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fat synthesis Flashcards

(104 cards)

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1
Q

3 questions to ask

A

do you have enough energy
do you have enough stored carbs
what should i do now

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2
Q

Fatty acid synthesis

A

you build fatty acids when you consume excess carbs

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3
Q

when dont you build fatty acids

A

when you consume excess fats

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4
Q

how does glucose get in the cell

A

it does not diffuse in the cell directly

2 transport mechanisms

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5
Q

what are the 2 transport mechanisms for getting glucose into the cell

A

sodium independently facilitated transport system

sodium monosaccharide co transport system

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6
Q

sodium independently facilitated transport system

A

glucose transporters GLUT

moves down the concentration gradient

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7
Q

sodium monosaccharide co transport system

A

ATP dependent
transports glucose AGAINST concentration gradient
epithelial cells of intestine, renal tubules and choroid plexus

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8
Q

What are two glucose transport proteins

A

GLUT 2

GLUT 4

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9
Q

glucose galactose and fructose
dietary glucose- out of the intestine (into the blood)
into the liver, kidney, pancreas B-cells
insulin independent

A

GLUT 2

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10
Q

glucose into muscle and adipose tissue
stimulated by insulin
stimulated by low energy charge (AMPkinase)
facilitated diffusion

A

GLUT 4

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11
Q

what are glucose transport statistics

A

in the absense of insulin only 5% of the total transporter pool is found on the cell surface
exercise or insulin result in a 10fold increase in glucose uptake in skeletal muscle
about 90% of insulin stimulated glucose uptake occurs in skeletal muslce
adipose tissue only accounts for 10% of insulin stimulated glucose uptake

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12
Q

what does exercise increase the number of

A

increases the number of GLUT 4 proteins in skeletal muscle

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13
Q

what does exercise stimulate the accumulation of

A

GLUT 4 in the cell membrane for 1-2 hours after exercise

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14
Q

what happens when adding a phosphate to glucose do

A

the glucose concentration in muscle remains low and glucose keeps coming

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15
Q

where is glucose

A

in the blood

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16
Q

what happens when muscle energy is low

A

glucose 6 phosphate runs through glycolysis prep step and krebs to make ATP

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17
Q

what happens when glycogen is low

A

glucose 6 phosphate is converted to glycogen

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18
Q

eating carbs does what

A

elevates blood glucose

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19
Q

when having a elevated blood glucose what happens

A

elevated insulin is caused

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20
Q

what happens with a elevated insulin

A

fat and muscle glucose transport

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21
Q

is the muscle full of glycogen after fat and muscle glucose transport

A

NO glucose is stored as glycogen

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22
Q

is the muscle full of glycogen after fat and muscle glucose transport

A

YES glucose goes to the liver

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23
Q

how does glucose enter the muscle

A

via facilitated diffusion

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24
Q

what does high energy and plenty of glycogen stores inhibit

A

PFK

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25
when PFK is inhibited what does it cuase glucose 6 phosphate to do
accumulate and inhibit hexokinase
26
what does higher glucose concentration in muscle inhibit
inhibits facilitated diffusion of glucose
27
glucose goes to the liver
glucokinase
28
glucokinase
lower affinity stimulated by insulin not inhibited by product
29
glucokinase does what
runs glycolysis
30
glycolysis runs for
energy and raw material
31
glucose goes to the liver ultimately for
fat building
32
glucokinase
lesser affinity for glucose not inhibited by its product stimulated by insulin stimulated by fructose
33
what does a increase of glucose satisfy
satisfies the low affinity of glucokinase
34
what is the liver a primary site for
for fructose metabolism
35
what does the liver express
frutokinase and triokinase
36
what does fructose stimulate
stimulates glucokinase
37
what is the liver a primary site for
fructose disposal
38
what are the enzymes essential for fructose metabolism and are highly expressed in the liver
fructokinase triokinase limited expression in muscle and adipose tissue
39
where is the fructose 1 phosphate pathway
in the liver
40
what is the entry point into glycolysis
glyceraldehyde 3 phosphate
41
what does a low dose of fructose cause
causes a 3fold increase in net liver glycogen synthesis
42
what do smaller amounts of fructose cause
causes the release of glucokinase from a regulatory protein
43
what does not inhibit glucose 6P
glucokinase
44
acetyl CoA to
FAT
45
where does fructose enter at
DHAP G3P
46
what does F6P normally binds to the regulatory protein and what is inhibited
glucokinase
47
F1P binds to the regulatory protein and GK is
set free and activated
48
fructose and fat the liver preferentially takes
in fructose
49
the liver has more what
fructokinase and triokinase enzymes
50
what does fructose stimulate
GK
51
what does fructose and fat produce
more acetyl CoA and ATP | building blocks and energy for building fatty acids
52
excess carbs and protein in the diet do what
synthesize FA | store as TAG
53
where is the pathway primarily
LIVER lactating mammary glands adipose tissue
54
what is the FA synthesis location
cytosol Beta oxidation
55
Building fat
Eating carbs raise blood glucose insulin is secreted glucose enters the cells
56
energy requiring
ATP
57
reduced conenzyme
nicotinamide adenine dinucleotide P (NADPH)
58
acetyl CoA supplies
carbons for the FA chain glycolysis>pyruvate>acetly CoA AA catabolism
59
Acetyl CoA needs to get to the matrix to the cytosol is a
problem
60
high sugar intake increases what
ATP production
61
what can the acetyl portion of acetyl CoA can be transported as
citrate into the cytosol
62
why do we need high energy
to build fat
63
citrate is where
in the inner mitochondrial membrane
64
citrate to acetyl CoA by
ATP added to ADP+Pi citrate lyase CoA added
65
carboxylation of acetyl CoA
acetyl CoA to malonyl CoA y acetyl CoA carboxylase coenzyme biotin
66
malonyl CoA inhibits what
CPT I and fat burning
67
what does the reaction of acetyl CoA and Malonyl CoA also require
CO2 | ATP
68
synthesis of malonyl CoA
acetyl CoA to Malonyl CoA by acetyl CoA carboxylase conenzyme biotin
69
what is the rate limiting and regulatory step of FA synthesis
acetyl CoA carboxylase ACC
70
Short term regulation of ACC inactive is a what
a protomer=subunit | polymerization= combining subunits
71
what is short term regulation of ACC activated by
citrate
72
what is short term regulation inactivated by
long chain fatty acyl CoA | end product=depolymerization
73
acetyl CoA carboxylase regulation is stimulated by
citrate | insulin
74
acetyl CoA carboxylase regulation is inhibited by
malonyl CoA palmitate-end product epineprine glucagon
75
metformin and type 2 diabetes
inhibtion of ACC activates AMPK inhibits ACC and fatty acid synthase lowers blood glucose
76
the reaction all part of fatty acid synthase the next four steps
condensation reduction dehydration reduction
77
condensation is Acetyl ACP and Malonyl ACP to?
Acetoacetyl ACP by beta ketoacyl ACP synthase
78
REduction Acetoacetyl ACP to D 3 hydroxybutyryl ACP by
beta ketoacyl ACP reductase
79
synthesis
``` cytosol acyl carrier protein adding 2 carbon units malonyl ACP NADPH consuming ATP ```
80
degradtion
``` Mitochondria Coenzyme A donating 2 carbons units acetyl CoA NADH FADH2 Making ATP ```
81
conditions that stimulate
``` high energy charge increased acetyl CoA increased NADH and FADH2 increased citrate increased sugar (glucose fructose) insulin ```
82
key enzymes
citrate lyase acetyl CoA carboxylase fatty acid syntase CRDR
83
TAG synthesis in the what
mitochondria
84
elongation is accomplished through
elongases and requires NADPH
85
desaturation is accomplished through
desaturates by adding double bonds
86
what are separate enzymatic processes
mitochondria | smooth ER
87
what can humans not create
double bonds beyond the 9-10th carbon
88
NADPH where does it come from
pentose phosphate pathway | malate-pyruvate in cytosol
89
NADPH source of electrons in?
synthesis
90
Fatty acids are what kind of molecules
highly reduced | remember reduction is gain of hydrogen and electrons
91
dehydraton D3 hydroxybutryrl ACP to Crotonyl ACP
by beta hydroxyacyl ACP dehydratase remove H2O
92
reduction 2 by Crotonyl ACP to Butyryl ACP by
Enoyl ACP reductase
93
Palmitate (16:0) when does this process stop
when we have 16 carbon palmiate
94
fatty acid synthesis
reduction dehydration reduction
95
fatty acid synthase
``` CRDR Condenses-adds molonyl CoA Reduces- with NADPH Dehydratase Reduces- with NADPH ```
96
release the fatty acid
palmitoyl thioesterase last step of FAS cleaves thioester bond and releases saturates palmitate
97
``` Update: Butyryl last 3 carbons are? still attached to? Transfer the butyryl chain to the what site? add another? when does growth stop ```
``` (4 carbons) hydrogen saturated ACP holding site (cysteine) add malonyl CoA and repeat at 16 carbons of palmitate ```
98
long term regulation ACC | high calorie/high carb diet
increase ACC synthesis which increase FA synthesis
99
long term regulation ACC | low calorie/ high fat diet
decrease ACC synthesis which decreases FA synthesis
100
long term regulation ACC | upregulated by insulin
increased response/increased receptors | increase ACC synthesis which increase FA synthesis
101
multi enzyme complex is
FA synthesis | one portion of the molecule is ACP
102
one portion of the molecule is ACP
acyl carrier protein ACP similar to coenzyme A terminal thiol group at the end of an arm
103
short term regulation of ACC | reversible phosphorylation
AMP- activated protein kinase AMPK- phosphorylates and inactivates ACC
104
short term regulation of ACC | reversible phosphorylation
can be activated by cAMP dependent PKA epinephrine and glucagon increase cAMP which phosphorylates and inactivates ACC insulin dephosphorylates and activates ACC

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