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132 Cards in this Set

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site of FA synthesis
cytosol
site of FA breakdown
mitochondria
shuttle used in fa synthesis
citrate shuttle
shuttle used in fa breakdown
carnitine shuttle
citrate -> malate -> pyruvate shuttle
citrate shuttle
purpose is to shuttle AcoA to cytoplasm for fa synthesis
citrate shuttle
site of acoA formation
mitochondria via pyruvate dehydrogenase
AcoA + OAA ->
citrate
has ability to cross the membrane in fa synthesis by joining acco to OAA
citrate
once citrate enters cytoplasm from citrate shuttle, it can break down to these....
OAA and AcoA
after OAA is used in citrate shuttle, what does it become and where does it go?
oaa -> malate -> pyruvate and then it reenters the mitochondria (in form of pyruvate)
rate limiting step of f.a. synthesis
AcoA carboxylase
describe steps of fa synthesis
-AcoA enters cytosol via citrate shuttle
-AcoA becomes malonyls CoA and is transferred to FAS (f.a. synthase)
-"OHOT" reactions occurs, and 2 c's of malonlylcoA are added to FA
-FAS is recharged with another malonyl coA and process continues.
normal end product of fatty acid anything
palmitic acid
carbon # of palmitic acid
16
atp's needed for fa synthesis/breakdown
c-1
nadh's needed for fa synthesis/breakdown
c-2
round's needed for fa synthesis/breakdown
c/2 - 1
occurs when atp production gets toogh high, inhibiting pyruvate dehydrogenase and pfk1
shunts to FA synthesis
most # of c's body can make for a FA
16 c's
space between ='s in fa's
3 c's apart
last C with =
C10
no ='s
saturated fa
with ='s
unsaturated FA
shuttles LONG chain fatty acids from cytosol to mitochondria for fa breakdown
carnitine shuttle
needed as cofactor in malonylcoA formation
biotin for AcoA carboxylase
steps of carnitine shuttle
-f.a. is enzymatically attached to carnitine and shuttled across mit. membrance to mitochondria.
-FA's are realeased for B-ox.
defect of carnitine shuttle
adrenal leukodystrophy
steps of beta-oxidation
-series of ox/hydration results in removal of 2-C groups as AcoA
-acoA -> kreb's
-if odd#, converted to propionyl coA and succinyl coA to enter krebs
b-ox yields atps...
1 nadh and 1 fadh2/turn = 5 atp
+ Acoa's that go to kreb's = 10 atp/molecule
odd # FA's become.....in fa breakdown
propionyl coA -> succinyl coA
required with fatty acid breakdown of odd chained fa's
biotin and b12
inhibitor of carnitine shuttle
malonyl coA
stimulated beta oxidation
epi
inhibits beta oxidation
insulin
essential fatty acids
linoeic and linolenic acid
helps form arachodonic acid
linoleic acid
becomes essential if linoleic acid isn't present
arachidonic acid
dependent on essential fatty acids
eiocosanoids
compounds used to form ketone bodies
fatty acids
amino acids
ketones formed from ketogenesis
acetone
acetoacetate
B-hydroxybutyrate
ketone that can penetrate the brain
B = beta hydroxybutyrate
situations when ketone bodies form
prolonged starbation
diabetic ketoacidosis
ketone excretion
urine
rate limiting enzyme of ketogenesis
hmgcoA synthase
atp's needed for fa synthesis/breakdown
c-1
nadh's needed for fa synthesis/breakdown
c-2
round's needed for fa synthesis/breakdown
c/2 - 1
occurs when atp production gets toogh high, inhibiting pyruvate dehydrogenase and pfk1
shunts to FA synthesis
most # of c's body can make for a FA
16 c's
space between ='s in fa's
3 c's apart
last C with =
C10
no ='s
saturated fa
with ='s
unsaturated FA
shuttles LONG chain fatty acids from cytosol to mitochondria for fa breakdown
carnitine shuttle
needed as cofactor in malonylcoA formation
biotin for AcoA carboxylase
steps of carnitine shuttle
-f.a. is enzymatically attached to carnitine and shuttled across mit. membrance to mitochondria.
-FA's are realeased for B-ox.
defect of carnitine shuttle
adrenal leukodystrophy
steps of beta-oxidation
-series of ox/hydration results in removal of 2-C groups as AcoA
-acoA -> kreb's
-if odd#, converted to propionyl coA and succinyl coA to enter krebs
b-ox yields atps...
1 nadh and 1 fadh2/turn = 5 atp
+ Acoa's that go to kreb's = 10 atp/molecule
study ketogenesis on your own
-
study beta oxidation by yourself
-
only 2 organs that can mobilize glycogen into glucose
adrenal cortex
kidney
glycogenesis/lysis occurs here
cytoplasm of muscle, liver, adipose, heart, adrenal cortex
rapidly metabolizes glucose from glycogen during exercise
skeletal muscle
storage depot to maintain blood sugar at appropriate levels
hepatocytes
protein that is a precursor of glycogenesis
glycogenin
sugar carrier used with glycogen synthesis
UDP
rate limiting enzyme of glycogenesis
glycogen synthase
creates alpha 1,4 linkages
glycogen synthase
adds glucose units to nonreducing end of existing alpha 1,4 linkages
glycogen synthesis
transfers 7-glucose long residues from non-reducing ends of chain, creating intenal branches with alpha 1,6 linkages
branching enzyme
branching enzyme
alpha 1,4 - alpha 1,6 glucosyl transferase
allosteric activator of glycogen synthesis
insulin
allosteric inhibitor of glycogen synthesis
glucagon/ epi (inhibits glycogen synthase)
breaks alpha 1,4 linkages until 4c's before branch point
glycogen phosphorylase
breaks alpha 1,4's on branches chain
debranching enzyme
takes off final nub; breaks alpha 1,6 and takes off last glucose
alpha 1,6 glucosidase
coverts glucose-1-ph of glycogenolysis to glucose-6-ph
phosphoglucomutase
glucose-6-ph is coverted to glucose by....., which enters......
glucose-6-phophorylase
glycolysis
instead of alpha 1,6 glucosidase, the heart has.....
alpha 1,4 glucosidase (yields free glucose directly)
abnormal glycogen metabolism leading to accumulation of glycogen within cells
glycogen storage diseases
deficiency of glucose 6 phosphatase
von gierke's type 1
glucose 6 phosphatase deficieny affects these 2 organs
liver
adrenal
3-4 month old with hepatomegaly and hypoglycemia, "doll facies"
type 1 glycogen storage disease = von gierke's
alpha 1,4 glucosidase deficiency
pompe's disease - type 2
glycogen storage disease with earliest death
pompe's
inheritance of glycogen storage disease
AR
acid maltase aka
alpha 1,4 glucosidase
infant with hypertrophic cardiomyopathy, hypotonia, failure to thrive, macroglossia, hs-megaly
pompe's disease - type 2
deficient debranching enzym
cori's disease
debranching enzyme aka...
alpha 1,6 blucosidase
milder form of type 1 with normal blood lactate levels
cori's
on muscle biospy, see many short branches
cori's
deficient skeletal muscle phosphorylase
mcardle's type 5
see high glycogen in muscle, pain in muscles, rhabdomyolysis
marcardle's
sites in body of pentose phosphate pathway
all sites of fatty acid or steroid synthesis -
lactating mammary glands
liver
adrenal cortex
glucose may enter this pathway without any atp use of producation
pentose phosphate pathway
in pentose pathway, nadph produced is used for these function
-fatty acid synthesis
-steroid synthesis
-glutathione reduction
-cytochrome p450
2 products of pentose phophate pathway
NADPH and
Ribose - 5 - ph
an alternative route for glucose oxidation
hmp shunt
hmp shunt occurs here in the cellsis
cytoplasm
2 types of reactions that occur in hmp shunt
oxidative and
nonoxidative
irreversible part of hmp shunt
oxidative reaction where glucose 6 ph -> ribose 5 phosphate
reversible part of hmp shunt
non-oxidative reaction where ribose 5 phosphate makes glyceraldehyde-3p and fructose-6-ph for entry into glycolysis
rate limiting enzyme of hmp shunt
glucose-6-phosphate dehydrogenase
enzyme for non-oxidative part of hmp shunt
transketolases
transketolases require this vitamin to function
thiamine
ribose 5 ph may be used for these pathways
ribose 5 ph -> nucleotide synthesis
g3p & F6p -> glycolytic intermediates
necessary to keep glutathione reduced
nadph
detoxifies free radicals and peroxisomes
glutathione
low nadph in rbc's
causes hemolytic anemia
rbc defense against oxidizeing agents
nadph
sources that may oxidize rbc membranes
fava beans
sulfonamides
primaquine
INH
antimalarials
metronidazole
presents with pallor, hemoglobinuria, jaundice, and could develop after eating beans
g6pd deficiency
prevalent amount mediterranian people
g6pd deficiency
altered hb that precipitates within the rbc
heinz bodies
inheritance of g6pd deficiency
x linked recessive
increased malarial resistance
g6pd deficiency
triglyceride synthesis begins with this compound
glycerol-3-ph
g-3-p in triglyceride synthese originates from these pathways
DHAP - glycolysis
from glycerol - glycerol kinase
backbone for all phospholipids
phosphatidic acid
carrier complex for lipids
CDP
phos. acid + CDP-choline ->
phosphatidyl choline/lecithin
bridges 2 g-3-p
cardiolipin
multiple spontaneous abortions
cardiolipin AD syndrome
physical sign of triglyceridemia
xantholesma
triglyceridemia increases the risk of.....
pancreatitis
mc causes of pancreatitis
alcohol
gallstones
trauma
backbone of sphingolipids
sphingosine
ceramide + udp-glucose ->
cerebroside
ceramide + dolichol ->
ganglioside