Cholesterol stabilizes membrane fluidity — not too fluid, not too rigid
Cholesterol in Membranes
Cholesterol is the membrane's fluidity buffer
At high temperatures: restrains phospholipid movement → prevents excess fluidity. At low temperatures: prevents tight packing → prevents solidifying. A Goldilocks molecule.
Why steroid hormones work differently from peptide hormones
Steroids are derived from cholesterol. Lipid-soluble → diffuse through membrane → bind intracellular receptors → directly regulate gene expression. Peptide hormones (insulin, glucagon) can't cross → bind surface receptors.
Beta-Oxidation
Beta-oxidation: fatty acids broken into 2-carbon acetyl-CoA units in mitochondria → ATP
Beta-Oxidation
How fatty acids are broken down to produce energy
Fatty acids are activated to acyl-CoA → enter mitochondria → each cycle removes 2 carbons as acetyl-CoA + produces FADH₂ + NADH. Acetyl-CoA enters Krebs cycle. Fat produces more ATP per gram than carbohydrates.
Glycerophospholipid Structure
Glycerophospholipids: glycerol + 2 fatty acids + phosphate + head group. The main membrane lipid.
Glycerophospholipid Structure
The dominant structural lipid in cell membranes
Glycerol backbone: position 1 and 2 — fatty acids (ester bonds). Position 3 — phosphate + head group (choline → phosphatidylcholine, serine → phosphatidylserine, ethanolamine, inositol). Head group determines charge and interactions. Phosphatidylserine: negatively charged, faces cytoplasm, flips to outer leaflet during apoptosis.
Lipid signaling molecules derived from arachidonic acid
Arachidonic acid (20-carbon PUFA) released from membrane phospholipids by phospholipase A₂. COX (cyclooxygenase) pathway: prostaglandins (inflammation, fever, pain) and thromboxanes (platelet aggregation, vasoconstriction). Lipoxygenase pathway: leukotrienes (bronchoconstriction, allergic response). Aspirin inhibits COX (cyclooxygenase) → reduces prostaglandins → anti-inflammatory.
Lipoproteins
Lipoproteins: transport lipids in blood. VLDL (Very Low Density Lipoprotein) → IDL (Intermediate Density Lipoprotein) → LDL (Low Density Lipoprotein — bad cholesterol). HDL (High Density Lipoprotein — good) takes cholesterol to liver.
Lipoproteins
How the body transports fats through the bloodstream
Lipoproteins: lipid + protein transport particles. VLDL (Very Low Density Lipoprotein): liver exports triglycerides. IDL (Intermediate Density Lipoprotein): intermediate product. LDL (Low Density Lipoprotein): delivers cholesterol to tissues — 'bad' because excess deposits in arterial walls. HDL: reverse cholesterol transport — removes cholesterol from tissues back to liver — 'good.' Apolipoproteins determine receptor binding.
VLDL
Liver exports triglycerides
LDL
Delivers cholesterol — 'bad'
HDL
Removes cholesterol — 'good'
Omega Fatty Acids
Omega-3 fatty acids: double bond at 3rd carbon from methyl end. Anti-inflammatory. EPA and DHA in fish oil.
Omega Fatty Acids
Naming convention and health significance of omega fatty acids
Omega (ω) position: carbon counting from the methyl end (omega end). Omega-3: double bond at 3rd carbon — EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) found in fish oil (anti-inflammatory, cardiovascular protection). Omega-6: double bond at 6th carbon — linoleic acid (pro-inflammatory in excess). Omega-9: oleic acid in olive oil (monounsaturated, neutral).
Waxes
Waxes: fatty acid ester of long-chain alcohol. Waterproofing in plants (cuticle), animals (earwax, fur).
Waxes
Simple lipids with waterproofing and protective functions
Wax: ester of long-chain fatty acid + long-chain alcohol. Very hydrophobic — excellent waterproofing. Plant cuticle wax: prevents water loss from leaves. Animal uses: earwax (cerumen), bee wax (honeycomb), spermaceti (whale), lanolin (sheep wool — water resistance). Hard solid at room temperature.
Free radicals (ROS): highly reactive molecules with unpaired electrons. Attack polyunsaturated fatty acids (PUFAs — fats with multiple double bonds) in membranes → lipid radical → chain reaction propagates. Damages membrane proteins and DNA. Antioxidants (vitamin E in membranes, vitamin C, glutathione) donate electrons to quench radicals. Linked to aging and atherosclerosis.
Mnemonic
What it means
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🎓 Common Exam Questions
Q: Describe the structure of the phospholipid bilayer and explain membrane fluidity.
A: Phospholipids are amphipathic: a glycerol backbone with two fatty acid tails (hydrophobic) and a phosphate-containing head group (hydrophilic). In aqueous environments they spontaneously form bilayers — heads face water, tails face inward. Fluid mosaic model (Singer-Nicolson, 1972): proteins float in a fluid lipid bilayer. Fluidity factors: unsaturated fatty acids (kinked tails) increase fluidity; saturated fatty acids decrease it; cholesterol acts as a fluidity buffer — at high temps it restricts movement (reduces fluidity); at low temps it prevents tight packing (prevents solidification). Temperature, fatty acid saturation, and cholesterol content all regulate membrane fluidity.
Q: Compare fatty acid synthesis and beta-oxidation — location, direction, and cofactors.
A: These are opposite processes occurring in different compartments — a key regulatory mechanism preventing futile cycling. Beta-oxidation: occurs in mitochondria; breaks fatty acids into 2-carbon acetyl-CoA units; produces NADH, FADH2, and acetyl-CoA; uses CoA; activated by carnitine transport into mitochondria. Fatty acid synthesis: occurs in cytoplasm; builds fatty acids 2 carbons at a time from acetyl-CoA; requires NADPH (from pentose phosphate pathway); uses ACP (acyl carrier protein); enzyme complex = fatty acid synthase. Reciprocally regulated: when energy is high (high ATP, high citrate), synthesis is promoted; when energy is low, beta-oxidation is promoted.
Q: Explain lipoprotein classes and their roles in cholesterol transport.
A: Lipoproteins transport hydrophobic lipids through the aqueous bloodstream. Chylomicrons: largest, least dense; carry dietary triglycerides from intestine to tissues. VLDL: made by liver; carries endogenous triglycerides to tissues; converted to IDL then LDL. LDL ("bad"): delivers cholesterol to peripheral tissues; taken up by LDL receptors; excess → atherosclerotic plaques. HDL ("good"): collects cholesterol from peripheral tissues and returns it to liver for excretion (reverse cholesterol transport). High LDL and low HDL correlate with cardiovascular disease risk. Statins block HMG-CoA reductase (rate-limiting step in cholesterol synthesis), lowering LDL.
Q: What are eicosanoids and what is their significance?
A: Eicosanoids are signaling lipids derived from 20-carbon polyunsaturated fatty acids, primarily arachidonic acid (an omega-6 fatty acid released from membrane phospholipids by phospholipase A2). Types: Prostaglandins (inflammation, pain, fever, platelet aggregation, uterine contraction). Thromboxanes (platelet aggregation, vasoconstriction). Leukotrienes (inflammation, bronchoconstriction in asthma). Prostacyclins (vasodilation, antiplatelet). NSAIDs (aspirin, ibuprofen) inhibit COX-1 and COX-2 enzymes that synthesize prostaglandins and thromboxanes — hence anti-inflammatory, analgesic, antipyretic effects. Aspirin irreversibly acetylates COX (hence antiplatelet effect lasting platelet lifetime ~10 days).
Q: How do steroid hormones differ from peptide hormones in their mechanism of action?
A: Steroid hormones (cortisol, testosterone, estrogen, progesterone, aldosterone, calcitriol) are lipid-soluble: they cross the plasma membrane freely, bind intracellular (cytoplasmic or nuclear) receptors, and the hormone-receptor complex acts as a transcription factor — directly regulating gene expression. Effects are slow (hours to days) but long-lasting. Peptide/protein hormones (insulin, glucagon, GH, ADH) are water-soluble: they cannot cross the membrane; they bind cell-surface receptors and trigger intracellular second messenger cascades (cAMP, IP3, Ca2+). Effects are rapid (seconds to minutes) but shorter-lived. This distinction is clinically important — oral administration works for steroids (lipid-soluble) but not peptides (degraded in GI tract).