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MCAT > concept 1d part2 > Flashcards

concept 1d part2 Flashcards

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MCAT flashcards
1
Q

dietary fat

A

consists mainly of triacylglycerols

remained comprised of cholesterol, cholesterol esters, phospholipids, and free fatty acids

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2
Q

lipid digestion

A

minimal in mouth and stomach
transported to the small intestines essentially intact where emulsification occurs
then pancreas secretes enzymes into the small intestine
these enzymes hydrolyze lipid components to 2-monoacylglycerol, free fatty acids, and cholesterol

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3
Q

emulsification

A

mixing of 2 normally immiscible liquids (for lipids its fat and water)
formation of emulsion increases surface area of lipid leading to greater enzymatic interactions and processing
aided by bile

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4
Q

bile

A

contains bile salts, pigments, and cholesterol
secreted by the liver and stored in the gallbladder
aids in emulsification

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5
Q

pancreatic secretions

A

pancreatic lipase, colipase, and cholesterol esterase

secreted into the small intestine to hydrolyze lipid components to 2-monoacylglycerol, free fatty acids, and cholesterol

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6
Q

micelles

A

clusters of amphipathic lipids that are soluble in the aqueous environment of intestinal lumen
water-soluble spheres w/ a lipid-soluble interior
vital in digestion, transport, and absorption of lipid-soluble substance from duodenum to ileum
formed by free fatty acids, cholesterol, 2-monoacylglycerol, and bile salts

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7
Q

structure of micelles

A

collections of lipids with their hydrophobic ends oriented toward center and charged ends oriented toward the aqueous environment
collect lipids within their hydrophobic center

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8
Q

absorption

A

micelles diffuse to brush border of intestinal mucosal cells and are absorbed
digested lipids pass through the brush border , where they are absorbed into the mucosa and re-esterified to form triacylglycerols and cholesterol esters and packaged
more water-soluble short-chain fatty acids absorbed by simple diffusion directly to bloodstream

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9
Q

chylomicrons

A

packed triacylglycerols and cholesterol lipids after absorption
along with apoproteins, fat-soluble vitamins, and other lipids

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10
Q

pathway of chylomicrons

A

leave the intestine via lacteals, the vessels of the lymphatic system
re-enter the bloodstream via the thoracic duct, a long lymphatic vessel that empties into the left subclavian vein at the base of the neck

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11
Q

postabsorptive state

A

at night
utilizing energy stores instead of food for fuel
fatty acids are released from adipose tissue and used for energy
decreased insulin, increased epinephrine, increased cortisol

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12
Q

hormone-sensitive lipase (HSL)

A

activated by decreased insulin
hydrolyzes triacylglycerols yielding fatty acids and glycerol
also activated by epinephrine and cortisol

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13
Q

mobilization of triacylglycerols

A

hydrolyzed in adipose tissue to glycerol and fatty acids then transported to the liver
glycerol participates in glycolysis or gluconeogenesis to form glucose
fatty acids undergo beta-oxidation to form acetyl-CoA for the citric acid cycle and ketone bodies

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14
Q

lipoprotein lipase (LPL)

A

necessary for the metabolism of chylomicrons and very-low-density lipoproteins
enzyme that can release free fatty acids from triacylglycerols in lipoproteins

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15
Q

free fatty acid transport

A

transported through the blood in association with albumin, a carrier protein

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16
Q

lipoprotein

A

transport mechanism for lipids within the circulatory and lymphatic systems
include chylomicrons and VLDL which transport triacylglycerols
HDL, IDL, and LDL which transport cholesterol and cholesteryl esters

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17
Q

structure of lipoproteins

A

phospholipid sphere with hydrophilic tail on inside and hydrophobic tail pointing out
cholesterol in the membrane
triacylglycerol (lipids) on the inside of the sphere
apoprotein B-100 spanning the membrane

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18
Q

types of lipoproteins

A 
chylomicrons (least dense) 
very-low-density lipoproteins (VLDL)
intermediate-density lipoproteins (IDL)
low-density lipoproteins (LDL)
high-density lipoproteins (HDL) (most dense)
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19
Q

chylomicrons

A

transport dietary triacylglycerols and cholesterol from intestines to tissues
least dense lipoprotein
highly soluble in lymphatic fluid and blood
assembly occurs in intestinal lining, results in nascent chylomicron containing lips and apolipoproteins

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20
Q

very-low-density lipoprotein (VLDL)

A

transport triacylglycerols from liver to tissues
metabolism similar to chylomicrons
produced and assembled in the liver
also contain fatty acids that are synthesized from excess glucose

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21
Q

intermediate-density lipoprotein (IDL)

A

picks up cholesterol from HDL to become LDL
picked up by the liver
VLDL with triacylglyceol removed
some processed in the bloodstream

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22
Q

low-density lipoproteins (LDL)

A

delivers cholesterol into cells
for biosynthesis, cell membranes
bile acids and salts are made from cholesterol in the liver

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23
Q

high-density lipoproteins (HDL)

A

picks up cholesterol accumulating in blood vessels
delivers cholesterol to liver and steroidogenic tissues
transfers apolipoproteins to other lipoproteins
synthesized in the liver and intestines, released as a dense protein-rick particle in blood

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24
Q

apoproteins

A

aka apolipoproteins
form of protein component of lipoproteins
receptor molecules and involved in signaling
5 types

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25
Q

types of apoproteins

A

apoA-I: activates LCAT, enzyme that catalyzes cholesterol esterification
apoB-48: mediates chylomicron secretion
apoB-100: permits uptake of LDL by the liver
apoC-II: activates lipoprotein lipase
apoE: permits uptake o chylomicron remnants and VLDL by the liver

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26
Q

cholesterol

A

ubiquitous component of all cells in the human body

role in synthesis of cell membranes, steroid hormones, bile acids, and vitamin D

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27
Q

cholesterol sources

A

most derive it from LDL or HDL

some is synthesized de novo which occurs in the liver and driven by acetyl-CoA and ATP

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28
Q

citrate shuttle

A

carries mitochondrial acetyl-CoA into the cytoplasm where synthesis occurs
NADPH, from pentose phosphate pathway, supplies reducing equivalents

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29
Q

synthesis of mevalonic acid

A

in the smooth ER
is the rate-limiting step in the cholesterol biosynthesis
catalyzed by 3-hydroxy-3-methylglutaryl (HMG) CoA reductase

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30
Q

regulation for cholesterol synthesis

A

increased levels of cholesterol inhibits further synthesis by feedback inhibition mechanism
insulin promotes cholesterol synthesis
control over de novo cholesterol synthesis is dependent on regulation of HGM-CoA reductase gene expression in the cell

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31
Q

specialized enzymes in cholesterol synthesis

A

lecithin-cholesterol acyltransferase (LCAT)

cholesteryl ester transfer protein (CEPT)

32
Q

lecithin-cholesterol acyltransferase (LCAT)

A

enzyme found in the blood stream that is activated by HDL apoproteins
adds a fatty acid to cholesterol
produces soluble cholesteryl esters, in HDL
HDL cholesteryl esters can be distributed to other lipoproteins like LDL

33
Q

cholesteryl ester transfer protein (CETP)

A

facilitates the transfer process

HDL cholesteryl esters distributed to IDL, which becomes LDL by acquiring these cholesterol esters from IDL

34
Q

fatty acids

A 
long-chain carboxylic acids 
carboxyl carbon is C1 
C2 is alpha-carbon 
found in the body occur as salts 
capable of forming micelles or esterified to other compounds, membrane lipids
35
Q

saturated fatty acids

A

fatty acid with no carbon-carbon double bonds

saturated with Hs

36
Q

unsaturated fatty acids

A

fatty acids with carbon-carbon double bonds
have one or more
humans only synthesis a few of these rest are from essential fatty acids in diet
double bonds generally in cis configuration

37
Q

2 essential fatty acids

A

alpha-linolenic acid
linoleic acid
poly-unsaturated fatty acids
role in cell membrane fluidity, critical for proper function of cell

38
Q

omega numbering system

A

also used for unsaturated fatty acids
designation describes the position of the last double bond relative to the end o the chain
identifies the major precursor fatty acid

39
Q

synthesis

A

used as fuel for body and supplied primarily bb diet
excess carbohydrate and protein acquired from diet converted to fatty acids and stored as triacylglycerol for energy
contemplate synthesis, do not rely directly on coding of nucleic acid (lipid and carbohydrate)

40
Q

fatty acid biosynthesis

A

occurs in liver
products subsequently transported to adipose tissue for storage
adipose synthesizes small amount

41
Q

fatty acid biosynthesis enzymes

A

acetyl-CoA carboxylase
fatty acid synthase
stimulated by insulin

42
Q

palmitic acid (palmitate)

A

primary end product of fatty acid synthesis

43
Q

acetyl-CoA shuttling

A

acetyl-CoA accumulates in mitochondrial matrix, needs to be moved to the cytosol for fatty acid biosynthesis
Acetyl-CoA is product of PDH complex
couples with oxaloacetyate to form citrate at beginning of citric acid cycle
isocitrate dehydrogenase is rate-limiting, as cell becomes e energetically satisfied, slows the citric acid cycle
causes citrate accumulation, can diffuse across membrane
cytosol citrate lyase splits it back to acetyl-CoA and oxaloacetate

44
Q

acetyl-CoA carboxylase

A

activates acetyl-CoA in the cytoplasm for incorporation into fatty acids
rate-limiting enzyme of fatty acid biosynthesis
requires biotin and ATP to function
adds CO2 to acetyl-CoA t po form malonyl-CoA
activated by insulin and citrate

45
Q

fatty acid synthase

A

palmitate synthase
palmitte is only fatty acid that humans can synthesize de novo
large multiple enzyme complex
found in cytosol
rapidly induced in the liver following a meal of carbohydrates bc of elevated insulin

46
Q

acyl carrier protein (ACP)

A

part of the multienzyme complex, fatty acid synthase

requires pantothenic acid (vitamin B5)

47
Q

activation of fatty acid synthase

A
  1. activation of the growing chain
  2. activation of malonyl-CoA with ACP
  3. bond formation b/w these activated molecules
  4. reduction of a carbonyl to a hydroxyl group
  5. dehydration, removal of H2O
  6. reduction to a saturated fatty acid
48
Q

triacylglycerol synthesis

A

triglyceride synthesis
formed by attaching three fatty acids (as fatty acyl-CoA) to glycerol
occurs primarily in the liver, and some in adipose tissue
from fatty acids and glycerol 3-phosphate
in liver packaged and sent to adipose tissue as VLD lipoproteins, leaving only small amount of stored triacylglycerols

49
Q

beta-oxidation

A

catabolism of most fatty acids

in the mitochondria, peroxisomal beta-oxidation also occurs

50
Q

alpha-oxidation

A

catabolism of branched-chain fatty acids

depending on branch points

51
Q

omega-oxidation

A

oxidation in which endoplasmic reticulum produces dicarboxylic acids

52
Q

activation of fatty acid metabolism

A

first become activated by attachment to CoA
catalyzed by fatty-cyl-CoA synthetase
product is fatty acyl-CoA or acyl-CoA

53
Q

fatty acid entry into mitochondria

A

short chain and medium chain fatty acids diffuse freely into mitochondria, where they are oxidized
long chain fatty acids (14-20C) are also oxidized in the mitochondria but require transport via a carnation shuttle
very long-chain fatty acids are oxidized elsewhere

54
Q

carnitine acyltransferase I

A

rate-limiting enzyme of fatty acid oxidation

55
Q

beta-oxidation in mitochondria

A

reverses the process of fatty acid synthesis by oxidizing and releasing molecules of acetyl-CoA (rather than reducing and linking)
repetition of four steps

56
Q

process of beta-oxidation

A 
each 4-step cycle accomplishing this 
releases one acetyl-CoA 
reduces NAD+ and FAD 
NADH and FADH2 are oxidized in ETC 
producing ATP 
acetyl-CoA is entered into the citric acid cycle (muscles and adipose) or stimulates gluconeogenesis by activating pyruvate carboxylase (liver)
57
Q

4 steps of beta-oxidation

A
  1. oxidation of the fatty acid to form a double bond
  2. hydration of the double bond to form a hydroxyl group
  3. splitting of the beta-ketoacid into a shorter acyl-CoA and acetyl-CoA
    process continues until the chain has been shorted to 2 carbons, creating final acetyl-CoA
58
Q

beta-oxidation of odd# fatty acids

A

undergo beta-oxidation in same manner until final cycle
final step yields one acetyl-CoA and on propionyl-CoA (from 5C fragment)
propionyl-CoA is converted to methylmalonyl-CoA

59
Q

propionyl-CoA carboxylase

A 
converts propionyl-CoA to methylmalonyl-CoA 
requires biotin (vitamin B7)
60
Q

methylmalonyl-CoA

A 
converted into succinyl-CoA 
catalyzed by methylmalonyl-CoA mutase 
requires cobalamin (vitamin B12)
61
Q

succinyl-CoA

A

a citric acid cycle intermediate

can be converted to malate to enter the gluconeogenic pathway in cytosol

62
Q

oxidation of unsaturated fatty acids

A

require 2 additional enzymes bc double bonds can disturb stereochemistry needed for oxidative enzymes to act on fatty acid
catalyzed by enoyl-CoA isomerase
once enough is liberated to isolate the bond within the first 3 carbons

63
Q

enoyl-CoA isomerase

A

rearranges cis double bonds at the 3,4 position to trans double bond at the 2,3 position

64
Q

2,4-dienoyl-CoA reductase

A

further reduction required for oxidation of polyunsaturated fatty acids
enzyme that is used to convert 2 conjugated double bonds to just one double bond at the 3,4 position
then undergo the same arrangement as monounsaturated fatty acids

65
Q

ketone bodies

A

liver converts excess acetyl-CoA from beta-oxidation of fatty acids during fasting state
acetoacetate and 3-hydroxybutyrate
used for energy in various tissues
muscles metabolize ketons as rapidly as liver releases them
this prevents accumulation in bloodstream

66
Q

after a week of fasting

A

ketones reach a concentration in the blood that is enough for the brain to begin metabolizing them
known as ketogenesis and ketolysis

67
Q

ketogenesis

A

occurs in the mitochondria of liver cells
when excess acetyl-CoA accumulates in fasting state
HMG-CoA synthase forms HMG-CoA
HMG-CoA lyase breaks down HMG-CoA into acetoacetate
which is reduced to 3-hydroxybutyrate
aceton is minor side product and will not be used as energy for tissues

68
Q

ketolysis

A

acetoacetate picked up from blood is activated in the mitochondria
catalyzed by succinyl-CoA acetoacetyl-CoA transferase (aka thiophorase)

69
Q

thiophorase

A

succinyl-CoA acetoacetyl-CoA transferase
enzyme in tissues outside the liver
3-hydroxybutyrate is oxidized to acetoacetate
liver cannot catabolized ketone bodies that it produces

70
Q

protein catabolism

A

rarely used as energy source but important for other functions
under extreme energy deprivation, can be used for energy
proteins must be digested and absorbed

71
Q

digestion of proteins

A

begins in the stomach with pepsin
continues with the pancreatic proteases secreted by zymogens
completed by the small intestine brush-boarder enzymes dipeptidase and amino peptidase

72
Q

produce of protein digestion

A

amino acids
dipeptides
tripeptides

73
Q

aborption of amino acids

A

and small peptides
through the luminal membrane
accomplished by secondary active transport linked to sodium
at the basal membrane simple and facilitated diffusion transports amino acids into bloodstream

74
Q

glucogenic amino acids

A

all but leucine and lysine

can be converted into glucose thought gluconeogenesis

75
Q

ketogenic amino acids

A

leucine, lysine, isoleucine, phenylalanine, threonin, tryptophan, and tyrosine
can be converted into acetyl-CoA and ketone bodies

76
Q

urea cycle

A

occurs in the liver

body’s primary way of removing excess nitrogen from the body

MCAT (18 decks)

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