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Principles of Biochemistry > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what is the structural role of lipids

A

comprise cell membranes in combination with specific protein molecules and thus control permeability of cells and regulate transport of metabolites

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2
Q

what is the energy source role of lipids

A

particularly triglycerides are an excellent source of energy, whether obtained from diet or tissue depots. Major portion of energy in mammals is derived from oxidation of free fatty acids originating from adipose tissue fat

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3
Q

what are the three major functions of lipids

A
  1. serve as structural components of biological membranes
  2. provide energy reserves, mostly in the form of triacylglycerols
  3. lipids and lipids derivates serve as vitamins and hormones
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4
Q

define lipids

A

biological molecules that are insoluble in aqueous solutions but soluble in organic solvents

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5
Q

what percentage of the body is triglycerides

A

13%

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6
Q

what percentage of the body is membrane lipids

A

2.5%

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7
Q

what are simple lipids

A

fatty acids and derivatives; cholesterol

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8
Q

are lipids hydrophobic or hydrophilic

A

lipids are poorly soluble in water, therefore needing special arrangements for transport in the blood and in tissues/fluids

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9
Q

what are complex lipids

A

contain additional molecular components: carbohydrate, proteins, etc.

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10
Q

what are aliphatic lipids

A

straight chain lipids

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11
Q

what are polar (amphipathic) lipids

A

contain ionizable/hydrophilic groups like: COO- or NH3+ or PO4- or SO4

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12
Q

what are neutral lipids

A

a long hydrocarbon chain with a carboxyl group at one end. Typical chain length between 16 and 20 carbons

for fatty “acids,” for the -OOH group has low ionization potential (rarely found as COO-)

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13
Q

what are the major components of lipids

A
  1. monocarboxylic
  2. unbranched chain # of carbons: 12-24
  3. mostly even number of carbons
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14
Q

what are the important roles of fatty acids

A

-building blocks for phospholipids and glycolipids
-target proteins to membranes
-high energy source of fuel
-fatty acid derivatives are used as hormones and intracellular messengers

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15
Q

what happens to the hydrophobicity of fatty acids as the chain length increases

A

increased

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16
Q

which fatty acid configuration is bent

A

cis unsaturated

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16
Q

describe the properties of saturated fatty acids

A

no multiple bonds; only single C-C bonds

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17
Q

which fatty acid configuration is the most abundant in nature

A

cis-configuration

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18
Q

how do fatty acids “pack” within stable aggregates

A

saturated/straight chain fatty acids pack tighter, and the more kinks it has, disrupts the van der waals interactions

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19
Q

describe the delta system nomenclature

A

counting starts from the carboxylic acid group

X is the number of C’s in the chain
Y is the number of double bonds

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20
Q

which fatty acids are nutritionally essential

A

linoleic acid and a-linolenic acid

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21
Q

what is arachidonic acid

A

a 20 carbon chain w 4 double bonds. A precursor, a straight chain fatty acid, that our body later converts to pyrogens that give us heat and fever

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22
Q

describe the omega nomenclature

A

start counting from the opposite end of the COOH group

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23
Q

why is the delta nomenclature useful

A

to describe biochemical reactions

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24
Q

why is the omega nomenclature useful

A

to track families of fatty acids in nutrition

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25
Q

what is the name of omega 6 fatty acid

A

linoleic acid

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26
Q

what is the name of omega 3 fatty acid

A

a-linolenic acid

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27
Q

why is it that omega 3 and 6 are nutritionally essential

A

bc animals can’t synthesize them and they therefore must be taken from our diet

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28
Q

what is oleic acid

A

omega 9 fatty acid

18:1;9

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29
Q

double bonds ________ the melting points of fatty acids

A

decrease

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30
Q

what fatty acids do fats and oils contain that are solid at room temperature

A

saturated/ trans unsaturated

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30
Q

what fatty acids fats and oils contain that are liquid even in the refrigerator

A

unsaturated fatty acids

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31
Q

describe the composition of olive oil

A

high in long chain unsaturated fatty acids, liquid state at 25 degrees C

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32
Q

describe the composition of butter

A

high in long chain saturated fatty acids that increase its melting point; soft solid at 25 degrees C

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33
Q

describe the composition of beef fat

A

highest portion of long-chain saturated fatty acids; hard solid at 25 degrees C

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34
Q

what are acylglycerols

A

glycerol + fatty acid

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35
Q

describe the structure of glycerophospholipids

A

glycerol backbone
-fatty acid
-fatty acid
-PO4-alcohol

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36
Q

describe the structure of sphingolipids

A

sphingosine
-fatty acid
-PO4-choline

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37
Q

describe the structure of sphingolipids

A

sphingosine
-fatty acid
-mono or oligosaccharide

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38
Q

describe the structure of galactolipids

A

glycerol backbone
-fatty acid
-fatty acid
-mono or disaccharide-SO4

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38
Q

what is the importance of carbiolipin

A

major lipid of inner mitochondrial membrane

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38
Q

what are phosphoacylglycerols

A

polar (amphipathic) lipids
-contain a phosphate group
-contain other ionizable groups
-key components of cell membranes
-used in food industry as emulsifying agents

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38
Q

what accumulates to cause Gaucher’s disease

A

glucosylceramide

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38
Q

what is the importance of plasmalogens

A

10% of phospholipid in muscle and nerves

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39
Q

what is unique about sphingolipids

A

do not have the glycerol backbone

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39
Q

what is dipalmitoyl phosphatidylcholine

A

lecithin, used to treat premie babies

pulmonary surfactant

normally made by type II alveolar cells of the lung to reduce surface tension at air-water interface of the alveolus

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39
Q

what are phosphatidylinositol compounds

A

phosphates added to sugars
-important cellular regulators of receptor-mediated signal transduction, Ca2+ transport, and metabolic events

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39
Q

what is the importance of platelet activating factor (PAF)

A

important in blood coagulation

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40
Q

what are steroids

A

compounds with a four ring structure called the “steroid nucleus” or “steroid skeleton”

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41
Q

what is the most abundant sterol in humans

A

cholesterol

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42
Q

what are the functions of cholesterol

A

component of cell membranes

precursor of bile acids

steroid hormones

vitamin D

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43
Q

how does cholesterol play a role in atheroslerosis

A

excess cholesterol in blood leads to plaque formation, causing an increase in blood pressure via narrowing of arterties. This causes a reduced ability to stretch and a clot formation leading to myocardial infarction or stroke

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44
Q

which steroids are produced from cholesterol

A

estradiol, testosterone, cortisol, progesterone

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45
Q

what are eicosanoids

A

derived from arachidonic acid

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46
Q

what is cyclooxygenase

A

COX enzyme

target of aspirin and non-steroidal anti-inflammatory drugs

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47
Q

what is thromboxane A2

A

stimulates platelet aggregation

raises BP

constricts coronary arteries

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48
Q

what is prostaglandin E1

A

inhibits platelet aggregation

lowers BP

relaxes coronary arteries

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49
Q

what are lipoproteins

A

lipids bound to other molecules

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50
Q

how is the lipid bilayer held together

A

by hydrophobic interaction between the tails of the membrane lipids

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50
Q

what forms the structural backbone of the membrane

A

lipids

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51
Q

how do membranes behave at body temperature

A

like a viscous liquid

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52
Q

what governs fluidity of a membrane

A

unsaturated fatty acid content of phospholipids and their chain length, and by cholesterol content of the membrane

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53
Q

saturated fatty acids/cholesterol = ?

A

more rigid membrane

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54
Q

high content of unsaturated fatty acids = ?

A

more fluid membrane

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55
Q

what is the current model of the membrane

A

fluid mosaic

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56
Q

what are the essential features of the biological membrane

A

existence of both integral and peripheral membrane proteins; hydrophobic proteins are located on the inner portion of the membrane while more water soluble proteins (glycoproteins) are found on the outer surface.

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57
Q

how are membrane-spanning segments formed

A

nonpolar alpha helices

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58
Q

what is a glycocalyx

A

the smooth hydrophilic coat of the membrane due to it being surrounded by the carbohydrate tails of glycolipids and glycoproteins

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59
Q

what can mechanically damage the membrane

A

crystalline material

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60
Q

what is the biological membrane particularly vulnerable to

A

to agents that disrupt hydrophobic interactions, like detergents and organic solvents

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61
Q

does passive diffusion require a carrier

A

no

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62
Q

does facilitated diffusion require a carrier

A

yes

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63
Q

does primary active transport require a carrier

A

yes

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64
Q

does secondary active transport require a carrier

A

yes

65
Q

does passive diffusion move against the gradient

A

no

66
Q

does facilitated diffusion move against the gradient

A

no

67
Q

does primary active transport move against the gradient

A

yes

68
Q

does secondary active transport move against the gradient

A

yes

69
Q

does passive diffusion need metabolic energy

A

no

70
Q

does facilitated diffusion need metabolic energy

A

no

71
Q

does primary active transport need metabolic energy

A

yes

72
Q

does secondary active transport need metabolic energy

A

yes

73
Q

does passive diffusion require ATP hydrolysis

A

no

74
Q

does facilitated diffusion require ATP hydrolysis

A

no

75
Q

does primary active transport require ATP hydrolysis

A

yes

76
Q

does secondary active transport require ATP hydrolysis

A

no

77
Q

what is example cargo of passive diffusion

A

steroid hormones; many drugs

78
Q

what is example cargo of facilitated diffusion

A

glucose in RBCs and at blood-brain barrier

79
Q

what is example cargo of primary active transport

A

Na+, K+ ATPase; Ca2+ ATPase

80
Q

secondary active transport

A

sodium (Na+) cotransport of glucose at kidney and intestine

81
Q

what are pores

A

allow passage of all small water soluble molecules

82
Q

what are channels

A

more selective than pores

narrow gate, formed by hydrophilic edges of amphipathic transmembrane alpha-helices, that interact with a specific solute and is permeable only for that solute

83
Q

what are transporters

A

aka membrane carriers

work somewhat like channels but undergo conformational changes during the transport cycle

84
Q

how is the energy barrier created in the membrane

A

there is an energetic cost to losing a shell of hydrogen and moving through the very hydrophobic lipid region

85
Q

how do you bypass the energy barrier?

A

proteins to facilitate diffusion such as transporters and permeases

86
Q

what are characteristics of carrier-mediated transport

A
  1. substrate-specific
  2. saturable
  3. can be selectively inhibited
87
Q

when does osmosis occur

A

when the concentration of the solvent is different on opposite sides of a porous membrane

88
Q

what is osmosis

A

diffusion of water across a semipermeable membrane

89
Q

what is osmolarity

A

total concentration of solute particles in a solution

90
Q

what is tonicity

A

how a solution affects cell volume (when a cell is “bathed in it”)

91
Q

how does active transport via atp-dependent transporters work

A

use the energy in ATP to drive movement of molecules/ions across the membrane

92
Q

what occurs to ATPase ion transporters during the transport cycle

A

phosphorylated

93
Q

what occurs to ABC during transport cycle

A

amino acid domains bind ATP

94
Q

what are the structures that make up the sodium-potassium pump

A

glycoprotein with 2 alpha and 2 beta subunits

95
Q

what are the three types of transporters

A
  1. antiporter
  2. symporter
  3. uniporter
96
Q

describe the difference between antiporter, symporter, uniporter

A

antiporter allows solute A and B to pass in opposite directions

symporter allows solute A and B to pass in the same direction

uniporter allows solute A and A to pass in opposite directions (GLUT1 glucose carrier)

97
Q

describe the regulation of intracellular calcium in myocardial cells

A

cardiotonic steroids reduce the sodium gradient and therefore the effectiveness of the Ca2+/Na+ antiporter in the plasma membrane

98
Q

what percentage of total calories in the western diet is triglycerides

A

35-40%

99
Q

what is the principal storage form of energy in the body

A

triglycerides

100
Q

how long can you live without food

A

52 days

101
Q

what are the 4 steps of fat metabolism

A
  1. digestions, absorption, and transport of dietary fat
  2. generation of metabolic energy from this fat
  3. storage of excess fat in adipose tissue
  4. metabolic links between triglycerides and other biomolecules, including carbohydrates and ketone bodies
102
Q

which yields more energy, glucose or palmitate

A

palmitate: 9 cal/g
glucose: 4 cal/g

103
Q

which three fatty acids are most abundant in adipose tissue

A
  1. oleic acid
  2. palmitic acid
  3. linoleic acid
104
Q

how does fatty acid degradation occur

A

by removing a carbon at the same end of the chain via “peeling off” and acetyl molecule

105
Q

what is Coenzyme A

A

a coenzyme, notable for its role in the synthesis and oxidation of fatty acids, and the oxidation of pyruvate in the TCA cycle

106
Q

how does fatty acid synthesis occur

A

carbon chain elongation occurs by adding a carbonyl group to the growing chain

107
Q

how much ATP is produced from beta oxidation

A

106

108
Q

what do defects in b-oxidation cause

A

muscle weakness and fasting hypoglycemia

109
Q

carnitine deficiency in the liver leads to _________

A

hypoketotic hypoglycemia during periods of extended fasting

110
Q

carnitine deficiency in skeletal muscle causes _______

A

muscle weakness and muscle cramps on exertion

111
Q

when patients show an unusual abundance of fat droplets in muscle and liver as well as some fatty degeneration of the liver, they have what?

A

generalized carnitine deficiency

112
Q

why does generalized carnitine deficiency cause abundance of fat droplets and fatty degeneration of liver

A

excess acyl-CoA that cannot be transported into the mitochondrion is diverted into triglyceride synthesis –> fat droplets

113
Q

how does skeletal muscle play into b-oxidation

A

covers major portion of energy needs from fatty acids at all times

114
Q

how does the liver play into b-oxidation

A

depends on fatty acids during fasting but not after a mixed meal

115
Q

at what steps does the body regulate fatty acid metabolism

A
  1. availability of fatty acids from adipose tissue (hormonal regulation of lipolysis)
  2. transport of fatty acid acyl-CoA into the mitochondria (down regulation of carnitine acyltransferase by manolyl-CoA)
  3. availability of coenzymes (NAD and FAD) to promote b-oxidation
116
Q

what are ketone bodies

A

water-soluble molecules that contain the ketone groups produced that fatty acids by the liver (ketogenesis)

117
Q

which acids are ketone bodies

A

acetone, acetoacetic acid, beta-hydroxybutyric acid

118
Q

ketone bodies are readily transported into tissues outside the ______, where they are converted into ______ which then enters the _________________ and is oxidized for energy

A

liver, acetyl-CoA, citric acid cycle

119
Q

when are ketone bodies produced

A

during periods of caloric restriction:
- low food intake, carbohydrate restrictive diets, starvation, prolonged exercise, alcoholism, type I diabetes

120
Q

ketone bodies are released into the blood ____ liver _____ stores are depleted

A

after, glycogen

121
Q

all major nutrients are degraded into ________

A

acetyl-CoA

122
Q

can fatty acids be converted to glucose?

A

no!

123
Q

what are the functions of dietary fats

A
  1. help the body absorb vitamins
  2. are a major energy fuel of hepatocytes and skeletal muscle
  3. are a component of myelin sheaths and all cell membranes
  4. are required at a higher level for infants and children than for adults
124
Q

what do fatty deposits in adipose tissue provide

A
  1. an easy-to-store concentrated source of energy
  2. a protective cushion around body organs
  3. an insulating layer beneath the skin
125
Q

what are bile salts

A

detergent-like substances created from cholesterol in liver and secreted from gallbladder to aid in digestion and absorption of lipids

126
Q

what is a bile salt made up of

A

bile acid and an associated cation, usually an amino acid (glycocholate, taurocholate)

127
Q

are bile salts amphipathic

A

yes

128
Q

how does a bile salt make a circular structure around a lipid

A

it is amphipathic. all water loving particles are on one side

129
Q

how are lipoproteins defined

A

by density

130
Q

what are chylomicrons

A

lightest, biggest; carries dietary fat away from intestine

131
Q

what are VLDL

A

next lightest to chylomicrons (very low density); carries fat away from liver

132
Q

what are HDL

A

heaviest, smallest; carries the “good cholesterol” to be metabolically changed/eliminated by liver actions

132
Q

what are LDL

A

the most cholesterol/the “bad” cholesterol; carries cholesterol away from liver –> can form plaques in bloodstream

133
Q

what is Apo C-II

A

an activator for lipases that hydrolyze triglycerides in lipoproteins

gets in the vicinity of LPL, an activate it

134
Q

what is Apo B-100

A

protein recognized by the LDL receptor in cholesterol transport

docks on hepatocyte which is upregulated the LDL receptor to catch it

135
Q

what is Apo E

A

has different allelic variants in humans; one of these (ApoE4) is associated with a higher risk of early-onset Alzheimer’s disease

136
Q

free cholesterol regulates its own concentration by action on these three important proteins

A
  1. ACAT: induced by cholesterol, which converts free cholesterol into highly insoluble cholesterol esters stored in the cell
  2. HMG-CoA reductase: repressed by cholesterol, the rate limiting enzyme of cholesterol biosynthesis
  3. LDL receptor: transcription of the gene for the receptor is repressed by cholesterol, reducing the uptake of LDL-cholesterol from blood
137
Q

which lipoprotein is needed for reverse cholesterol transport

A

HDL

138
Q

how does HDL perform reverse cholesterol transport

A

accepts cholesterol from cells throughout the body and brings it to the liver, which secretes it into bile either as such or after its conversion to bile acids

139
Q

what are statins

A

specific, reversible, competitive inhibitors of HMG-CoA reductase

140
Q

what are the risks of hypertriglyceridemia and CAD

A

-accumulation of chylomicron remnants
-accumulation of VLDL remnants
-generation of small, dense LDL
-associated with low HDL (poor reverse transport)
-increased coagulability of blood

141
Q

what is the function of Apo A-I

A

activates LCAT; present in chylomicrons and HDL

142
Q

what is the function of ApoE

A

mediates remnant uptake; present in all lipoproteins except LDL

143
Q

what is the function of B 48

A

chylomicron exocytosis; present in chylomicron and chylomicron remnant

144
Q

what are the signs of atherosclerosis

A

chest pain (angina) or tightness, heart attack or stroke

145
Q

what is the cause of atherosclerosis

A

inefficient reverse cholesterol transport –> fatty acid streaks in arteries

146
Q

what is the treatment for atherosclerosis

A

drugs to lower cholesterol (statins, etc.)

147
Q

what is familial hypercholesterolemia

A

genetic disorder

very high LDL cholesterol levels in the blood and early cardiovascular disease. Many FH patients have mutations in the gene for LDL receptor protein, which normally removes LDL from circulation, or for apolipoportein B which is the part of LDL that binds with the LDL receptor

148
Q

what are the signs of familial hypercholesterolemia

A

“xanthomas” (yellowish cholesterol deposits), angina, chest tightness; heart attack or stroke

149
Q

what are the causes of familia hypercholesterolemia

A

loss of function mutation to ApoB100 or to LDL receptor –> inefficient LDL cholesterol transport

150
Q

what is the treatment for familial hypercholesterolemia

A

statins, etc

151
Q

what are the signs of hypertriglyceridemia

A

elevated fasting plasma TG seen in blood

152
Q

what are the causes of hypertriglyceridemia

A

multiple causes, including loss of function mutation of several genes

153
Q

what is the treatment for hypertriglyceridemia

A

niacin to lower TG and statins to lower cholesterol

154
Q

what is Tangier disease

A

near complete absence of HDL

155
Q

what are the signs of tangier disease

A

orange tonsils
lymphadenopathy
heptatosplenomegaly
peripheral neuropathy

156
Q

what are the causes of tangier disease

A

familial genetic mutation of ABCA1 causes failure to load pre-HDL particle w free cholesterol

–> no reverse cholesterol transport
–> cellular accumulation of cholesterol

157
Q

what is the treatment for tangier disease

A

none

158
Q

what is LCAT deficiency

A

lipoprotein cholesterol cannot be processed to cholesterol esters

159
Q

what are the signs of LCAT deficiency

A

corneal clouding, mild anemia, protein in urine, renal failure

160
Q

what are the causes of LCAT deficiency

A

familial genetic mutation to LCAT causes failure to convert free cholesterol to cholesterol esters

–> lipoprotein accumulation of free cholesterol

161
Q

what is the treatment for LCAT deficiency

A

symptom relief: corneal transplant, kidney dialysis

162
Q

what is CETP deficiency

A

a benign condition in which the cholesterol esters formed by LCAT cannot be transferred from HDL to other lipoproteins

163
Q

what are the signs of CETP deficiency

A

elevation of HDL cholesterol but LDL is normal or low

HDL particles are oversized with abundant cholesterol ester and very little triglyceride

164
Q

what doe having a CETP deficiency do for you

A

lowers risk of cardiovascular morbidity and mortality

165
Q

what are the signs of abetalipoproteinemia

A

fat malabsorption –> failure to thrive; steatorrhea (presence of excess fat in feces)

166
Q

what are the causes of abetalipoproteinemia

A

familial genetic mutation to microsomal triglyceride transfer protein (MTTP) –> unable to assemble triglyceride-rich lipoproteins

167
Q

what is the treatment for abetalipoproteinemia

A

dietary restriction on TG; substitute with medium chain fatty acids, linoleic acid, vitamin E

168
Q

describe the 5 hyperlipoproteinemia symptom types

A

1: hyperchylomicronemia –> inherited deficiency of LPL or apoE-II, systemic lupus erythematosus
2: hypercholesterolemia –> primary: familial hypercholesterolemia; secondary –> obesity, poor diet, hypothyroidism, diabetes mellitus, nephrotic syndrome
3: dysbetalipoproteinemia –> elevated chylomicron and VLDL remnants; caused by homozygosity for apoE-2 (does not bind to hepatic apoE receptors)
4: hypertriglyceridemia –> elevated VLDL; caused by diabetes mellitus, obesity, alcoholism, poor dietary habits
5: elevated chylomicrons and VLDL; caused by obesity, diabetes, alcoholism, contraceptives

169
Q

the more visceral fat there is in the body, the more ______ the person is to insulin

A

resistant

170
Q

what are the two most important metabolic regulators

A

insulin and glucagon

171
Q

insulin and glucagon are both secreted by ______

A

pancreas

172
Q

where are insulin and glucagon synthesized in the pancres

A

islets of langerhans

173
Q
A

Principles of Biochemistry (1 decks)

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