LIPIDS: Study Guide Flashcards
L1: What are the definitions for amphipathic and adipocyte
amphipathic: (lipids) have both hydrophilic and hydrophobic parts
adipocyte: a cell specialized for the storage of fat, found in connective tissue
L1: What are the definitions for steroid nucleus and polymorphism
steroid nucleus: non-liner structure built on a tetracyclic platform
polymorphism: multiple stable structures/states. Facilitate membrane stability and lipid : protein interactions
L1: What are the definitions for carboxyl terminus and omega carbon
carboxyl terminus: the end of a peptide or protein’s primary structure
omega carbon: the last carbon in the chain, farthest from the carboxyl group
L1: What are the major elements required for life present in fatty acids
Carbon, Hydrogen, Oxygen (not NPS)
L1: What are the four classes of lipids? (which have FAs/ involved in membranes)
Triacylglycerides (FA), Phospholipids (FA, membranes), Glycolipids (FA, membranes), Steroids (membranes)
L1: Why are lipids not considered to be “true polymers”?
generally large biomolecule, not a lot of monomers, monomers are not interlinked
L1: Why are lipids water-insoluble, yet amphipathic?
-they are primarily nonpolar (water-fearing) carbon-carbon or carbon-hydrogen bonds
-they are soluble in nonpolar organic solvents
-they have a hyrophillic polar end and a hydrophobic nonpolar
L1: What do saturated, unsaturated, omega-3 and omega-6 fatty acids look like?
Saturated - composed of carbon-carbon single bonds (stearic acid)
Unsaturated - one or more carbon- carbon double or triple bonds
Omega-3 / Omega-6 - refer to the location of the first carbon-carbon double bond, if you start counting from the ω end.
L1: Are trans fats saturated and unsaturated? What do they look like?
Trans fat: unsaturated fat, unnatural, has to be synthesized synthetically. Hydrogens are split across the double bond (one up and one down)
Unsaturated: one or more carbon-carbon double/triple bonds (usually cis)
L1: Describe the naming process for fatty acids (X:X)
The first X (:X) is the total carbons in the fatty acid
The second X (X:) is the total carbon-carbon double bonds
L1: Which type of saturated FA has a higher melting point: a shorter FA or a longer FA?
-a longer fatty acid chain would have a higher melting point
-melting point decreases when bonds are added, more carbons= higher melting points
L1: Which type of unsaturated FA has a higher melting point: monounsaturated or polyunsaturated?
Monounsaturated
L1: Compare and contrast phosphoglycerides with sphingolipids and with glycoglycerolipids.
phosphoglycerides(phospholipid): found in the plasma membrane
- have 2 fatty acids
-platform: glycerol
sphingolipid (phospholipid): found in the nervous system
-have 1 fatty acid
-platform: sphingosine
glycoglycerolipid (glycolipid): found in plant cell membrane
-lipid with carb monomers covalently attached
L1: Compare and contrast glycosphingolipids with glycoglycerolipids and with sphingolipids.
Glycosphingolipids = animal cells, for eukaryotic membranes, a glycolipid, only 1 FA (like sphingolipids)
Glycoglycerolipds = plant cells, for eukaryotic membranes, a glycolipid
Sphingolipid = NS mainly, 1 FA, platform - sphingosine, ex. sphingomyelin, phospholipid
L1: What is the hydrophobic effect? How does it impact membrane formation?
-the phenomenon by which nonpolar molecules aggregate to avoid contact with polar molecules, mainly water (entropy-driven association)
-this effect drives membrane formation (the membrane is stabilized with non-covalent interactions)
-nonpolar tails and polar heads
L1: Explain why membranes are asymmetric, noncovalent assemblies.
asymmetric as outer surface hydrophilic but internal space hydrophobic and certain lipids found mostly on one outer surface
noncovalent as stabilized by noncovalent interactions
L1: Explain why membranes have polarity. Can asymmetry play a role?
-asymmetric as outer surface hydrophilic but internal space hydrophobic and certain lipids found mostly on one outer surface
-noncovalent assembly as stabilized by noncovalent interactions
-membranes are polar because negatively charged heads are on the exterior and uncharged tails on the interior
L1: what do peripheral and integral membrane proteins look like?
Peripheral proteins are the ones outside the bilayer/membrane - on one side of the membrane of the other
integral proteins are embedded in the bilayer/membrane - span entire membrane
L1: Do all cellular organelles have the same membrane composition?
No, membrane-bound organelles are only found in eukaryotic cells
-membrane composition differs depending on the organelle’s function
L1: Why does cholesterol, FA chain length and degree of unsaturation impact fluidity
(eukaryotes) more cholesterol = more membrane rigidity = less fluid
(prokaryotes) shorter chain and cis unsaturation = less membrane rigidity = more fluid (adjusting Carbon-Carbon double bonds)
L2: What is the difference between lateral and transverse diffusion
-lateral diffusion: move along one side of the membrane
-transverse: flipping sides on the membrane
L2: Define what a nuclear hormone receptor is
Found in nucleus, can be bound to ligand lipids, and bind to DNA and alter gene expression
L2: what is the difference between kinase and phosphatase
kinase: an enzyme that attaches a phosphate group to a protein
phosphatase: an enzyme that removes a phosphate group from a protein
L2: what are the differences between simple diffusion, passive transport, and active transport
Passive transport :
Facilitated diffusion - with concentration gradient, moving charged and large molecule, polar, need protein to cross ((uniport) carrier-mediated and channel mediated)
Simple diffusion - don’t need protein, high to low concentration, small/uncharged, going with concentration gradient, small uncharged molecules (like CO2 and O2) cross by this
Active transport : uniport and cotransport (moving 2 molecules at once, could be with or against gradient). pump mediated, transfer from low to high, against concentration gradient, require ATP. pumps use active - also move water-soluble molecules via hydrophilic “hole”
L2: Are transporters peripheral or integral membrane proteins? What about receptors?
-integral membrane proteins that function as channels or pumps
-Both are integral membrane proteins that facilitate cellular functions.
L2: How does signal transduction pathway operate
process by which molecular stimuli are transmitted through a cell
1. stimulus triggers release of a primary messenger
2. primary messenger is recognized by a receptor
3. information is relayed to cell’s interior by second messengers
4. second messengers activate or inhibit effector molecules
5. signal cascade is terminated
L2: what is the difference between primary and secondary messengers
primary messenger:
-extracellular signals
-do not readily diffuse across membranes
-interact with receptors to initiate intracellular activity
Secondary messenger:
-intracellular signals
-do readily diffuse across membranes, amplifying a signal
-interact with effector molecules to trigger effector molecules
L2: Why are lipid-derived primary messengers able to bind to nuclear hormone receptors but protein-derived primary messengers cannot?
-composition of the lipid is more suitable for binding versus the protein (TA said this?)
L2: Compare and contrast the structure of a 7TM / GPCR with a dimeric protein receptor.
- Both integral membrane proteins
-ligand will bind to extracellular 7TM receptors and intracellular nuclear hormones receptors
** add to this slide
L2: What happens when a receptor recognizes a primary messenger?
Information is then relayed to cell’s interior by second messenger
L2: How does the insulin signal transduction pathway work
- High glucose triggers insulin (primary msg) release
- insulin interacts with insulin receptor
- activated receptor facilitates the synthesis of PIP3 (second msg)
- PIP3 facilitates activation of AKT 9 (an effector)
L2: Explain how insulin increases glucose uptake in muscle cells, focusing on activated protein kinase B (Akt) and GLUT4.
GLUT moves glucose into the cell & protein kinase helps GLUT move to the surface
Insulin (hormone) released by pancreatic β-cells when blood glucose-rich
Stimulates liver to synthesize glycogen
Stimulates muscle and fat cells to uptake glucose
L2: How is the insulin signal transduction pathway shutdown?
termination of insulin signaling depends on dephosphorylation
- dephosphorylation of the second messenger
L3: What is the definition of catabolism and peroxisome
catabolism: breaking down - breaking 1 molecule down to liberate energy
peroxisome: organelle containing oxidative enzymes
L3: what are some examples of edible items that contain lipids and some that do not
-found within foods that contain vegetable oils or fats (some spices or herbs)
-inorganic food additives (like sugar/salt) lack this biomolecule
L3: Do digestive enzymes cleave covalent bonds or noncovalent interactions?
cleave covalent bonds using water
L3: how are lipids digested (name the lipases/where)
Lipids are digested by a set of digestive enzymes, which cleave bonds using water
-Mouth: saliva contains lingual lipase
-Stomach: gastric lipase cleave TAGS
-Small intestine: bile salts insert into lipid droplets
Small intestine: pancreatic lipases cleave TAGS/DAGS
L3: How are FAs transported across the mitochondrial inner membrane?
requires activation and channels - organelle has 2 membranes; inner one is highly impermeable
activation by attaching FA to coenzyme A, catalyzed by enzyme acyl CoA synthetase, reaction reversible but driven forward by ATP hydrolysis
L3: what are the four steps of the B-oxidation pathway (where/ what organelles/ does it occur in humans)
-this pathway primarily occurs within the mitochondria of skeletal muscle cells
1. Oxidation by FAD by dehydrogenase
2. Hydration by hydratase
3. Oxidation by NAD+ dehydrogenase
4. Thiolysis by coenzyme A
-yes it occurs in humans, lipid synthesis
L3: How do you calculate how many rounds of b-oxidation are necessary to metabolize a FA
you divide the number of carbons by 2 and subtract 1
ex. 15/2 = 7.5 -1 = 6.5
(round down if half carbon)
L3: The ß-oxidation pathway generates acetyl CoA and propionyl CoA. What happens to each of these products?
With an odd fatty acid chain, propionyl CoA is converted to succinyl CoA (which enters cellular respiration via the citric acid cycle)
L3: Can the human body metabolize very long-chain fatty acids? What about unsaturated fatty acids?
Yes, it’s just difficult. Very long chain (22+ Carbons) sent to peroxisome first then acyl group shortened via peroxisomal B-oxidation pathway, then transported to mitochondria for standard B-oxidation pathway.
Yes, unsaturated fatty acids can be metabolized
L3: Glycerol metabolism generates glyceraldehyde 3-phosphate. What happens to this product? Where [organ(s)] does glycerol metabolism occur in humans?
during lipid digestion/lipolysis, glycerol is separated from fatty acids in TAGS
-sent to the liver, which is phosphorylated by glycerol kinase
-G3P is an intermediate of glycolysis and gluconeogenesis
L3: Ketolysis generates acetyl CoA. What happens to this product? Where [organ(s) and organelle(s)] does ketolysis occur in humans?
acetyl CoA enters cellular respiration via the citric acid cycle
-metabolism occurs primarily within the mitochondria of the brain, heart, and skeletal muscle cells
-products enter cellular respiration (ketogenesis occurs primarily in the liver)
L3: Refer to the cellular respiration pathway, where are fatty acids and glycerol entering
fatty acids: come from fats, enter as an intermediate into pyruvate oxidation, and prepares to enter the citric acid cycle
glycerol: come from fats, and enter into glycolysis as the “backbone” (G3P) and prepares to enter pyruvate oxidation
L4: what is the definition of anabolism and committed step
Anabolism: building up (make more complex molecules)
committed step: irreversible reaction that “dedicated” atoms to that pathway and the final product. in fatty acid synthesis, used to regulate overall pathway
L4: what are the four repeating steps in fatty acids synthesis
- Condensation
- reduction of the carbonyl group
- dehydration
- reduction of the double bond
(steps repeat until palmitate (16:0) made- extending fatty acids by 2 each time)
L4: To synthesize an odd chain FA, would acetyl CoA or propionyl CoA be activated? What about for an even chain FA?
Propionyl CoA would be activated, not acetyl CoA
Even chain first reaction is condensation of malonyl ACP with acetyl ACP
L4: Why are PUFAs an essential dietary component?
Polyunsaturated fatty acids are mainly localized in cell membranes.
-they play a role in membrane fluidity, reduce inflammation, and blood clotting, regulate blood pressure and cell signaling
L4: Can the human body synthesize trans fats? If not, where are they coming from?
No, we cannot synthesize them on our own. They come from our diet
L4: How can you tell if a FA was synthesized by human enzymes
(IDK!)
triacylglycerides, most synthesis (80%) occurs in ER of intestinal cells via monoacylglycerol pathway.
Phospholipids synthesis occurs in ER of most cells vis kennedy pathway
glycolipds synthesis occurs in most cells and involves the ER and golgi complex
-look for trans fatty acids (our body can’t synthesize) or if there are double bonds past a certain point
L4: How is fatty acid synthesis regulated
The committed step in fatty acid synthesis consequently, will be used to regulate overall pathway
L4: Where [organ(s) and organelle(s)] does cholesterol synthesis occur in humans?
part 1 occurs in the cytoplasm; part 2/3 occur in the ER
-synthesized in the liver from acetyl CoA
L4: How are statins able to lower cholesterol? why are diet changes recommended for someone taking statins?
They’re a competitive inhibitor of HMG CoA reductase, mimic enzymes substrate so compete for binding in active site, if statin is bound, then cholesterol synthesis declines
L4: How is cholesterol synthesis regulated
-cholesterol synthesis is controlled via HMG CoA reductase
1. HMG CoA reductase gene expression
2. hormones (insulin/ glucagon)
3. oxygenated-cholesterol derivatives
4. phosphorylation
L4: How do LDL and HDL differ, in terms of cholesterol destination?
LDL - low density; transporters cholesterol from liver to body - labeled “bad cholesterol” as contributes to artery cholesterol buildup
HDL - high density; transports cholesterol from body to liver - labeled “good cholesterol” as scavenges cholesterol from arteries
where are triacylglycerols made?
majority occurs in the ER of intestinal cells via the monoacylglycerol pathway
where are phospholipids made?
synthesis occurs in the ER of most cells via the Kennedy pathway
where are glycolipids made? what is the enzyme?
synthesis occurs in most cells and involves the ER/Golgi
-key enzyme (ceramide glucosyltransferase)
