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Science
Biology
Biochemistry
Cholesterol Metabolism
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Gravity
Block 5
Terms in this set (74)
What is cholesterol a precursor for?
- Bile salts
- Steroid hormones
- Vitamin D
What is need for synthesis of cholesterol to occur?
- A well fed state (both energy and carbon skeletons available)
- Cholesterol supply is low
What molecules synthesize HMG CoA?
Acetyl CoA (3 molecules)
Where does cholesterol synthesis occur?
In the cytoplasm
What is the rate limiting step of cholesterol synthesis?
The conversion of HMG CoA to mevalonate
What enzyme is responsible for the conversion of HMG CoA to mevalonate?
HMG CoA Reductase
What cofactor is required by HMG CoA Reductase?
NADPH
What is needed to make one molecule of cholesterol?
6 molecules of mevalonate
What is needed to make one molecule of mevalonate?
3 molecules of acetyl CoA
How many molecules of acetyl CoA are needed to make one molecule of cholesterol?
18 molecules
What enzyme is responsible for Smith-Lemli-Opitz Syndrome?
7-dehydrocholesterol reductase
(involved in conversion of lanosterol to cholesterol)
In what 3 ways is cholesterol synthesis regulated?
- Influencing the rate of transcription of the HMG CoA reductase gene
- influencing the activity of HMG CoA reductase
- influencing the turnover of HMG CoA reductase
What are 2 ways of enhancing the transcription of HMG CoA reductase gene?
- Via SREBP and SCAP complex
- Via insulin
What occurs between SCAP and sterols when sterol levels are high?
- SCAP binds to sterols and retains the SCAP-SREBP complex on the ER and in the INACTIVE state
What occurs between SCAP and sterols when sterol levels are low?
- SCAP does not bind to sterols
- SCAP-SREBP complex transported to the golgi and modified to an ACTIVE form
- Complex moves to nucleus and binds an SRE (enhancer)
- Increases synthesis of cholesterol
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Why were sulfur and phosphorus used in Hershey's experiment?
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Several different antigens can be detected in blood tests. The following four traits were tested for each individual shown: $$ \begin{array}{ll} \text{ABO type} & \text{$\left(I^{A} \text { and } I^{B} \text { codominant }, i \text { recessive }\right)$}\\ \text{Rh type} & \text{$\left(R h^{+} \text {dominant to } R h^{-}\right)$}\\ \text{MN type} & \text{$(M \text { and } N \text { codominant })$}\\ \text{$\mathrm{Xg}^{(\mathrm{a})}$ type} & \text{$\left(X g^{(a+)} \text { dominant to } X g^{(a-)}\right)$}\\ \end{array} $$ All of these blood type genes are autosomal, except for $\mathrm{Xg}^{(\mathrm{a})},$ which is X linked. $$ \begin{array}{lllll} \text{Mother} & \text{$\mathrm{AB}$} & \text{$\mathrm{Rh}^{-}$} & \text{$\mathrm{MN}$} & \text{$\mathrm{Xg}^{(\mathrm{a}+)}$}\\ \text{Daughter} & \text{$\mathrm{A}$} & \text{$\mathrm{Rh}^{+}$} & \text{$\mathrm{MN}$} & \text{$\mathrm{Xg}^{(\mathrm{a}-)}$}\\ \text{Alleged father 1} & \text{$\mathrm{AB}$} & \text{$\mathrm{Rh}^{+}$} & \text{$\mathrm{M}$} & \text{$\mathrm{Xg}^{(\mathrm{a}+)}$}\\ \text{Alleged father 2} & \text{$\mathrm{A}$} & \text{$\mathrm{Rh}^{-}$} & \text{$\mathrm{N}$} & \text{$\mathrm{Xg}^{(\mathrm{a}-)}$}\\ \text{Alleged father 3} & \text{$\mathrm{B}$} & \text{$\mathrm{Rh}^{+}$} & \text{$\mathrm{N}$} & \text{$\mathrm{Xg}^{(\mathrm{a}-)}$}\\ \text{Alleged father 4} & \text{$\mathrm{O}$} & \text{$\mathrm{Rh}^{-}$} & \text{$\mathrm{MN}$} & \text{$\mathrm{Xg}^{(\mathrm{a}-)}$}\\ \end{array} $$ a. Which, if any, of the alleged fathers could be the real father? b. Would your answer to part a change if the daughter had Turner syndrome (the abnormal phenotype seen in XO individuals)? If so, how?
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