Cholesterol & Steroids Flashcards
cholesterol synthesis requires
acetyl CoA, NADPH, & ATP
rate limiting enzyme for cholesterol synthesis
HMG CoA reductase
where does cholesterol synthesis occur
cytoplasm
steps of acetyl coA to HMG coA
2 acetyl CoA to acetylacyl CoA via thiolase. acetylacyl CoA to HMG CoA via HMG CoA synthase
function of HMG CoA reductase
takes HMG CoA to mevalonate. uses 2 NADPH. irreversible step because it releases CoA
inhibitors of HMG CoA reductase
cholesterol, statins, glucagon.
activator of HMG CoA reductase
insulin
explain sterol independent inactivation of HMG CoA reductase
high levels of AMP activate AMPkinase to phosphorylate HMG CoA reductase and render it inactive.
statins are what kind of inhibitors of HMG CoA reductase
competitive
low cholesterol promotes the release of which stimulatory protein
SREBP (causes the liver to produce more HMG CoA reductase)
degradation of HMG CoAR due to high levels of cholesterol or Mevalonate, is done by
proteosomes tagging with ubiquitin
lipoprotein with highest amount of cholesterol
LDL
increases the amount of LDL receptors on the cell surface to lower serum LDL
statins
converts cholesterol to cholesterol ester for storage
ACAT
enzyme needed for double bond formation in the b ring of cholesterol
7-dehydrocholesterol reductase
disorder associated with absent 7-dehydrocholesterol reductase
SLOS- causes severe mental retardation
some cholesterol is modified by bacteria to form
cholestanol & coprostanol
most abundant organic components of bile
PC and bile salts
primary bile acids
cholic acid & chenodeoxycholic acid
rate limiting enzyme for synthesis of bile acids
7-alpha-hydroxlase (puts OH on carbon 7)
7-alpha-hydroxlase is inhibited by
cholic acid
amino acids involved in bile salt formation
taurine and glycine
four functions of bile
eliminates excess cholesterol in feces, prevents gallstone formation, help with digestion of TAGs and help absorb vitamins
rate limiting step for steroid synthesis
conversion of cholesterol to pregnenolone via desmolase (cyp11a, p450)
transports cholesterol into mitochondria
StAR
how does desmolase modify cholesterol in rate limiting step
shortens hydrocarbon chain and hydroxylates steroid nucleus.
what does the rate limiting step of steroid synthesis require
NADPH and O2
hormone secreted from zona glomerulosa
aldosterone
hormone secreted from zona fasiculata
cortisol
hormones secreted from zona reticularis
dihydrotestosterone, estradiol
peptide that signals cortisol release
ACTH
peptide that signals aldosterone release
Ang II or Ang III
peptide that signals estradiol release
FSH
peptide that signals progesterone and testosterone release
LH
how is cortisol transported in the blood
bound to transcortin and albumin
raises bp & fluid volume. increases Na+ reabsorption
aldosterone
precursor to testosterone and estradiol
DHEA, and androstenedione
patient has buffalo hump, hyperglycemia, abnormal hair growth
cushings (too much cortisol)
disorder that is the opposite of cushings
addisons.
CAH that presents with patient unable to make glucocorticoids, mineralocorticoids, and androgens
3-beta-hydroxysteroid dehydrogenase deficiency. (Unable to take pregnenolone to progesterone)
CAH that presents with patient unable to make glucocorticoids and androgens. patient has normal aldosterone
17-alpha-hydroxylase deficiency. (unable to take progesterone to 17-a-hydroxyprogesterone)
CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens
21-alpha-hydroxylase deficiency (unable to take progesterone to 11-deoxycortiocosterone) (unable to take 17-alpha-hydroxyprosterterone to 11-deoxycortisol)
CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens. also have increased deoxycorticosterone
11-beta1- hydroxylase deficiency (unable to take 11-deoxycortisol to cortisol) (unable to take 11-deoxycortiocosterone to corticosterone)
