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Topics covered: Classification of lipids, Classification of fatty acids, Saturated fatty acids
Lipids are hydrophobic or amphipathic organic molecules, insoluble in water but soluble in non-polar solvents.
• Fats (Triacylglycerols) → glycerol + 3 fatty acids
• Waxes → long-chain fatty acids + long-chain alcohols
Contain additional non-lipid groups
• Phospholipids → fatty acids + alcohol + phosphate
– Glycerophospholipids (lecithin, cephalin)
– Sphingophospholipids (sphingomyelin)
• Glycolipids → fatty acids + carbohydrate
– Cerebrosides
– Gangliosides
• Lipoproteins → lipid + protein (transport forms)
Formed during hydrolysis of other lipids
• Fatty acids
• Steroids (cholesterol)
• Fat-soluble vitamins (A, D, E, K)
• Eicosanoids
• Carotenoids
• Squalene
• Prostaglandins
Fatty acids are long-chain hydrocarbons ending in a carboxyl group (-COOH).
• Saturated fatty acids
• Unsaturated fatty acids
– Monounsaturated (one double bond)
– Polyunsaturated (multiple double bonds)
• Short-chain (<6 carbons)
• Medium-chain (6–12 carbons)
• Long-chain (13–20 carbons)
• Very-long chain (>20 carbons)
• Essential fatty acids (EFAs) → linoleic, linolenic (cannot be synthesized)
• Non-essential fatty acids → synthesized by the body
• Cis fatty acids → naturally occurring
• Trans fatty acids → industrial hydrogenation, associated with heart disease
Fatty acids containing no double bonds; all carbon atoms are “saturated” with hydrogen.
• Acetic acid (2C)
• Butyric acid (4C)
• Caproic acid (6C)
• Caprylic acid (8C)
• Capric acid (10C)
• Lauric acid (12C)
• Myristic acid (14C)
• Palmitic acid (16C)
• Stearic acid (18C)
• Arachidic acid (20C)
• Animal fats (ghee, butter)
• Coconut oil
• Palm oil
• Dairy products
• Meat
• Solid at room temperature
• High melting point
• No susceptibility to oxidation (unlike PUFA)
• Excess intake → increased LDL cholesterol
• Risk of atherosclerosis & cardiovascular disease
• Butyric acid supports colonic mucosal health
• Medium-chain triglycerides (MCTs) used in malabsorption disorders
Fatty acids containing one or more double bonds in their carbon chain.
• Monounsaturated fatty acids (MUFA) → 1 double bond
• Polyunsaturated fatty acids (PUFA) → ≥ 2 double bonds
• MUFA: Oleic acid (18:1)
• PUFA: Linoleic (18:2), Linolenic (18:3), Arachidonic acid (20:4)
• Liquid at room temperature
• Lower melting point than saturated fats
• Refined oils rich in unsaturated fatty acids
• Linoleic acid (18:2)
• Alpha-linolenic acid (18:3)
• Arachidonic acid (20:4)
• EPA (20:5)
• DHA (22:6)
• Fluidity of membranes
• Precursor of eicosanoids (prostaglandins, leukotrienes)
Fatty acids not synthesized by humans; must be supplied by diet.
• Linoleic acid (ω-6)
• Alpha-linolenic acid (ω-3)
• Arachidonic acid (essential if linoleic acid deficient)
• Dry scaly skin
• Hair loss
• Poor wound healing
• Growth retardation
• Alpha-linolenic acid (ALA)
• EPA, DHA (fish oils)
Benefits
• Anti-inflammatory
• Improves heart health
• Essential for brain/retina
• Linoleic acid
• Arachidonic acid
Functions
• Growth, reproduction
• Pro-inflammatory eicosanoid precursor
Ideal ratio: 1:4
Modern diet: 1:20 (excess inflammation)
• Natural form
• Creates a bend in chain
• ↑ membrane fluidity
• Healthier
• Formed by hydrogenation of oils
• Straight-chain, behaves like saturated fat
• ↑ LDL, ↓ HDL
• Associated with atherosclerosis & heart disease
• Insoluble in water
• Soluble in ether, chloroform
• Hydrophobic (some amphipathic)
• Hydrolysis → fatty acids + glycerol
• Hydrogenation → solid fat formation
• Oxidation → rancidity
• Saponification → soap formation
Glycerol + 3 fatty acids
• Simple TAG → same FA
• Mixed TAG → different FAs
• Major energy reserve
• Stored in adipose tissue
• Provides insulation, protection
• High TAG → risk of pancreatitis
• Low TAG → malnutrition, fat malabsorption
Oxidative damage to PUFA in cell membranes by free radicals.
• Initiation → free radical attack
• Propagation → chain reaction
• Termination → antioxidants stop cycle
• Membrane damage
• Cell injury, aging
• Seen in liver diseases, CCl₄ toxicity
• Vitamin E, vitamin C, glutathione, superoxide dismutase
Compound lipids are lipids containing additional non-lipid components (phosphate, carbohydrate, proteins).
Contain:
• Fatty acids
• Alcohol (glycerol or sphingosine)
• Phosphate
• Nitrogenous base (choline, ethanolamine)
Includes:
• Glycerophospholipids
• Sphingophospholipids
Contain:
• Fatty acids
• Carbohydrate (galactose, sialic acid)
• Sphingosine
Includes:
• Cerebrosides
• Gangliosides
• Lipid + protein
• Transport vehicles for TAG, cholesterol, phospholipids
• Types: chylomicrons, VLDL, LDL, HDL
• Fatty acids + carbohydrate + sulfonic acid
• Fatty acids + amino alcohols
Lipids containing phosphate, essential part of cell membranes and lipoproteins.
Alcohol = glycerol
Examples:
• Lecithin (phosphatidylcholine)
• Cephalin (phosphatidylethanolamine)
• Phosphatidylserine
• Phosphatidylinositol
• Cardiolipin
Cardiolipin is a unique diphosphatidylglycerol phospholipid found almost exclusively in the inner mitochondrial membrane.
It contains:
• Glycerol + 2 phosphatidic acid units
• Total of 4 fatty acids
• Highly acidic (two phosphate groups)
Cardiolipin is formed by linking two phosphatidylglycerol molecules through an additional glycerol unit.
This produces a twin phospholipid structure with:
• Central glycerol
• Two phosphatidic acids
• Four long-chain fatty acids in total
This unique architecture makes it essential for mitochondrial membrane stability.
Cardiolipin is concentrated in:
• Inner mitochondrial membrane (IMM)
• Particularly abundant in tissues with high energy demand:
– Heart
– Skeletal muscle
– Liver
– Kidney
Cardiolipin binds tightly to:
• Complex I
• Complex III
• Complex IV
• ATP synthase
Maintains the structure and function of the electron transport chain (ETC).
Helps maintain proton gradient and optimal function of oxidative phosphorylation.
Cardiolipin undergoes oxidation during apoptosis → facilitates release of cytochrome c, triggering programmed cell death.
Because bacteria contain cardiolipin, antibodies to cardiolipin are clinically significant (see below).
• Defect: TAZ gene mutation (encodes tafazzin).
• Impairs cardiolipin remodeling.
• Leads to:
– Dilated cardiomyopathy
– Skeletal muscle weakness
– Neutropenia
– Growth delay
This is the classic disorder linked to cardiolipin.
Seen in:
• Antiphospholipid syndrome (APS)
• Systemic lupus erythematosus (SLE)
Effects:
• Hypercoagulability
• Recurrent miscarriages
• Thrombosis (venous & arterial)
Anticardiolipin antibodies are used in diagnosis of APS.
Abnormal cardiolipin → impaired ETC →
• Muscle weakness
• Lactic acidosis
• Exercise intolerance
Seen in:
• Mitochondrial myopathies
• Multiple acyl-CoA dehydrogenase deficiency
• Aging-related mitochondrial dysfunction
Ischemic damage alters cardiolipin composition → reduces ETC activity → worsens cardiac dysfunction.
Cardiolipin is synthesized from phosphatidylglycerol, which is also a surfactant component.
Thus mitochondrial defects affecting cardiolipin synthesis may also affect phosphatidylglycerol turnover.
• Cardiolipin = diphosphatidylglycerol with 4 fatty acids
• Located in inner mitochondrial membrane
• Stabilizes ETC complexes & ATP synthase
• Required for oxidative phosphorylation
• Mutated in Barth syndrome (dilated cardiomyopathy)
• Anticardiolipin antibodies → antiphospholipid syndrome
• Reduced in mitochondrial myopathies & ischemic heart disease
• Formed from phosphatidylglycerol
Functions:
• Membrane structure
• Surfactant
• Second messengers (IP₃, DAG)
Alcohol = sphingosine
Example:
• Sphingomyelin
Functions:
• Myelin sheath structure
• Nerve conduction
Artificial spherical vesicles composed of phospholipid bilayers.
• Drug delivery systems
• Gene delivery (DNA/RNA transport)
• Model membranes for research
• Stabilize and transport hydrophobic drugs
• Aqueous core surrounded by one or more phospholipid bilayers
• Amphipathic nature allows hydrophilic and hydrophobic drug entrapment
Most abundant glycerophospholipid in human tissues.
• Glycerol
• 2 fatty acids
• Phosphate
• Choline
• Important membrane component
• Major pulmonary surfactant (Lecithin : Sphingomyelin ratio used for fetal lung maturity)
• Lipoprotein structure (VLDL export from liver)
• Respiratory Distress Syndrome (RDS) → low lecithin in premature infants
• Lecithin: Sphingomyelin ratio > 2:1 indicates mature fetal lungs
Enzymes that hydrolyze specific bonds of phospholipids.
• Removes fatty acid at C-1 of glycerol
• Removes fatty acid at C-2
• Releases arachidonic acid → prostaglandins & leukotrienes
• Found in venom, pancreas
• Removes both C-1 and C-2 fatty acids
• Splits phosphate-containing head group
• Cleaves PIP₂ → DAG + IP₃ (second messengers)
• Removes alcohol (choline/ethanolamine)
• Converts PC → phosphatidic acid
• Snake venom contains potent phospholipase A2 → membrane destruction
• Excess activation → inflammation
• Defects in phospholipid metabolism → neurological disorders
Mixture of phospholipids & proteins that reduces surface tension inside alveoli.
• Dipalmityl phosphatidylcholine (DPPC) → the key surfactant.
• Also contains phosphatidylglycerol & surfactant proteins (SP-A, SP-B, SP-C, SP-D).
• Prevents alveolar collapse at end-expiration
• Improves lung compliance
• Respiratory Distress Syndrome (RDS)
– Due to low surfactant in premature infants
– Lecithin : Sphingomyelin ratio > 2:1 = lung maturity
• Maternal steroids enhance fetal surfactant synthesis.
A glycerophospholipid composed of:
• Glycerol backbone
• Two fatty acids
• Phosphate group
• Glycerol as the head group
It is one of the major phospholipids in cell membranes and plays a key role in lung surfactant.
• Glycerol + fatty acid at C-1 and C-2
• Phosphate at C-3
• Another glycerol molecule attached to phosphate
This forms a phosphatidyl-glycerol-phosphate unit, later dephosphorylated to phosphatidylglycerol.
Phosphatidylglycerol is synthesized from:
Phosphatidic acid
Converted to CDP-diacylglycerol
Reacts with glycerol-3-phosphate
Final dephosphorylation yields phosphatidylglycerol
This is the pathway used in lung cells (type II pneumocytes) for surfactant synthesis.
Phosphatidylglycerol is the second most abundant surfactant phospholipid after DPPC (dipalmitoyl phosphatidylcholine).
Its presence is crucial because:
• It enhances spreading and stability of DPPC
• It appears late in gestation (~34–36 weeks), so it is used as a marker of fetal lung maturity
• Helps maintain membrane curvature
• Important for mitochondrial membranes
• Serves as a precursor for cardiolipin
• Used in amniotic fluid analysis
• Presence of phosphatidylglycerol indicates low risk of Respiratory Distress Syndrome (RDS)
• Appears after L:S (lecithin:sphingomyelin) ratio becomes > 2:1
In premature infants:
• Low DPPC + low phosphatidylglycerol
→ alveolar collapse
→ severe respiratory distress
Maternal steroids increase surfactant production and increase phosphatidylglycerol levels.
• Phosphatidylglycerol is required for cardiolipin synthesis
• Cardiolipin maintains mitochondrial membrane function
• Abnormal cardiolipin is seen in Barth syndrome and mitochondrial disorders
• Phosphatidylglycerol = glycerol + phosphate + glycerol
• Essential for lung surfactant → appears late in gestation
• Marker of fetal lung maturity in amniotic fluid
• Precursor to cardiolipin
• Deficiency → higher risk of RDS in preterm infants
• Located in mitochondria and lung tissue prominently
A glycerophospholipid containing ethanolamine.
• Structural component of cell membranes
• Important in blood coagulation
• Precursor for formation of phosphatidylcholine
• Brain and nervous tissue
Ether phospholipids where fatty acid at C-1 is replaced by unsaturated ether linkage.
• Phosphatidylethanolamine plasmalogen → abundant in nerve tissue
• Phosphatidylcholine plasmalogen → present in heart muscle
• Membrane stabilizers
• Antioxidant properties
• Reduced in Zellweger syndrome (peroxisomal disorder)
Lipids containing sphingosine instead of glycerol.
Sphingomyelin (phospholipid)
Glycosphingolipids
– Cerebrosides
– Sulfatides
– Globosides
– Gangliosides
• Myelin sheath integrity
• Cell recognition, adhesion
• Signal transduction
Contain carbohydrate + ceramide with no phosphate.
• Cerebrosides
• Sulfatides
• Globosides
• Gangliosides
• Found in nerve & muscle membranes
• Brain white matter
• Cell signaling & recognition
• Ceramide + one sugar (glucose or galactose)
• Glucocerebroside
• Galactocerebroside (major myelin component)
• Gaucher Disease
– Glucocerebrosidase deficiency
– Hepatosplenomegaly, bone pain, “crumpled tissue paper” macrophages
• Ceramide + oligosaccharide containing sialic acid (NANA)
• Cell surface receptors
• Neurotransmission
• Brain development
• Tay-Sachs Disease
– Hexosaminidase A deficiency
– Accumulation of GM₂ ganglioside
– Cherry-red spot on macula, neurodegeneration
• Steroid nucleus = cyclopentanoperhydrophenanthrene ring
• 27-carbon molecule
• Hydroxyl at C-3, double bond between C-5 and C-6
• Membrane fluidity regulator
• Precursor of:
– Bile acids
– Steroid hormones
– Vitamin D
– Lipoproteins
• High LDL → atherosclerosis
• Gallstones → excess cholesterol precipitation
• Smith-Lemli-Opitz syndrome → cholesterol biosynthesis defect
Bioactive lipids derived from arachidonic acid (20:4).
• Prostaglandins (PG)
• Thromboxanes (TX)
• Leukotrienes (LT)
• Lipoxins
• Inflammation
• Platelet aggregation
• Bronchial tone regulation
• Renal blood flow
• NSAIDs block COX → ↓ prostaglandins
• Asthma → leukotrienes cause bronchoconstriction
• Low-dose aspirin → inhibits TXA₂ → antiplatelet effect
• Enzyme: Hexosaminidase A
• Accumulation: GM₂ ganglioside
• Features: neurodegeneration, cherry-red macula
• Enzyme: Glucocerebrosidase
• Accumulation: Glucocerebroside
• Features: hepatosplenomegaly, bone crises, “crumpled tissue paper” cells
• Enzyme: Sphingomyelinase
• Accumulation: Sphingomyelin
• Features: hepatosplenomegaly, neurodegeneration, cherry-red spot
• Enzyme: Galactocerebrosidase
• Accumulation: Galactocerebroside
• Features: optic atrophy, severe demyelination
• Enzyme: Arylsulfatase A
• Accumulation: Sulfatides
• Features: progressive demyelination
• Enzyme: α-galactosidase A
• Accumulation: Ceramide trihexoside
• Features: angiokeratomas, renal failure, neuropathy
• Not a sphingolipidosis, but peroxisomal disorder
• ↓ plasmalogens
• Features: hypotonia, seizures, craniofacial abnormalities
Lipids that contain additional non-lipid components such as phosphate, carbohydrate, nitrogen base, or protein.
• Phospholipids (contain phosphate)
• Glycolipids (contain carbohydrate)
• Lipoproteins (contain proteins)
• Sulfolipids (contain sulfate)
• Aminolipids (contain amino groups)
Phospholipids containing glycerol as the backbone.
• Glycerol
• Two fatty acids
• Phosphate
• Nitrogenous base (choline, ethanolamine, serine, inositol)
• Phosphatidylcholine (Lecithin)
• Phosphatidylethanolamine (Cephalin)
• Phosphatidylserine
• Phosphatidylinositol (PI)
• Cardiolipin
• Major part of cell membranes
• Surfactant (DPPC)
• Signal transduction (PIP₂ → IP₃ & DAG)
• Lipoprotein assembly (VLDL formation in liver)
Lipids containing sphingosine as the backbone instead of glycerol.
• Sphingosine
• Fatty acid (forms ceramide)
• Carbohydrate OR phosphate group
• Head group (varies by type)
Sphingomyelin – contains phosphate
Cerebrosides – contain one sugar
Globosides – multiple sugars
Gangliosides – sugars + sialic acid
Sulfatides – sulfate group
• Cell membrane stability
• Neuronal insulation (myelin)
• Cell recognition and adhesion
• Signal transduction
A sphingophospholipid: sphingosine + fatty acid (ceramide) + phosphate + choline.
• Myelin sheath
• Cell membranes (especially nerve tissue)
• Electrical insulation
• Cell signaling
• Membrane stability
• Niemann–Pick disease → sphingomyelinase deficiency
– Hepatosplenomegaly, neurodegeneration, cherry-red macula
Glycolipids with ceramide + a single sugar (glucose or galactose).
• Glucocerebroside
• Galactocerebroside (abundant in myelin)
• Important in white matter
• Role in nerve conduction and myelin stability
• Gaucher disease
– Glucocerebrosidase deficiency
– “Crumpled tissue paper” macrophages
– Hepatosplenomegaly, bone pain
Glycosphingolipids with ceramide + oligosaccharide + sialic acid (NANA).
• Neuronal membranes
• Synaptic junctions
• Gray matter
• Cell recognition
• Neurodevelopment
• Modulation of synaptic transmission
• Tay–Sachs disease
– Hexosaminidase A deficiency
– Accumulation of GM₂ ganglioside
– Neurodegeneration, cherry-red macula, no hepatosplenomegaly
• Compound lipids contain phosphate or carbohydrate.
• Glycerophosphatides are glycerol-based phospholipids (lecithin, cephalin).
• Sphingolipids are sphingosine-based lipids.
• Sphingomyelin = ceramide + phosphate + choline.
• Cerebrosides = ceramide + single sugar.
• Gangliosides = ceramide + oligosaccharide + sialic acid.
• Clinical disorders: Niemann–Pick, Gaucher, Tay–Sachs.
Extra Note :
Sulfatides are sulfated glycolipids belonging to the glycosphingolipid family.
They consist of:
• Ceramide (sphingosine + fatty acid)
• Galactose
• Sulfate group added to the galactose
They are also called sulfogalactocerebrosides.
A ceramide backbone is attached to a galactose molecule, which is further esterified with sulfuric acid, producing a negatively charged lipid.
This structure gives sulfatides strong acidic properties and allows interaction with proteins in nerve tissue.
Sulfatides are abundant in:
• Myelin sheath (white matter)
• Oligodendrocytes
• Schwann cells
• Renal tubular cells
• Gastrointestinal mucosa
Sulfatides help maintain:
• Compact structure of myelin
• Saltatory conduction
• Adhesion between myelin lamellae
Important for:
• Immune cell adhesion
• Axonal–glial communication
• Trafficking of membrane proteins
Contribute to formation of lipid rafts, influencing signal transduction.
Key disorder involving sulfatides
• Enzyme deficiency: Arylsulfatase A
• Result: Accumulation of sulfatides in CNS & PNS
• Pathology: Myelin destruction → “metachromatic staining” of deposits
• Features:
– Progressive motor loss
– Hypotonia
– Developmental delay
– Vision & hearing loss
– Peripheral neuropathy
This is the classic sulfatide storage disease.
• Myelin breakdown alters sulfatide composition
• Used as potential biomarker for demyelinating activity
• Changes in renal sulfatides observed in early diabetic nephropathy
• Altered sulfatide levels seen in gastric and colon cancers
• May modulate immune evasion
Sulfatides are degraded in lysosomes.
Steps:
Arylsulfatase A removes the sulfate group
Remaining galactocerebroside is further broken down by galactosidases
Failure of the first step → Metachromatic leukodystrophy.
• Sulfatides = sulfated galactocerebrosides
• Major lipids of myelin
• Synthesized in Golgi apparatus
• Degraded by arylsulfatase A
• Deficiency → Metachromatic leukodystrophy
• Important in nerve conduction, membrane adhesion, lipid rafts
• Excess sulfatides → demyelination disorders
• Lipids are hydrophobic or amphipathic molecules essential for energy storage, membranes, signaling, and insulation.
• Simple lipids → fats (TAGs) and waxes; compound lipids → phospholipids, glycolipids, lipoproteins; derived lipids → fatty acids, steroids, eicosanoids.
• Fatty acids may be saturated, unsaturated, essential, cis/trans, short- or long-chain.
• Essential fatty acids → linoleic (ω-6) and α-linolenic (ω-3); deficiency causes dry skin, poor wound healing, growth failure.
• Unsaturated fatty acids increase membrane fluidity; trans fats behave like saturated fats and increase cardiovascular risk.
• Triglycerides are the main storage lipids; high levels can trigger pancreatitis.
• Phospholipids are major membrane components; lecithin is key surfactant; cephalin is found in brain; plasmalogens are reduced in peroxisomal disorders.
• Phosphatidylglycerol and DPPC form the backbone of lung surfactant; absence → neonatal RDS.
• Cardiolipin is unique to the inner mitochondrial membrane and stabilizes ETC complexes; altered in Barth syndrome and mitochondrial diseases.
• Sphingolipids contain sphingosine; important for myelin and signal transduction.
• Cerebrosides = ceramide + one sugar; gangliosides = ceramide + oligosaccharide + sialic acid; sulfatides = sulfated cerebrosides.
• Cholesterol is a steroid alcohol with 27 carbons and rigid ring structure; precursor of bile acids, vitamin D, steroid hormones.
• Eicosanoids (prostaglandins, thromboxanes, leukotrienes) derive from arachidonic acid and regulate inflammation, vasoconstriction, bronchial tone, platelet function.
• Lipid peroxidation damages membranes; prevented by vitamin E, vitamin C, glutathione.
• Lipid storage disorders = enzyme defects in sphingolipid degradation → Gaucher, Tay-Sachs, Niemann–Pick, Krabbe, MLD, Fabry.
• High LDL increases atherosclerosis risk; HDL is protective; trans fats increase LDL and decrease HDL.
• Omega-3 fatty acids (EPA, DHA) reduce inflammation and improve cardiovascular health.
• Myelin lipids (cerebrosides, sulfatides, sphingomyelin) are essential for nerve conduction; defects cause progressive neurological disease.
A water-insoluble, hydrophobic or amphipathic organic molecule.
Long-term energy storage and metabolic fuel.
Linoleic and α-linolenic acids → humans lack enzymes to introduce double bonds beyond C-9.
The position of the first double bond from the methyl end (C-3 for omega-3, C-6 for omega-6).
It raises LDL, lowers HDL, and increases atherosclerosis risk.
It is the key surfactant lipid; used in L:S ratio to assess fetal lung maturity.
A diphosphatidylglycerol found in the inner mitochondrial membrane; essential for ETC stability.
Ceramide + one sugar; abundant in white matter and myelin.
Cell recognition, neurodevelopment, and synaptic function.
GM₂ ganglioside accumulation in retinal ganglion cells.
Glucocerebrosidase.
It forms part of the myelin sheath and contributes to nerve conduction.
Free radical–driven oxidation of polyunsaturated fatty acids → membrane damage.
Prostaglandins → inflammation
Thromboxanes → platelet aggregation
Leukotrienes → bronchoconstriction
Controls fluidity, stabilizes lipid bilayer, reduces permeability.
Low surfactant (mainly DPPC & phosphatidylglycerol).
Emulsification of fats and aiding lipid digestion.
Metachromatic leukodystrophy.
They reduce triglycerides, inflammation, and platelet aggregation.
Hydrophilic head + hydrophobic fatty acid tails.
A. Oleic acid
B. Palmitic acid
C. Linoleic acid
D. Stearic acid
A. Omega-3 fatty acids
B. Saturated fatty acids
C. Polyunsaturated fatty acids
D. Short-chain fatty acids
A. Phosphatidylserine
B. Dipalmitoyl phosphatidylcholine
C. Cardiolipin
D. Sphingomyelin
A. Outer mitochondrial membrane
B. Inner mitochondrial membrane
C. Golgi apparatus
D. Lysosomal membrane
A. Gaucher disease
B. Zellweger syndrome
C. Tay-Sachs disease
D. Fabry disease
A. Phosphate
B. Nitrogen base
C. Carbohydrate
D. Glycerol
A. Sulfate
B. Sialic acid (NANA)
C. Phosphate
D. Ceramide + one sugar
A. Lecithin
B. Ceramide
C. Cardiolipin
D. Phosphatidylglycerol
A. GM2 ganglioside
B. Glucocerebroside
C. Ceramide trihexoside
D. Sphingomyelin
A. Arylsulfatase A
B. Hexosaminidase A
C. Glucocerebrosidase
D. Sphingomyelinase
A. Prostaglandins
B. Steroid hormones
C. TAGs
D. Bile acids
A. Increase platelet aggregation
B. Increase LDL
C. Reduce inflammation
D. Raise trans-fat levels
A. Arylsulfatase A
B. Hexokinase
C. Lipoprotein lipase
D. Ceramidase
A. Phospholipid
B. Triglyceride
C. Cholesterol ester
D. Free cholesterol
A. Sphingomyelin
B. Phosphatidylinositol
C. Lecithin
D. Cardiolipin
A. Butter
B. Coconut oil
C. Hydrogenated vegetable oils
D. Olive oil
A. Renal function test
B. Fetal lung maturity test
C. Liver function test
D. Lipid profile
A. Cholesterol
B. PUFA in membranes
C. Short-chain fatty acids
D. Triglycerides in adipose tissue
A. Phosphatidylserine
B. Cholesterol
C. Arachidonic acid
D. Ceramide
A. Auer rods
B. “Crumpled tissue paper” macrophages
C. Onion skin macrophages
D. Foamy macrophages
A. Omega-3 FA
B. Phosphatidylglycerol
C. Cholesterol
D. Ceramide
A. Ceramide
B. Sulfatide
C. Sphingomyelin
D. Phosphatidylcholine
A. Ergosterol
B. Sitosterol
C. Cholesterol
D. Lanosterol
A. Triglyceride
B. Cholesterol ester
C. Lecithin
D. Ganglioside
A. Steroid hormones
B. Eicosanoids
C. Amino acids
D. Ketone bodies
1-C
2-B
3-B
4-B
5-B
6-C
7-B
8-C
9-D
10-B
11-A
12-C
13-A
14-B
15-A
16-C
17-B
18-B
19-B
20-B
21-B
22-B
23-C
24-B
25-B
A hydrophobic or amphipathic molecule insoluble in water.
It contains both a hydrophilic head and hydrophobic tail.
Triglycerides (triacylglycerols).
Linoleic acid (ω-6) and α-linolenic acid (ω-3).
Humans cannot introduce double bonds beyond carbon 9.
Saturated have no double bonds; unsaturated have one or more double bonds.
An unsaturated fatty acid with trans configuration, acting like saturated fat.
Phospholipids.
DPPC — dipalmitoyl phosphatidylcholine.
A key surfactant lipid; appears late in fetal development.
Inner mitochondrial membrane.
Stabilizes ETC complexes and ATP synthesis.
Barth syndrome.
A phospholipid with glycerol backbone.
Lecithin and cephalin.
A phospholipid with an ether linkage at carbon-1.
A lipid containing sphingosine backbone.
Ceramide.
A sphingophospholipid containing phosphate + choline.
Niemann–Pick disease.
Ceramide + one sugar (glucose or galactose).
Gaucher disease.
Ceramide + oligosaccharide + sialic acid (NANA).
Hexosaminidase A.
Sulfated galactocerebrosides.
Arylsulfatase A.
A 27-carbon steroid with four fused rings.
Bile acids, steroid hormones, vitamin D.
Regulates fluidity and stability.
Arachidonic acid.
Prostaglandins, thromboxanes, leukotrienes.
Phospholipase A2.
Free-radical oxidation of polyunsaturated fatty acids causing membrane damage.
Vitamin E.
Reduce inflammation, improve cardiac health.
Cerebrosides, sulfatides, sphingomyelin.
Assessment of fetal lung maturity.
Emulsification and absorption of dietary lipids.
Arachidonic acid.
Increase LDL and decrease HDL.
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