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biochem 410 and 411 > 411 exam 3 > Flashcards

411 exam 3 Flashcards

1
Q

what is the purpose of B-oxidation?

A
  • break down triacylglycerols because they are insoluble and must be emulsified to be digested
  • fatty acids –> acetyl CoA to generate ATP
  • create a carbonyl group on the beta-C
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1
Q

what is emulsification?

A
  • fat globules broken down into soluble droplets (facilitated by bile salts and lipases)
  • adds solubility characteristics to fats to make micelles
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2
Q

bile salts

A
  • amphiphilic molecules
  • synthesized from cholesterol in liver and stored in gall bladder until released into small intestines for digestion
    *** produce solubilized fat globules **
  • ex: taurocholic acid used in fat digestion
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3
Q

interfacial activation

A

rate enhancement of lipase when it comes into contact with water
includes: bile salts, mixed micelles of phosphatidylcholine, and colipase

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4
Q

where does protein and lipid digestion begin?

A

protein: stomach (protease-pepsin)
lipid: small intestines (amylase, protease, lipase, nuclease)

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5
Q

functions of liver, gall bladder, and pancreas

A

liver: make bile
gall bladder: concentrate and store bile
pancreas: make enzymes for small intestines

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6
Q

what does pancreatic lipase do?

A

breaks down micelle for transport into small intestinal cell

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7
Q

chylomicrons

A
  • formed in intestinal mucosal cells
  • highly soluble for release into intestinal lymph vessels
  • dietary TAG, cholesterol, cholesteryl esters, apoproteins, vitamins
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7
Q

VLDL

A
  • dietary TAGs, cholesterol, choelsteryl esters
  • made in liver by choelsterol- rich chylomciron remnants and TAGs
  • transport TAGs and FAs from liver to tissue
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7
Q

IDL

A
  • formed from the remnnts of VLDL after TAGs are removed
  • transition particle between TAG transport (VLDL) and cholesterol transport (LDL)
  • some IDL reabsorbed by liver, other IDL pick up cholesteryl esters from HDL to form more LDL
  • ENDOGENOUS PATHWAY
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8
Q

LDL functions and type of pathway

A

1) deliver cholesterol to cells, where it is used in membranes
2) for biosynthesis of bile salts in liver
3) for synthesis of steroid hormones

ENDOGENOUS PATHWAY

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9
Q

HDL

A
  • made in liver and intestines and released in blood stream
  • protein-rich
  • cholesterol recovery- picks up excess cholesterol from blood and brings back to liver
  • delivers cholesterol to steroidogenic tissues (adrenal glands, ovaries, testes)

ENDOGENOUS PATHWAY

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10
Q

apoproteins

A
  • protein part of lipoproteins
  • dictate interactions in lipoproteins
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11
Q

what lipoproteins has no association with ApoE?

A

LDL

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12
Q

ApoA1

A
  • binding occurs in chylomicrons and HDL
  • add hydrophilicity to transport in a soluble env.
  • homotetratemer that can wrap around HDL particle
  • to help clear fats and cholesterol from WBC and HDL picks it up
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13
Q

ApoB-100

A
  • LDL-receptors are transmembrane glycoproteins
  • receptors target ApoB in clathrin-coated vesicles for endocytosis
  • ApoB and cholesteryl-esters are hydrolyzed –> amino acids, f.a., and cholesterol
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14
Q

ApoE

A
  • found in VLDL and IDL because of conversion of lipoproteins in the endogenous pathway
  • enhance binding to LDL (recpetors are primarily in liver but also CNS)
  • defects in ApoE4: cant clear out amiloid peptides –> alzheimers
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15
Q

where does Beta oxidation happen?

A

mitochondrial matrix

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16
Q

what do ABCG1 and ABCA1/4 do?

A

ABCG1: controls tissue lipid levels and efflux of cellular cholesterol to HDL
ABCA1: mediates efflux of cholesterol and phospholipids to lipid-poor apolipoproteins like ApoA-I to form nHDL

17
Q

how do ApoA1 work clear cholesterol?

A
  1. facilitates interactions with SR-B1 receptor within HDL at liver
  2. HDL binds to SR-B1 and transfers lipids to cell
  3. depleted HDL (remHDL) dissociates from receptor and reenters circulation for scavenging cholesterol
18
Q

what transports FA into mitochondria?

A

carnitine

19
Q

what is Acyl CoA Synthetase used in the conversion of?

A

Fatty acid –> Fatty Acid-CoA

(activation of fatty acid)

20
Q

how do fats and glycogen differ in energy?

A

fat: energy for 2-3 months
glycogen: energy for 1 day (30 ATP/ glucose ox)

21
Q

what is uptake of free fatty acids?

A
  • come from adipocyte (fat storage cells)
  • stored fats are mobilized for energy production (animals)
  • low energy, fasting state
  • when when body deals with energetic demands because diet is not enough
22
Q

what does HSL do?

A
  • produces free fatty acids
  • hydrolyses TAG in fat droplets
23
Q

albumin

A
  • blood protein
  • aids in transport of hydrophobic fatty acids in blood
24
Q

CD36

A

transporter that lets FA into muslce cell cytosol

25
Q

where are FA activated and what are the ATP investments?

A
  • cytosol of muscle cells
  • 2 ATP
26
Q

NNT and ROS

A
  • NNT in mitochondria converts NADH to NAD+ and NADP+ to NADPH
  • if don’t do its job, NADPH lowers and ROS increases (will have to go through more glucose to keep up)
27
Q

B-oxidation in peroxisomes

A
  • carnitine acultransferase recognize and shorten very long FA (>22C)
  • sent to mitochondria for further degradation if under 8C
  • NOT sent into ETC. Make 1.5 less ATP
  • calatase is present to get rid of H2O2
  • glyoxysome is the plant equivalent to peroxisomes
28
Q

ketone bodies

A
  • quick and temporary source of fuel and energy for brain, heart, and mouscle
  • for brain during starvation
  • transportable forms of acetyl-CoA (v soluble –> quick source of ATP)
  • acetone, acetoacetate, B-hydrohybutane
29
Q

what will acetoacetate and B-hydroxybutyrate ultimately get converted to?

A

acetyl-CoA

30
Q

how are ACC isoforms same and different?

A
  • catalyize the same reaction
  • differ in kinetics
  • differ in regulation
  • based on tissue specificity
31
Q

where is ACC1 and ACC2 found?

A
  • ACC1: adipose tissue (where FA synthesis occurs)
  • ACC2: tissues where FA does not occur
  • liver has both
32
Q

how do ACC1 and ACC2 work together?

A

ACC1 makes malonyl-Coa, and CC2 uses that for regulatory role to inhibit acyl import

33
Q

NAFLD

A
  • non-alcoholic fatty liver disease
  • hepatic accumulation of excess triglycerides
  • secretion into plasma as VLDL
  • cardiovascular disesae is leading cause of mortaility for patients with NAFLD
34
Q

what happens to FA after it reaches 16C in synthesis?

A

goes to ER or mitochondria

35
Q

what are eicosanoids?

A
  • local hormones that signal for swelling, pain
  • synthesis in ER triggered by injury and inflammation
  • enzyme cleaves out FA and become local signals through cyclooxogenase
  • not transported in the blood stream
  • stored in cell membrane as C2-esterphosphatidylinositolor other phospholipids that when are hydroluzed by phospholipase are utilized in metabolism that is cell specific
  • cycolyzed signals of FA
  • exert effects at very low concentations, and have very short half lifes
  • release is stimulated by histamines, hormones, and proteases
  • thromboxan A2 is produced by plateletes to stimalted platelet aggregation
36
Q

what does PLA2 release?

A

arachidonic acid (precursor of eicosanoids)

37
Q

how do medicines work with arachidonate?

A

prevent FA from cyclooxidizing

38
Q

how does aspirin work?

A

prevents biosynthesis of prostogladins via acetylation of of a serine residue that block arachidonate from reaching active site of COX

39
Q

how are B-ox and FA synthesis tags different?

A
  • B-ox: AMP
  • FA synth: ACP; serine

both have cysteamine and phosphopantetheine group

40
Q

what enzyme is known as condensing enzyme?

A

B-ketoacyl-ACP synthase (KS)

41
Q

animals can’t desaturate FA beyond ______

A

∆9

42
Q
A

biochem 410 and 411 (4 decks)

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