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
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
3
Q
what are the three major functions of lipids
A
- serve as structural components of biological membranes
- provide energy reserves, mostly in the form of triacylglycerols
- lipids and lipids derivates serve as vitamins and hormones
4
Q
define lipids
A
biological molecules that are insoluble in aqueous solutions but soluble in organic solvents
5
Q
what percentage of the body is triglycerides
A
13%
6
Q
what percentage of the body is membrane lipids
A
2.5%
7
Q
what are simple lipids
A
fatty acids and derivatives; cholesterol
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
9
Q
what are complex lipids
A
contain additional molecular components: carbohydrate, proteins, etc.
10
Q
what are aliphatic lipids
A
straight chain lipids
11
Q
what are polar (amphipathic) lipids
A
contain ionizable/hydrophilic groups like: COO- or NH3+ or PO4- or SO4
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-)
13
Q
what are the major components of lipids
A
- monocarboxylic
- unbranched chain # of carbons: 12-24
- mostly even number of carbons
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
15
Q
what happens to the hydrophobicity of fatty acids as the chain length increases
A
increased
16
Q
which fatty acid configuration is bent
A
cis unsaturated
16
Q
describe the properties of saturated fatty acids
A
no multiple bonds; only single C-C bonds
17
Q
which fatty acid configuration is the most abundant in nature
A
cis-configuration
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
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
20
Q
which fatty acids are nutritionally essential
A
linoleic acid and a-linolenic acid
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
22
Q
describe the omega nomenclature
A
start counting from the opposite end of the COOH group
23
Q
why is the delta nomenclature useful
A
to describe biochemical reactions
24
why is the omega nomenclature useful
to track families of fatty acids in nutrition
25
what is the name of omega 6 fatty acid
linoleic acid
26
what is the name of omega 3 fatty acid
a-linolenic acid
27
why is it that omega 3 and 6 are nutritionally essential
bc animals can't synthesize them and they therefore must be taken from our diet
28
what is oleic acid
omega 9 fatty acid
18:1;9
29
double bonds ________ the melting points of fatty acids
decrease
30
what fatty acids do fats and oils contain that are solid at room temperature
saturated/ trans unsaturated
30
what fatty acids fats and oils contain that are liquid even in the refrigerator
unsaturated fatty acids
31
describe the composition of olive oil
high in long chain unsaturated fatty acids, liquid state at 25 degrees C
32
describe the composition of butter
high in long chain saturated fatty acids that increase its melting point; soft solid at 25 degrees C
33
describe the composition of beef fat
highest portion of long-chain saturated fatty acids; hard solid at 25 degrees C
34
what are acylglycerols
glycerol + fatty acid
35
describe the structure of glycerophospholipids
glycerol backbone
-fatty acid
-fatty acid
-PO4-alcohol
36
describe the structure of sphingolipids
sphingosine
-fatty acid
-PO4-choline
37
describe the structure of sphingolipids
sphingosine
-fatty acid
-mono or oligosaccharide
38
describe the structure of galactolipids
glycerol backbone
-fatty acid
-fatty acid
-mono or disaccharide-SO4
38
what is the importance of carbiolipin
major lipid of inner mitochondrial membrane
38
what are phosphoacylglycerols
polar (amphipathic) lipids
-contain a phosphate group
-contain other ionizable groups
-key components of cell membranes
-used in food industry as emulsifying agents
38
what accumulates to cause Gaucher's disease
glucosylceramide
38
what is the importance of plasmalogens
10% of phospholipid in muscle and nerves
39
what is unique about sphingolipids
do not have the glycerol backbone
39
what is dipalmitoyl phosphatidylcholine
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
39
what are phosphatidylinositol compounds
phosphates added to sugars
-important cellular regulators of receptor-mediated signal transduction, Ca2+ transport, and metabolic events
39
what is the importance of platelet activating factor (PAF)
important in blood coagulation
40
what are steroids
compounds with a four ring structure called the "steroid nucleus" or "steroid skeleton"
41
what is the most abundant sterol in humans
cholesterol
42
what are the functions of cholesterol
component of cell membranes
precursor of bile acids
steroid hormones
vitamin D
43
how does cholesterol play a role in atheroslerosis
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
44
which steroids are produced from cholesterol
estradiol, testosterone, cortisol, progesterone
45
what are eicosanoids
derived from arachidonic acid
46
what is cyclooxygenase
COX enzyme
target of aspirin and non-steroidal anti-inflammatory drugs
47
what is thromboxane A2
stimulates platelet aggregation
raises BP
constricts coronary arteries
48
what is prostaglandin E1
inhibits platelet aggregation
lowers BP
relaxes coronary arteries
49
what are lipoproteins
lipids bound to other molecules
50
how is the lipid bilayer held together
by hydrophobic interaction between the tails of the membrane lipids
50
what forms the structural backbone of the membrane
lipids
51
how do membranes behave at body temperature
like a viscous liquid
52
what governs fluidity of a membrane
unsaturated fatty acid content of phospholipids and their chain length, and by cholesterol content of the membrane
53
saturated fatty acids/cholesterol = ?
more rigid membrane
54
high content of unsaturated fatty acids = ?
more fluid membrane
55
what is the current model of the membrane
fluid mosaic
56
what are the essential features of the biological membrane
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.
57
how are membrane-spanning segments formed
nonpolar alpha helices
58
what is a glycocalyx
the smooth hydrophilic coat of the membrane due to it being surrounded by the carbohydrate tails of glycolipids and glycoproteins
59
what can mechanically damage the membrane
crystalline material
60
what is the biological membrane particularly vulnerable to
to agents that disrupt hydrophobic interactions, like detergents and organic solvents
61
does passive diffusion require a carrier
no
62
does facilitated diffusion require a carrier
yes
63
does primary active transport require a carrier
yes
64
does secondary active transport require a carrier
yes
65
does passive diffusion move against the gradient
no
66
does facilitated diffusion move against the gradient
no
67
does primary active transport move against the gradient
yes
68
does secondary active transport move against the gradient
yes
69
does passive diffusion need metabolic energy
no
70
does facilitated diffusion need metabolic energy
no
71
does primary active transport need metabolic energy
yes
72
does secondary active transport need metabolic energy
yes
73
does passive diffusion require ATP hydrolysis
no
74
does facilitated diffusion require ATP hydrolysis
no
75
does primary active transport require ATP hydrolysis
yes
76
does secondary active transport require ATP hydrolysis
no
77
what is example cargo of passive diffusion
steroid hormones; many drugs
78
what is example cargo of facilitated diffusion
glucose in RBCs and at blood-brain barrier
79
what is example cargo of primary active transport
Na+, K+ ATPase; Ca2+ ATPase
80
secondary active transport
sodium (Na+) cotransport of glucose at kidney and intestine
81
what are pores
allow passage of all small water soluble molecules
82
what are channels
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
what are transporters
aka membrane carriers
work somewhat like channels but undergo conformational changes during the transport cycle
84
how is the energy barrier created in the membrane
there is an energetic cost to losing a shell of hydrogen and moving through the very hydrophobic lipid region
85
how do you bypass the energy barrier?
proteins to facilitate diffusion such as transporters and permeases
86
what are characteristics of carrier-mediated transport
1. substrate-specific
2. saturable
3. can be selectively inhibited
87
when does osmosis occur
when the concentration of the solvent is different on opposite sides of a porous membrane
88
what is osmosis
diffusion of water across a semipermeable membrane
89
what is osmolarity
total concentration of solute particles in a solution
90
what is tonicity
how a solution affects cell volume (when a cell is "bathed in it")
91
how does active transport via atp-dependent transporters work
use the energy in ATP to drive movement of molecules/ions across the membrane
92
what occurs to ATPase ion transporters during the transport cycle
phosphorylated
93
what occurs to ABC during transport cycle
amino acid domains bind ATP
94
what are the structures that make up the sodium-potassium pump
glycoprotein with 2 alpha and 2 beta subunits
95
what are the three types of transporters
1. antiporter
2. symporter
3. uniporter
96
describe the difference between antiporter, symporter, uniporter
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
describe the regulation of intracellular calcium in myocardial cells
cardiotonic steroids reduce the sodium gradient and therefore the effectiveness of the Ca2+/Na+ antiporter in the plasma membrane
98
what percentage of total calories in the western diet is triglycerides
35-40%
99
what is the principal storage form of energy in the body
triglycerides
100
how long can you live without food
52 days
101
what are the 4 steps of fat metabolism
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
which yields more energy, glucose or palmitate
palmitate: 9 cal/g
glucose: 4 cal/g
103
which three fatty acids are most abundant in adipose tissue
1. oleic acid
2. palmitic acid
3. linoleic acid
104
how does fatty acid degradation occur
by removing a carbon at the same end of the chain via "peeling off" and acetyl molecule
105
what is Coenzyme 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
how does fatty acid synthesis occur
carbon chain elongation occurs by adding a carbonyl group to the growing chain
107
how much ATP is produced from beta oxidation
106
108
what do defects in b-oxidation cause
muscle weakness and fasting hypoglycemia
109
carnitine deficiency in the liver leads to _________
hypoketotic hypoglycemia during periods of extended fasting
110
carnitine deficiency in skeletal muscle causes _______
muscle weakness and muscle cramps on exertion
111
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?
generalized carnitine deficiency
112
why does generalized carnitine deficiency cause abundance of fat droplets and fatty degeneration of liver
excess acyl-CoA that cannot be transported into the mitochondrion is diverted into triglyceride synthesis --> fat droplets
113
how does skeletal muscle play into b-oxidation
covers major portion of energy needs from fatty acids at all times
114
how does the liver play into b-oxidation
depends on fatty acids during fasting but not after a mixed meal
115
at what steps does the body regulate fatty acid metabolism
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
what are ketone bodies
water-soluble molecules that contain the ketone groups produced that fatty acids by the liver (ketogenesis)
117
which acids are ketone bodies
acetone, acetoacetic acid, beta-hydroxybutyric acid
118
ketone bodies are readily transported into tissues outside the ______, where they are converted into ______ which then enters the _________________ and is oxidized for energy
liver, acetyl-CoA, citric acid cycle
119
when are ketone bodies produced
during periods of caloric restriction:
- low food intake, carbohydrate restrictive diets, starvation, prolonged exercise, alcoholism, type I diabetes
120
ketone bodies are released into the blood ____ liver _____ stores are depleted
after, glycogen
121
all major nutrients are degraded into ________
acetyl-CoA
122
can fatty acids be converted to glucose?
no!
123
what are the functions of dietary fats
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
what do fatty deposits in adipose tissue provide
1. an easy-to-store concentrated source of energy
2. a protective cushion around body organs
3. an insulating layer beneath the skin
125
what are bile salts
detergent-like substances created from cholesterol in liver and secreted from gallbladder to aid in digestion and absorption of lipids
126
what is a bile salt made up of
bile acid and an associated cation, usually an amino acid (glycocholate, taurocholate)
127
are bile salts amphipathic
yes
128
how does a bile salt make a circular structure around a lipid
it is amphipathic. all water loving particles are on one side
129
how are lipoproteins defined
by density
130
what are chylomicrons
lightest, biggest; carries dietary fat away from intestine
131
what are VLDL
next lightest to chylomicrons (very low density); carries fat away from liver
132
what are HDL
heaviest, smallest; carries the "good cholesterol" to be metabolically changed/eliminated by liver actions
132
what are LDL
the most cholesterol/the "bad" cholesterol; carries cholesterol away from liver --> can form plaques in bloodstream
133
what is Apo C-II
an activator for lipases that hydrolyze triglycerides in lipoproteins
gets in the vicinity of LPL, an activate it
134
what is Apo B-100
protein recognized by the LDL receptor in cholesterol transport
docks on hepatocyte which is upregulated the LDL receptor to catch it
135
what is Apo E
has different allelic variants in humans; one of these (ApoE4) is associated with a higher risk of early-onset Alzheimer's disease
136
free cholesterol regulates its own concentration by action on these three important proteins
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
which lipoprotein is needed for reverse cholesterol transport
HDL
138
how does HDL perform reverse cholesterol transport
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
what are statins
specific, reversible, competitive inhibitors of HMG-CoA reductase
140
what are the risks of hypertriglyceridemia and CAD
-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
what is the function of Apo A-I
activates LCAT; present in chylomicrons and HDL
142
what is the function of ApoE
mediates remnant uptake; present in all lipoproteins except LDL
143
what is the function of B 48
chylomicron exocytosis; present in chylomicron and chylomicron remnant
144
what are the signs of atherosclerosis
chest pain (angina) or tightness, heart attack or stroke
145
what is the cause of atherosclerosis
inefficient reverse cholesterol transport --> fatty acid streaks in arteries
146
what is the treatment for atherosclerosis
drugs to lower cholesterol (statins, etc.)
147
what is familial hypercholesterolemia
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
what are the signs of familial hypercholesterolemia
"xanthomas" (yellowish cholesterol deposits), angina, chest tightness; heart attack or stroke
149
what are the causes of familia hypercholesterolemia
loss of function mutation to ApoB100 or to LDL receptor --> inefficient LDL cholesterol transport
150
what is the treatment for familial hypercholesterolemia
statins, etc
151
what are the signs of hypertriglyceridemia
elevated fasting plasma TG seen in blood
152
what are the causes of hypertriglyceridemia
multiple causes, including loss of function mutation of several genes
153
what is the treatment for hypertriglyceridemia
niacin to lower TG and statins to lower cholesterol
154
what is Tangier disease
near complete absence of HDL
155
what are the signs of tangier disease
orange tonsils
lymphadenopathy
heptatosplenomegaly
peripheral neuropathy
156
what are the causes of tangier disease
familial genetic mutation of ABCA1 causes failure to load pre-HDL particle w free cholesterol
--> no reverse cholesterol transport
--> cellular accumulation of cholesterol
157
what is the treatment for tangier disease
none
158
what is LCAT deficiency
lipoprotein cholesterol cannot be processed to cholesterol esters
159
what are the signs of LCAT deficiency
corneal clouding, mild anemia, protein in urine, renal failure
160
what are the causes of LCAT deficiency
familial genetic mutation to LCAT causes failure to convert free cholesterol to cholesterol esters
--> lipoprotein accumulation of free cholesterol
161
what is the treatment for LCAT deficiency
symptom relief: corneal transplant, kidney dialysis
162
what is CETP deficiency
a benign condition in which the cholesterol esters formed by LCAT cannot be transferred from HDL to other lipoproteins
163
what are the signs of CETP deficiency
elevation of HDL cholesterol but LDL is normal or low
HDL particles are oversized with abundant cholesterol ester and very little triglyceride
164
what doe having a CETP deficiency do for you
lowers risk of cardiovascular morbidity and mortality
165
what are the signs of abetalipoproteinemia
fat malabsorption --> failure to thrive; steatorrhea (presence of excess fat in feces)
166
what are the causes of abetalipoproteinemia
familial genetic mutation to microsomal triglyceride transfer protein (MTTP) --> unable to assemble triglyceride-rich lipoproteins
167
what is the treatment for abetalipoproteinemia
dietary restriction on TG; substitute with medium chain fatty acids, linoleic acid, vitamin E
168
describe the 5 hyperlipoproteinemia symptom types
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
the more visceral fat there is in the body, the more ______ the person is to insulin
resistant
170
what are the two most important metabolic regulators
insulin and glucagon
171
insulin and glucagon are both secreted by ______
pancreas
172
where are insulin and glucagon synthesized in the pancres
islets of langerhans
173
