chp 12 Flashcards
(175 cards)
1
Q
What is the main enzyme that digests triacylglycerols in the small intestine?
A
pancreatic lipase
2
Q
What is the role of bile salts in fat digestion?
A
They emulsify dietary fats, increasing surface area for lipase action.
3
Q
Into what products does pancreatic lipase break down triacylglycerols?
A
Fatty acids and monoacylglycerols.
4
Q
What type of cells absorb the products of lipid digestion?
A
Enterocytes
5
Q
How are short- and medium-chain fatty acids transported after absorption?
A
They enter the bloodstream directly and bind to serum albumin for transport to the liver.
6
Q
What happens to long-chain fatty acids inside enterocytes?
A
They are re-esterified into triacylglycerols in the smooth ER.
7
Q
What is a chylomicron composed of?
A
Triacylglycerols, dietary cholesterol, phospholipids, and ApoB-48.
8
Q
What is the function of ApoB-48 in chylomicrons?
A
It is the structural apolipoprotein that helps assemble and stabilize nascent chylomicrons.
9
Q
How do nascent chylomicrons enter the bloodstream?
A
Through the lymphatic system and then into the bloodstream via the thoracic duct.
10
Q
What proteins are transferred to nascent chylomicrons by HDL to make them mature?
A
ApoC-II and ApoE.
11
Q
activates lipoprotein lipase
A
ApoC-II
12
Q
What does lipoprotein lipase do
A
It hydrolyzes triacylglycerols in chylomicrons into fatty acids and glycerol.
13
Q
How are the products of LPL action used in the body?
A
Fatty acids are either stored in adipose tissue or used for energy by muscle; glycerol goes to the liver.
14
Q
How is LPL activity regulated by hormones?
A
Insulin activates LPL in adipose tissue; glucagon activates LPL in skeletal and cardiac muscle
15
Q
lpl in adipose tissue is activated by ?
A
insulin
16
Q
lpl is activates in skeletal and cardiac muscle by ?
A
glucagon
17
Q
What condition results from LPL deficiency?
A
Hypertriglyceridemia (elevated blood triacylglycerols).
18
Q
wt does the insulin do to the hormone sensitive lipase after eating ?
A
inhibits it after eating
19
Q
In fasting/exercise, glucagon or epinephrine
Activates wt ?
A
lipolysis (breakdown of tags to release eenergy )
20
Q
why is tags important ?
A
energy balance and controlling free fatty acid levels
21
Q
wdym by endogenous pathway ?
A
how the liver makes and transport lipids like cholestrol and triglycrides to body using lipoproteins such as VLDL
22
Q
Lpl removes around 90% of TGs in chylomicrons , the remnants are removed from the blood by who and how
A
by liver cells via the binding of ApoE to chylomicron remnant receptors
23
Q
wt are the fates of cholestrol in the liver ?
A
Be esterified (joined with fatty acids) → then packed into lipoproteins (like VLDL) to be transported in the blood.
Be converted into bile acids → which help digest fats in the intestine.
Be secreted directly into bile → and stored in the gallbladder or released into the intestine.
24
Q
when is insulin released ?
A
when blood glucose is high after meals
25
glucagon activates who ?
lipolysis
26
why is Tg cycle imporant
we have always enough fatty acids available when needed
27
wt happens to the excess fatty acids
FFAs are toxic to cells in high levels so the body re-esterifies them (converts them back to TAGS for storage safely in fat cells )
28
tags are made from
fatty acids + glycerol-3-phosphate
29
Fatty acids are released from TAGs into blood by
Glucagon (during fasting)
Epinephrine (during stress or exercise)
Insulin stops this breakdown (because insulin is a storage hormone).
30
VLDL role
delivers tags to tissues especially adipose
31
how do u activate fatty acids
u mix fatty acid with COA + ATP and u get acyl-coA
32
Acyl-COA is added using wt and wt ?
ATP and COA
33
palmitate and oleate helps forming wt
the structurre of membranes (phosphollipids)
34
Glyceroneogenesis
It's making glycerol-3-phosphate (the glycerol backbone for TAGs/phospholipids)
35
wts the thing that makes Glyceroneogenesis unique?
not from glucose or glycerol — instead, from:
Pyruvate
Alanine
Glutamine
Malate
OAA (oxaloacetate)
36
Glyceroneogenesis is important during wt ?
important during fasting or stress when glucose is low but fat synthesis still needs glycerol.
37
wt are the enzymes that play a role in glyceroneogenesis
1- mitochondrial pyruvate carboxylase (PC)
2- cytoplasmic isoform of phosphoenolpyruvate carboxykinase
38
PC AND PEPCK-C are found where ?
adipose tissue and liver and kidneys and mmary glands
39
glyceroneogensis is more active in where more ?
brown adipocytes than in white adipocytes
40
TRIACYLGLYCEROL HYDROLYSIS = Lipolysis
This is breaking down TAGs (fats) into fatty acids + glycerol
41
wt are the hormones that start lipolysis ?
Epinephrine
Norepinephrine
42
ATGL is made more when wt is active ?
PPARγ (a transcription factor) is active
43
who cant use fatty acids for ruel ?
brain and red blood cells thye need glucose or ketones
44
who loves fatty acids and relies on them for most of its energy ?
cardiac muscle
45
fatty acid breakdown takes place where ?
in mitochondria also in peroxisomes for very long fatty acids
46
in b oxidation fatty acids are broken down into wt ?
acetyl-COA
47
in b oxidation it breaks the bond between wt and wt ?
a carbon and b carbon
48
When is the fatty acids synthesized?
happens when nutrients are high esp carbs
49
b oxidation
removes 2 carbon from the carboxyl end , so the b carbon is oxidized and acetyl CoA is released
50
a oxidation is used for wt ?
branched-chain fatty acids (like phytanic acid).
51
how does a oxidation works ?
Removes 1 carbon at a time from the α-carbon (carbon #2 from the carboxyl end).
52
ω-Oxidation (omega oxidation) happens where ?
Happens at the methyl end (ω-carbon, farthest from carboxyl).
53
when is w oxidation used ?
Used when β-oxidation is impaired or overwhelmed.
54
what is b oxidation ?
the process of breaking down fatty acids in the mitochondria to get energy in the form of acetyl-CoA, NADH, and FADH₂
55
regulation of b oxidation in muscles happens more when ?
when energy is needed
56
Stops β-hydroxyacyl-CoA dehydrogenase
NADH
57
Stops thiolase
Acetyl-CoA
58
Blocks CAT-I, so fatty acids can’t enter mitochondria
Malonyl-CoA
59
What is the primary purpose of β-oxidation in cells?
To generate acetyl-CoA, NADH, and FADH₂ from fatty acids for ATP production
60
Before entering the mitochondria, how are fatty acids activated?
Fatty acids react with ATP and CoA to form Acyl-CoA via acyl-CoA synthetase.
61
Why is carnitine needed in β-oxidation of long-chain fatty acids?
The inner mitochondrial membrane is impermeable to acyl-CoA, so carnitine transports fatty acids into the matrix.
61
What enzyme forms acyl-carnitine from acyl-CoA?
Carnitine acyltransferase I (CAT-I)
62
What happens to acyl-carnitine inside the mitochondrial matrix?
CAT-II converts it back to acyl-CoA and free carnitine.
63
Name the 4 main steps of β-oxidation (in order).
Oxidation (acyl-CoA dehydrogenase)
Hydration (enoyl-CoA hydratase)
Oxidation (β-hydroxyacyl-CoA dehydrogenase)
Cleavage (thiolase)
64
Which coenzymes are reduced during β-oxidation?
FAD → FADH₂ and NAD⁺ → NADH
65
What is the final product of each β-oxidation cycle?
1 Acetyl-CoA, 1 FADH₂, and 1 NADH
66
What molecule inhibits CAT-I and prevents β-oxidation?
Malonyl-CoA
67
Which molecules inhibit enzymes during β-oxidation?
NADH inhibits β-hydroxyacyl-CoA dehydrogenase
Acetyl-CoA inhibits thiolase
68
Palmitoyl-CoA oxidation gives
108 ATP But 2 ATP are used to activate fatty acid → net is 106 ATP
69
How much ATP is produced per carbon atom in palmitic acid?
106 ÷ 16 = 6.6 ATP per carbon
70
How does glucose compare to palmitic acid in energy yield per carbon?
Glucose gives 5 ATP/carbon; palmitic acid gives more because it's more reduced.
71
Where does peroxisomal β-oxidation occur and for which fatty acids?
In peroxisomes, for very long-chain fatty acids
72
What is the role of peroxisomal β-oxidation?
It shortens long fatty acids to medium-chain fatty acids to be sent to mitochondria for full oxidation.
73
Is ATP produced directly in peroxisomal β-oxidation?
no
74
What enzyme catalyzes the first oxidation step in peroxisomes?
Acyl-CoA oxidase, which sends electrons to O₂, making H₂O₂
75
What detoxifies H₂O₂ in peroxisomes?
Catalase breaks it down to water (H₂O)
76
What other enzymes are used in peroxisomal β-oxidation?
Enoyl-CoA hydratase
3-hydroxyacyl-CoA dehydrogenase
β-ketoacyl-CoA thiolase
77
What is the purpose of ketogenesis?
To manage excess acetyl-CoA during fasting or diabetes, converting it to ketone bodies.
78
What are the 3 ketone bodies?
Acetoacetate
β-hydroxybutyrate
Acetone
79
Where are ketone bodies produced?
In the liver mitochondria
80
What enzyme condenses 2 acetyl-CoA molecules into acetoacetyl-CoA?
Acetoacetate-CoA thiolase
81
What enzyme forms HMG-CoA from acetoacetyl-CoA and another acetyl-CoA?
HMG-CoA synthetase
82
What enzyme breaks HMG-CoA into acetoacetate and acetyl-CoA?
HMG-CoA lyase
83
How is β-hydroxybutyrate formed?
By reducing acetoacetate
84
How is acetone formed?
By spontaneous decarboxylation of acetoacetate when its concentration is high
85
What is ketosis and when does it happen?
Ketosis is ketone body production during starvation or uncontrolled diabetes. If excessive, it causes ketoacidosis.
86
Which tissues use ketone bodies?
Cardiac and skeletal muscle
Brain (after prolonged fasting)
Enterocytes and adipocytes
Muscles also use it to save protein
87
ketogenesis takes place in ?
matrix of liver mitochondria
88
What is the final product of odd-chain FA β-oxidation?
1 Acetyl-CoA + 1 Propionyl-CoA
89
What happens to Propionyl-CoA?
It's converted to Succinyl-CoA, a TCA cycle intermediate.
90
Why does oxidation of unsaturated fatty acids require extra enzymes?
Because their cis double bonds interfere with β-oxidation, and must be converted to trans.
91
What enzyme helps convert cis-β,γ bonds to trans-α,β bonds?
Enoyl-CoA isomerase
92
What does enoyl hydratase do in unsaturated FA oxidation?
Hydrates the trans-α,β double bond to allow β-oxidation to continue.
93
Example of a monounsaturated FA and how it’s oxidized?
Oleic acid — undergoes 3 cycles of β-oxidation, then requires enoyl-CoA isomerase to convert its Δ³-cis bond to trans-Δ².
94
What enzyme converts Propionyl-CoA to D-methylmalonyl-CoA?
Propionyl-CoA carboxylase (needs biotin)
95
How is D-methylmalonyl-CoA converted to L-methylmalonyl-CoA?
By Methylmalonyl-CoA racemase
96
What enzyme converts L-methylmalonyl-CoA to Succinyl-CoA?
Methylmalonyl-CoA mutase (needs vitamin B₁₂)
97
Where does α-oxidation occur in humans?
In peroxisomes
98
Why can't phytanic acid undergo β-oxidation directly?
Because of a methyl group on the β-carbon (C-3) blocking the reaction.
99
What is the first step in phytanic acid oxidation?
Conversion to α-hydroxyphytanoyl-CoA by phytanoyl-CoA hydroxylase (needs O₂, Fe²⁺, ascorbate)
100
What happens to α-hydroxyphytanoyl-CoA?
It’s decarboxylated to pristanal
→ by α-hydroxyphytanoyl-CoA lyase (needs TPP)
101
How is pristanal further processed?
Converted to pristanic acid by aldehyde dehydrogenase
Needs NADP⁺
102
What happens to pristanic acid?
It undergoes β-oxidation after esterification with CoASH
103
What are the final products of pristanic acid oxidation?
3 Acetyl-CoA
3 Propionyl-CoA
1 Isobutyryl-CoA
104
Where does fatty acid biosynthesis mainly occur in the body
In the cytoplasm, mainly in the liver
105
What triggers fatty acid synthesis?
When the diet is low in fat and high in carbohydrates or protein.
106
How many Acetyl-CoA, NADPH, and ATP are needed to make palmitate (16C fatty acid)?
8 Acetyl-CoA, 14 NADPH, 7 ATP
107
What are the four sources of NADPH used in synthesis?
Pentose phosphate pathway
Isocitrate dehydrogenase (2 & 3)
Malic enzyme
Aldehyde dehydrogenase (omega & alpha oxidation)
108
Where does fatty acid synthesis occur in the cell?
In the cytoplasm.
109
What enzyme complex is used for synthesis?
Fatty acid synthase.
110
What are the two phases of fatty acid synthesis?
Carboxylation of Acetyl-CoA → Malonyl-CoA
Sequential 2C additions to grow the fatty acid chain
111
What enzyme catalyzes the carboxylation of Acetyl-CoA?
Acetyl-CoA carboxylase (ACC)
112
What coenzyme does ACC need?
Biotin
113
What are the 3 domains of ACC?
BCCP (biotin carboxyl carrier protein)
BC (biotin carboxylase)
CT (carboxyltransferase)
114
Where is ACC1 found and what does it do?
In lipogenic tissues (liver, adipose, mammary glands) → for synthesis.
14. Where is ACC2 found and what does it do?
115
Where is ACC2 found and what does it do?
In oxidative tissues (heart, skeletal muscle) → regulates oxidation by inhibiting CAT-I.
116
What activates ACC allosterically?
Citrate
117
What inhibits ACC allosterically?
almitoyl-CoA (causes depolymerization)
118
What inhibits ACC by covalent modification?
Phosphorylation by AMPK
PKA (via cAMP)
Glucagon and epinephrine (inhibit PP2A)
119
What activates ACC by covalent modification?
Insulin (via PP2A dephosphorylation)
120
fatty acid synthesis takes place in ?
cytoplasm , liver is the mjor site for this process
121
What is the role of ACP in fatty acid synthesis?
CP (acyl carrier protein) holds and transfers growing fatty acid chains using a flexible arm with a phosphopantetheine group
122
What’s the first step of fatty acid synthesis?
Transfer of an acetyl group (from acetyl-CoA) and a malonyl group (from malonyl-CoA) to ACP.
123
Which enzyme transfers acetyl and malonyl groups to ACP?
Malonyl/acetyl transferase (MAT).
124
What does KS (β-ketoacyl synthase) do?
Catalyzes condensation between acetyl and malonyl groups, forming acetoacetyl-ACP.
125
What’s the role of KR (β-ketoacyl-ACP reductase)?
Reduces acetoacetyl-ACP to β-hydroxybutyryl-ACP using NADPH.
126
What does DH (β-hydroxyacyl-ACP dehydratase) do?
Removes water (dehydration) from β-hydroxybutyryl-ACP to form crotonyl-ACP.
127
Where does fatty acid elongation and desaturation occur?
In the cytoplasm or from the diet, primarily by ER enzymes.
128
Why is fatty acid elongation and desaturation important?
Regulates membrane fluidity
Produces fatty acid precursors like eicosanoids and myelin lipids.
129
How does cold temperature affect fatty acids?
It increases unsaturation to maintain membrane fluidity.
130
What does ER fatty acid chain elongation require?
Malonyl-CoA, NADPH, and cycles of condensation, reduction, dehydration, and reduction
131
What are the intermediates in ER elongation?
They are CoA esters, not a large multienzyme complex
132
What cofactors are needed for fatty acid desaturation?
NADH and O₂.
133
What enzymes are involved in desaturation?
Cytochrome b5 reductase and oxygen-dependent desaturases.
134
What is the connection between elongation and desaturation?
They work together to produce polyunsaturated fatty acids like arachidonic acid from linoleic acid.
135
Q: Where does fatty acid β-oxidation occur?
In the mitochondria.
136
Where does fatty acid synthesis occur?
In the cytoplasm.
137
What are the substrates for β-oxidation?
Acyl-CoA, FAD, NAD⁺, CoASH.
138
What are the products of β-oxidation?
Acetyl-CoA, FADH₂, NADH.
139
What are the substrates for fatty acid synthesis?
Acetyl-CoA, NADPH.
140
What are the products of fatty acid synthesis?
Palmitate, NADP⁺, CO₂, CoASH.
141
What happens in the REDOX step of β-oxidation?
FAD and NAD⁺ are reduced to FADH₂ and NADH.
142
What does HYDRATION do in β-oxidation?
Converts enoyl to hydroxyacyl intermediate.
143
What is the role of DEHYDRATION in fatty acid synthesis?
Converts hydroxyacyl to enoyl.
144
What is the role of NADPH in synthesis?
REDOX—reduces keto and enoyl intermediates.
145
What regulates β-oxidation when energy is high?
NADH and acetyl-CoA inhibit β-HADH and thiolase.
146
What does malonyl-CoA inhibit?
CAT-I (Carnitine Acyltransferase I), blocking fatty acid entry into mitochondria.
147
What is the effect of high insulin/glucagon ratio on β-oxidation?
Increases malonyl-CoA → inhibits β-oxidation
148
What does AMPK do?
Inhibits fatty acid and TAG synthesis by phosphorylating ACC1 and glycerol-3-phosphate acyltransferase.
149
What activates AMPK?
High AMP levels (low energy status).
150
What does AMPK activation do to malonyl-CoA?
It activates malonyl-CoA decarboxylase (MCD), reducing malonyl-CoA levels and relieving inhibition of β-oxidation.
151
What pathways does AMPK promote?
Catabolic pathways like β-oxidation and glycolysis.
152
How does insulin affect ACC1?
Activates phosphoprotein phosphatase 2A, which dephosphorylates and activates ACC1.
153
How does insulin promote fatty acid synthesis?
By activating ATP-citrate lyase and pyruvate dehydrogenase in adipocytes.
154
How does insulin inhibit lipolysis?
By phosphorylating and inhibiting hormone-sensitive lipase
155
How does epinephrine affect lipolysis?
A: Stimulates hormone-sensitive lipase via phosphorylation, increasing lipolysis.
156
How does glucagon increase fatty acid oxidation?
Possibly by activating CAT-I (mechanism not fully understood).
157
What are the two main transcription factor families in lipid regulation?
SREBPs and PPARs.
158
What is SREBP-1c’s role in metabolism?
Upregulates genes for fatty acid synthesis and NADPH production in response to insulin
159
What inhibits SREBP-1c?
Glucagon and long-chain fatty acids.
160
Q: What does SREBP2 regulate?
Genes involved in cholesterol metabolism.
161
What activates PPARα and what does it do?
Activated by fasting; promotes fatty acid oxidation and ketogenesis
162
What does PPARγ do?
Promotes fat storage and glucose uptake in adipose tissue (works with insulin and SREBP1).
163
What stimulates PPAR activity?
Lipid molecules like saturated/unsaturated fatty acids and prostaglandins.
164
What does ChREBP do?
In response to glucose, promotes enzymes that convert excess sugars into fatty acids (e.g., ACC, fatty acid synthase).
165
Q: Where does phospholipid synthesis occur in eukaryotic cells?
A: At the interface of the smooth endoplasmic reticulum (SER) and cytoplasm.
166
Q: Why does the fatty acid composition of the SER membrane change?
A: To increase membrane fluidity by replacing saturated fats with unsaturated ones through phospholipases and acyltransferases.
167
How is phosphatidylethanolamine (PE) synthesized?
Ethanolamine is phosphorylated → reacts with CTP → forms CDP-ethanolamine → reacts with diacylglycerol → forms PE.
168
Q: How is phosphatidylcholine (PC) synthesized?
Choline is phosphorylated → reacts with CTP → forms CDP-choline → reacts with diacylglycerol → forms PC.
169
Q: How else can PC be synthesized?
A: From PE via methylation (3 steps) by phosphatidylethanolamine-N-methyltransferase using S-adenosylmethionine (SAM) as a methyl donor.
170
Q: How is phosphatidylserine (PS) formed in animals?
A: By reaction of CDP-diacylglycerol with serine in the SER.
171
Q: How can PS be converted to PE?
A: Through decarboxylation of PS in the mitochondria.
172
Q: What is phospholipid turnover?
A: It is rapid, meaning phospholipids are constantly synthesized and degraded.
173
Q: What do phospholipases do?
A: Degrade phosphoglycerides by cleaving specific bonds.
174
Q: What are the roles of phospholipases A1 and A2?
A1 hydrolyzes ester bond at C-1
A2 hydrolyzes ester bond at C-2
