Term
what are the essential fatty acids?
what can they be converted into?
when does the semi-essential FA become essential? |
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Definition
Linoleic Acid
α-linoleic acid
can be converted into a semi-essential FA, arachidonic acid
when linoleic acid is absent in one's diet
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Term
what is arachadonic acid a precursor to?
how do these differ from hormones
name 3 examples |
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Definition
ecosanoids
these are produced in small amounts and act on v. short distances.
not t/p in blood stream
short half life
Thromboxane, Prostaglandins/prostacyclins, Leukotrines |
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Term
what enzyme converts Arachadonic acid to thromboxane?
4 inhibitors |
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Definition
Cyclooxygenase
inhibitors COX1&2
Aspirin
Indomethecin
Phenylbutazone
corticosteroids & celecoxib inhibit COX2 |
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Term
| name 4 promotors of cyclooxygenase |
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Definition
cytokines
endotoxin
GF's
Tumors |
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Term
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Definition
in tissues for maintenance of gastric tissue
renal homeostasis
platelet aggregation |
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Term
where is COX2 made?
in response to what? |
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Definition
in a limited amount of tissues
in response to products of activated immune & inflammatory cells |
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Term
| why would a MI patient rather eat fish oil than seed oil |
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Definition
| the thromboxane produced from fish oil is less potent than that from seed oil, thus less chance of thrombus formation |
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Term
| 4 symptoms of essential FA deficiency |
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Definition
scaly dermatitis (cell membranes need FA's)
hair loss (same as above)
poor wound healing (no thromboxane synth)
infertility, reduced growth, inability to fight infection |
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Term
what is a chylomicron?
what's it's main component? |
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Definition
| it's what carried the FA's through the blood stream, it's made of proteins around the FA's thus it's water soluble |
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Term
what does LPL (lipoprotein lipase) do?
where are they not found in the body?
which one's get stimulated by insulin? |
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Definition
it's what hydrolyzes the FA's from the chylomicrons for intake into various cells (like storage in adipose tissue)
these are not found in the brain / liver.
insulin stimulate the ones on adipose tissue |
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Term
| what's the main component of adipose tissue? |
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Definition
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Term
| what are two advantages to using FA's for stored energy rather than glycogen / starch? |
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Definition
β-oxidation yields more energy
FA's carbon chains can get more reduced
they're hydrophobic so there's no water-weight |
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Term
| what is insulin's effect on adipose tissue after a meal? |
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Definition
LPL (lipoprotein lipase) activity increases
it stimulates adipose tissue to make triglycerides |
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Term
| describe affect of glucagon on adipose tissue |
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Definition
a hormone sensitive lipase cleaves the triglyceride into glycerol & FA's. the FA's get t/p via albumin in blood stream for ATP synthesis etc.
the glycerol gets used in gluconeogenesis |
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Term
name 2 hormones that act through
cAMP & Kinase A |
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Definition
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Term
| name two hormones that stimulate protein stynthesis |
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Definition
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Term
| failure to oxidize FA's would result in what? |
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Definition
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Term
what does carnitine do?
where is it mostly found?
what inhibits it? |
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Definition
needed for t/p of long chain FA's across inner mitochondrial membrane
97% is found in muscle
Malonyl-CoA (intermediate in FA synthesis) inhibits it! |
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Term
what's the rate limiting step for β-oxidation?
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Definition
CPT (carnitine palmitoyl transferase)
it's used to link the carnitine to the acyl for t/p across the mito membrane |
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Term
what's the main function of β-oxidation?
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Definition
to release all the Carbon atoms as Acetyl-Coa to be used in the TCA cycle
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Term
| what does Acyl-Coa Dehydrogenase do? |
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Definition
it makes a double bond in the carbon chain
it's the first step in β-oxidation
it uses the Flava proteins (FAD & FADH) |
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Term
how does the cell break down very long chain FA's?
what are they converted to?
do they yield alot of energy
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Definition
in the peroxisomes they are converted by Acyl-CoA oxidase (instead of Acyl-CoA dehydrogenase)
they're converted to octanoyl-CoA and then passed on to carnitine for t/p into mito for β-oxidation
not as efficient as medium chain FA's |
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Term
| what is zellweger syndrome |
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Definition
| defect in peroxisomes, thus no long chain FA oxidation |
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Term
X-linked Adrenoleukodystrophy
what goes wrong in cells?
what are three symptoms? |
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Definition
can't t/p long chain FA's into peroxisome thus get buildup of them in other places
leads to:
reduction in plasmalogens
adrenocortical insufficiency
white matter abnormalities in cerebrum |
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Term
break down of phytanic acid:
by what process? why?
what are the products? |
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Definition
by α-oxidation, because it has methyl groups that β-oxidation can't handle
products are a
3 Carbon propionyl CoA & Acetyl CoA |
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Term
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Definition
lack the phytanic-oxidase enzyme, thus get accumulation of phytanic acid
neurological disorder
Rx - dietary restriction |
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Term
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Definition
pt lacks the methylmalonic-CoA mutase
also due to lack of Vit B12
the enzyme is needed to oxidase odd chain fatty acids like propionyl-CoA to make succinyl-CoA |
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Term
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Definition
made during FA synthesis
acts as feedback inhibition of FA breakdown |
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Term
when and where are ketone bodies used?
what hormones cause/stop their synthesis? |
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Definition
they are a reserve form of energy for use during starvation states
the brain uses them for energy to spare the glucose for RBC's
epinephrine & glucagon stimulate ketone body formation, insulin stops it |
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Term
what's the precursor for ketone bodies?
where does the ketone body synthesis occur?
what do we measure for in ketoacidosis?
what's the major plasma ketone body? |
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Definition
Acyl-CoA
in the mitochondria
measure acetoacetate in pt's urine (B-hydroxybutyrate is not in the urine)
Beta-hydroxybutyrate
these two are both ketones
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Term
where does acetone come from?
what disease is it associated with? |
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Definition
from spontaneous decarboxylation of acetoacetate
in a diabetic crisis one would smell this on the pt's breath (acidic smell) |
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Term
| what enzyme is needed to use ketone bodies (acetoacetate) |
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Definition
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Term
ketoacidosis:
associated with what disease?
how can we pick it up in our pt?
what happens to their keto bodies? |
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Definition
type I diabetes
fruity odor on breath
ketone bodies lose an H |
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Term
medium chain Acyl-CoA dehydrogenase deficiency
1. name 2 causes
2. name 6 symptoms |
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Definition
1. caused by hypoglycin poison
people w/ 2 copies of a mutant MCAD allele
2. decrease use of FA's as fuel (so don't get ketone bodies for brain to use, or Acetyl-CoA for gluconeogenesis)
more glucose must be oxidized to compensate
omega-oxidation increases
high level of acids in urine
high level of FA's in plasma
fat accumulation in liver |
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Term
Reyes syndrome / SIDS (sudden infants death syndrome)
cause?
symptom?
Rx? |
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Definition
impaired activation of pyruvate carboxylase
ketone body production impaired
Rx - low fat diet, high carb diet
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Term
Carnitine deficiency
7 symptoms
Rx? |
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Definition
low rate of t/p of long chain FA's
high level FA's in blood
hypoglycemia
low ketone levels
muscle weakness / pain
release of myoglobin / CK into blood
impaired gluconeogenisis
Rx - give carnitine |
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Term
what's the rate limiting step for fatty acid synthesis?
what 2 things does this enzyme require? |
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Definition
Acetyl-CoA carboxylase
it also requires ATP & Biotin |
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Term
| Acetyl-CoA carboxylase activity is regulated by: |
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Definition
Activating:
citrate
dephosphorylation due to hormone (insulin)
Inhibiting:
Palmitoyl-CoA allosterically
phosphorylation by a cAMP dependent protein kinase A (due to glucagon / epinephrine)
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Term
what effect does an oxidizing agent have on long chain FA's (LCFA) ?
what's the role of Vit E & Vit C |
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Definition
an oxidizing agent will take a H thus leaving a free radical, so the LCFA takes a H from it's neighbor. keeps going till,
Vit E donates a H leaving itself a radical
Vit C donates a H to Vit E, and then leaves the body. |
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