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Define the following:
2. Insulin resistance
3. Inborn errors of metabolism
1. Atherosclerosis - lipid infiltration in the subendothelial space in vasculature
2. Insulin resistance - lipid deposition in non-adipose tissues contributes to development of T2D
3. Inborn errors - defects in energy production or metabolism of certain lipid species
1. What is the major storage form of energy? In what specific form?
2. What does brain use as fuel during starvation?
3. What is usually used as short-term energy?
4. What does starvation shape? What does it do?
1. Lipids --> TAGs in adipose tissue.
2. Ketone bodies (mainly B-hydroxybutyrate) over glucose
4. Metabolic adaptations - glucose really falls off, while fats and ketones step in to take care of fuel needs during starvation.
1. What are the physiologic roles of lipids (4)
2. What are the pathologic roles of lipids? (5)
3. Define lipids
4. What can lipids organize into? Through what type of interactions?
5. What are the 3 major functions of lipids?
1. Membrane constituents, energy storage, signaling molecules, intra/extracellular shuttles
2. Neuropathies, obesity, T1D, T2D, atherosclersosi
3. Lipids - molecules that are soluble in organic solvents (metahnol & chloroform) and weakly soluble in water
4. Lipids can organize into large, supramolecule structures through noncovalent interactions (membranes, lipid droplets)
5. (1) Energy storage (2) Mediators of signaling molecules (3) membrane constituents
1. What are the 2 major classes of lipids?
2. What happens to [FA] in plasma during fasting?
3. What number of Cs are there usually in fatty acids? (even or odd) Why?
4. Are there high or low concentrations in cells?
5. What is the charge of fatty acids in neutral pH?
1. Simple and membrane
3. Even, bc they're synthesized in 2-C blocks
1. What are the 3(or 5) types of simple lipids?
2. What are the types of membrane lipids? (1-2, 2-2, 3)
1. Fatty acids, M/D/TAGs, waxes
2. Phospholipids - glycerophospholipids, sphingomyelins
Glycolipids - cerebrosides, gangliosides
1. Are FAs polar or nonpolar?
2. What does saturated vs. unsaturated mean? How many 2x bonds are there usually?
3. What types of double bonds generally exist in FAs?
4. Describe how to name saturated fatty acids? How to name unsaturated fatty acids? (2)
1. Both! They're amphiphilic (polar carboxy head, neutral hydrocarbon tail)
2. Saturated - only single bonds. Unsaturated - double bonds exist. There are usually 1-6
4. Saturated - C(# of C):(# of double bonds) - C18:0
- 5. Unsaturated fatty acids
- (1) Counting from C: C18:2
- (2) Counting from C: C18:29 (only include C with first double bond)
1. What determines MP of FAs? (2)
2. At physiological temp, what form will most fats be in?
3. Why is trans fat dangerous?
4. What are essential fatty acids? Why are they essential?
5. What od fats and oils consist mostly of?
1. Length (longer FAs tend to be more solid) and Saturation (more saturation, higher MP)
2. Liquid form --> why fats form lipid droplets.
3. More difficult to degrade in body, can act as signaling molecules to increase de novo lipogenesis in the liver.
4. Linoleic (n-6) --> Arachidonic acid and Linolenic acid ---> EPA, DHA (n-3)
Bc humans don't have the desaturases to create double bonds at these specific places.
5. Triglycerols aka triglycerides
1. Why do unsaturated FAs have lower melting points?
2. What are triacylglycerols?
3. What is their main function? In animals where do synthesize/storage mainly occur?
4. What are other names for triacylglycerols?
5. What is one of the primary sources of energy during starvation?
1. Bc they have a "permanent kink" in their tail, lowering MP due to entropy.
2. Water-insoluble substances that are fatty acid triesters of glycerol
3. To store energy. Adipocytes (specialized cells).
4. Triglycerides, TGs, TAGs
5. TGs secreted from liver.
1. What type of FAs can be added onto glycerol backbones? 4
2. What type of bond exists bt glycerol and FAs in TGs?
3. How are TGs named?
4. How are TGs stored in cells? Where in cell? Describe structure (inside/outside)
5. What type of tissues do you usually find TAGs in? What does it mean if you find TAGS in other tissues?
1. Saturated, monounsaturated, polyunsaturated, or a combo
2. Ester bond.
3. According to constituents 1-myristoyl-2-steraoyl-3-palmitoyl-glycerol.
4. As lipid droplets in cytosol.
- Neutral lipid core - TGs, CEs.
- Outer layer: phospholipid monolayer with proteins on outside.
5. White adipose tissue; if you see TAGs in other tissues (liver, heart) SIGN OF PATHOLOGY.
1. What do DAGs do in terms of signaling, very generally?
2. What enzyme specifically generates it? From what?
3. What does DAG, in turn do? What else activates this?
4. What does excess DAG activation of PKC cause? (3)
- 1. Secondary messenger
- 2. Phospholipase C from the membrane lipids
3. Activates PKC in signaling cascade; Ca2+ also activates PKC
4. Heart failure, insulin resistance, and other pathophysiological conditions
1. Define what a wax is structurally
2. Is it hydrophobic or hydrophilic?
3. As length increases what happens to rigidity and solidity? What is this like?
4. What are the 2 major types of phospholipids?
5. What is another name for phospholipids? (2)
1. Fatty acid esterified to fatty alcohol
2. Almost completely hydrophobic (except for OH group)
3. Increases rigidity and solidity --> like all other lipids
4. Glycerophospholipids and sphingomyelin
5. Glycerophospholipids or phosphoglycerides.
1. What is the major role of phospholipids?
2. What is it composed of? (5)
3. Are they polar or nonpolar?
4. What are common classes of glycerophospholipids?
5. What is the defining characteristic of PLs?
6. What is made from phosphatidylcholine?
1. Major lipid component of membrane
2. Glycerol backbone, 2 HC chains from FAs, phosphate group, head group
3. Amphiphilic - polar head, nonpolar tail
4. Ethanolamine, water, choline, serine, glycerol
5. Head group (also phosphate group!)
1. What do membranes provide overall?
2. What do they contain to allow communication?
3. What do they for enzymes?
4. What do they do for electrical signals?
5. What is membrane formation driven by?***
1. Selective permeability barrier
2. Molecular receptors (often proteins) to receive external signals. Cell-cell comm is often mediated by clel membranes (can occur through direct cell-cell contact & through soluble mediators.
3. Support and regulate enzymatic rxns - involved in energy conversion processes (e.g., generation of ATP)
4. Provide support for generation/propagation of electric signals (nerve impulse transmission & neuromuscular control)
5. Membrane formation is driven by entropy - phospholipids will naturally form PL bilayer (polar heads on outside and nonpolar tails on inside) bc it is the lowest entropy
1. What determines membrane fluidity?
2. What do membranes contain as much of as they do lipids?
3. Is phospholipid distribution in a membrane symmetrical or asymmetrical? Describe which of the PLs listed are more abundant on inside or outside:
- Phosphatidylserine?** why?
1. Composition of saturated vs. unsatuated acyl groups
2. Proteins. They also contain a nominal amount of carbohydrates too (i.e., oligosaccharides, glycolipids, etc)
Outside: more total, more sphingomyelin, phosphatidylcholine.
Inside: more phosphatidylethanolamine and phosphatidylserine.
- Phosphatidylserine is important bc when cells die, it flips from inside to outside, signaling macrophages to come eat them.
1. How do FFAs enter membranes? (3)
2. How do phospholipids change? What are these both role-wise?
1. Short/Medium-chain fatty acids enter freely. They are (1) Adsorbed (2) Flip-flopped from outer to inner) and (3) desorbed
2. DAG <--> Phosphatidic acid can interconvert via DAG kinase and Phosphatidic acid phosphatase (2)
Signaling molecules for different pathways. Increasing/decreasing them via DAG/PAP can regulate these pathways.
1. What does phosphatidylinositol do? When?
2. What does it produce?
3. What do its products do?
4. How is phosphatidylinositiol involved with insulin signaling?
1. Phosphatidylinositol acts as a second messenger when its cleaved producing DAG
- 2. DAG --> activates PKC
- Inositol --> causes release of IC Ca2+ (another 2ndary messenger) --> enzyme activation and hormonal responses!
4. It is a mediator.
- 1. Insulin binds to IR
- 2. Activates phosphatidylinositol-3-kinase --> phosphatidyl triphosphate (PIP3)
3. PIP3 activates Akt which has many insulin consequences.
1. What are liposomes?
2. Describe structure.
3. What are liposomes used for?
4. What are sphingolipids mainly used for?
5. What is the above derived from? (don't need to know)
6. What are their N-acyl fatty acid derivatives called overall? Name 3 specific examples.
7. Describe what each of the examples above do.
1. In aq solutions, amphiphilic molecules form vesicles aka liposomes.
2. Small spheres with surface defined by bimolecular lipid layer and aqueous interior.
3. Drug delivery - liposomes fuse with cells and release contents.
4. major components of biological membranes
5. Sphingolipids are derived from C-18 amino alcohols sphingosine and dihydrosphingosine and their homologues.
6. Ceramides. Sphingomyelin, cerebrosides, ganglosides.
7. Sphingomyelin - ceramides with phosphocholine/phosphoethanolamine head groups - important for myelin sheath
Cerebrosides - ceramides with headgroups that consist of single sugar residue (found in cerebral membranes)
Gangliosides - ceramides with head groups consisting of more than one sugar residue (growth & differentiation)
1. What is the backbone of sphingolipids?
2. What are the 2 major sphingolipids? (2)
3. What is important about sphingolipids?
4. Main functions? (2)
1. Sphingosine (long chain amino alcohol, NOT glycerol!)
2. Sphingosine and dihydrosphingosine
3. Can interconvert to CERAMIDES
1. Name what ceramide can induce? (3)
2. Name what structural role ceramide holds? By converting to what? What does it do?
3. What class do sphingolipids go under
4. What is Niemann-Pick disease? Symptoms of A vs. B?
1. Apoptosis, inflammation, glucose metabolism
2. Ceramide can also form SPHINGOMYELIN --> myelin sheath, plasma membranes, and helps with signal transduction.
4. Niemann-Pick Disease
- Lack of acid sphingomyelinase in lysosomes --> can't metabolize sphingomyelin to ceramide.
Sphingomyelin builds up inside cells within lysosomes
- A - neurologic disease (early death)
- B - enlarged livers and spleen and respiratory problems.
1. What are the 3 main types of sphingolipids? What class do they belong under?
2. Define glycolipids
1. Sphinomyelins (phospholipids), cerebrosides (glycolipids) and gangliosides (glycolipids)
2. Glycolipid - sphingolipids whose polar head group consists of carb units
1. Main roles of cerebrosides and gangliosides? (2)
3. What tissues are they mostly found in? Are they found in other tissues too?
3. What are malfunctions of ganglioside metabolism associated with? Example?
4. What enzyme is important in ganglioside turnover? What happens if there's a deficiency?
5. What is the structure of sterols?
6. What is the precursor?
7. What are the 2 best known sterols? Difference bt them?
1. Components of cell-surface membranes, constitute a significant fraction of brain lipids
2. Brain, but found in other tissues to lesser degree
3. Hereditary diseases (i.e., Tay Sachs disease)
4. Hexosaminidase A - hydrolyzes glycosidic bond connected to head group which encourages turnover of these molecules. Deficiency --> Tay Sach's Disease
5. Cyclic ring structure
6. Acetyl CoA
7. Cholesterol (animals) & ergosterol (plants)
1. Sources of cholesterol? (2)
2. How much is synthesized per day?
3. Where are major sites of chol synthesis? 2
4. What is major source of chol in humans?
5. What is major role of cholesterol?
6. What % of free chol is found in membranes?
7. What is rate-limiting step of cholesterol synthesis? What is it inhibited by? (3)
8. What is cellular cholesterol homeostasis regulated by?
1. Dietary (animal) ~0.6 g/day; endogenous (cholesterol de novo synthesis.
2. 1 g/day
3. Liver & intestine
4. De novo synthesis
5. Cell membrane component
7. HMG CoA Reductase. Inhibited by mevalonate, cholesterol, and statin drugs.
1. What is plasma membrane cholesterol maintained by? (3)
2. What are the main functions of cholesterol? (5)
3. Where are steroid hormone receptors found?
4. What % of fat calories are present as TGs? What are examples? (4) Where are they from?
5. What are the important dietary lipids to keep track of? 4
1. (1) Balance of newly synthesized cholesterol, (2) cholesterol uptake from plasma lipoproteins, and (3) efflux of cellular cholesterol out of cells.
2. (1) Cholesteryl esters (storage & circulation), (2) bile salts (lipid absorption/chol excretion), (3) steroid hormones (glucocorticoids --> cortisol/aldosterone, estrogen/testosterone,), (4) vitamin D synthesis, (5) membrane fluidity in membrane.
3. Inside nucleus.
4. 95. Palmitate/stearate (animals), oleate/linolenic (plants)
5. TGs (dietary), phospholipids (lecithin - dietary/biliary), sterols (cholesterol - dietary/biliary), fat-soluble vitamins (ADEK)
Describe mechanism of dietary lipid digestion (8)
- 1. Dietary lipids enter stomach intact
- 2. Lingual/gastric lipase hydrolyze medium/short-chain FAs from ONLY TGs from sn-3 position --> DGs.
3. TAG, DAG, C, CE, and PL --> SI + bile salts --> micelles
4. Pancreatic/intestinal enzymes act on micelles
5. Short-chain FAs move directly into portal vein toward liver.
6. Glycerol, long-chain FAs, cholesterol are absorbed into enterocyte with help of transfer proteins (does NOT require energy!)
MAG, DAG, and lysophosphatides are absorbed into enterocyte via diffusion.
7. Enterocyte ER - DAGs + MAGs + FFAs --> TAGs, lysophsophatides + FA --> phosphatidic acid, C --> CE.
8. Reformed lipids, along with ApoB48, form chylomicron that leaves enterocyte by endocytosis into lymph. Other apolipoproteins are transferred to chylomicrons from other lipoprotein complexes.
What are the important digestion factors in lipid digestion? (5)
Location of action?
- Where does lipid digestion begin?
What happens in gastric phase of digestion?
- Main enzymes 2
- Main targets
- Important in? Why?
- What can be absorbed in stomach?
- - Mouth and stomach
- - Lingual/Gastric lipase
- - TGs with short/medium-chain fatty acids
- - Important in infants/young children consuming high amounts of milk (milk contains lots of TGs with short/med chains)
- short-chain fatty acids
INTRALUMINAL PHASE OF DIGESTION:
1. Overall, what happens? (4)
2. What is the purpose of bile salts?
3. Where are bile salts made? Where are they stored? What hormone causes it to contract?
4. What are components of bile? (7)
5. What are bile salts synthesized from? (1) Enzymes?
6. Where is it resorbed? What happens to it then? Key concept?
7. What inhibits hepatic bile synthesis? Via what enzyme?
1. Bile salts (emulsification of dietary lipids) --> lipolysis via lipase/colipase, other enzymes --> micelle formation (solubilization) --> translocation of lipolytic products across etnerocyte.
2. Emulsify fat into smaller, accessible droplets.
3. liver, gall bladder, CCK
4. Bile acid/salts (80:20), cholesterol, phospholipids (lecithin), pigments (bilirubin, biliverdin), water, bicarbonate, electrolytes.
5. Cholesterol. Cholesterol 7a-hydroxylase and sterol-27 hydroxylase --> cholate + chenodeoxycholate.
6. Ileum. Portal circulation --> liver. Bile salts are recycled.
7. Resorption of bile acids --> inhibition of cholesterol 7a-hydroxylase.
1. What happens to dietary lipids after they're emulsified by bile? Liberating? (4) Forming? (1) That is absorbed by? (1)
2. What is the principal enzyme in TG digestion?
3. What is ^ secreted from? In response to? Optimum pH activity? What does it also need (hormone and substrate) to raise pH to this level?
4. What is most important enzyme in TG synthesis?
1. Broken down by lipases, phospholipase and colipase --> liberated free fatty acids, DAGs, LPAs, MGAs will form mixed micelle that will be absorbed by enterocytes.
1. What is pancreatic lipase inhibited by? How?
2. What solves the problem?
3. How is ^ secreted? Where is it activated? By what?
4. How does lipase act?
5. What breaks down phospholipids?
ALL ESTER BONDS MUST BE HYDROLYZED
1. Physiological concentrations of bile salts bc bile salts displace lipase from substrate.
3. From intestine as pro-colipase. Activated by trypsin
4. Lipase acts to hydrolyze ester bonds at sn-1 and sn-3 position of triglycerides.
5. Phospholipase A2: phospholipid --> lipophospholipid + FA.
1. Why are FFA packaged into TGs?
2. What else is repackaged? (3)
3. What are the enzymes involved? (4) include substrates & products
- 1. Bc high levels of FFA are toxic in plasma
- 2. cholesterols, phospholipids, MAGs
- 3. (1) MGAT/ (2)DGAT: MAGs/DAGs + FFAs --> TAGs
- (3) AGPAT (acylglycerol 3-phosphate acyl transferase): LPA (lysophosphatidic acid) --> PA
- (4) ACAT (acyl-CoA cholesterol transferase): cholesterol--> CE
4. What is cholesterol's transport protein into enterocytes? What drug inhibits this protein?
5. What protein helps package TG into chylomicrons?What shouldn't you confuse this with?
6. What happens to chylomicron formed? (3)
7. Where does chylomicron go?
4. Niemann-Pick C1-Like -1 Protein(NPC1L1 protein) Ezemtimibe.
5. MTP (mirosomal triglyceride transfer protein) Ezemtibe. Mitochondrial trifunctional protein (inborn errors/B-oxidation)
6. Secretory vesicles containing chylomicron form--> fuses with basolateral membrane --> releases chylomicron containing dietary TAGs, CEs, fat-soluble vitamins, phospholipids, and proteins into lymphatic circulation.
7. Lymphatic system ---> heart (#1), skeletal muscle, adipose tissue) --> liver as chylomicron remnants.