Chang Flashcards
(30 cards)
This is the initial acceptor of fatty acids during TAG synthesis
Glycerol Phosphate
This enzyme catalyzes DHAP –> Glycerol Phosphate
Glycerol Phosphate Dehydrogenase
Where is glycerol kinase enzyme present? (Glycerol Phosphate
liver ONLY
This _____ contains a fatty acid and/or a steroid.
lipid
Fatty acids make: ____, _____, ____
triacylglycerol
phospholipid
glycolipid
Triacylglycerol is ____-based.
glycerol
Phospholipids are ____ and ___ based.
glycerol based or sphingosine based
Glycolipids are ___-based
sphingosine-based
Glycerol-based phospholipids are called:
glycerophospholipids (phosphoglycerides)
Phosphoglycerides are formed from:
Phosphatidic acid + alcohol
Common phosphoglycerides
phosphatidyl serine; phosphatidylcholine; phosphaethanolamine; phosphatidylglycerol --> cardiolipin SEGC
Sphingosine based phospholipids: 1) and 2)
Sphingomyelin
Ceramide
Glycolipids (formed from ceramide)
How to degrade sphingomyelin
First understand that serine contributes to making sphingomyelin.
Serine –> Sphingomyelin –> (enzyme: sphingomyelinase, a type of Phospholipase C) ceramide
Ceramide –> (enzyme: ceramidase) free FAs + sphingosine
Nieman Pick Type A or B
Can’t degrade sphingomyelin due to not having sphingomyelinase
- Hepato/splenomegaly
- Cherry red macular spot (accumulation of sphingolipids)
Phosphoglyceride degradation
Phospholipid –> (enzyme: Phospholipase A1, A2, C, or D) Lysophosphoglyceride
A2 can then produce arachadonic acid
Structure of cholesterol
Sterol nucleus (4 rings) with 8-10 C’s at C17 and a hydroxyl at C3 (that’s what a sterol is)
Does most plasma cholesterol exist in an esterified form?
a) Y
b) N
yes
Where is cholesterol made?
all tissues but esp in liver, INTESTINE, adrenal cortex, reproductive tissues, and brain
What is the pathway of cholesterol synthesis?
2 Acetyl CoA –> Acetoacetate –> HMG CoA Reductase –> Mevalonic acid –> 5’ pyrophosphomevalonic acid –> IPP –> DPP –> GPP –> FPP –> Squalene –> Lanosterol –> Cholesterol
If you have a mutation in the enzyme that takes you from lanosterol to cholesterol, this is…
It’s the last precursor sterol.
enzyme: 7-dehydrocholesterol-7-reductase
Results in Smith-Lemli-Opitz syndrome
Pathway of cholesterol BREAKDOWN
1) LDL binds LDL(r)
2) LDL(r) gets internalized and taken up - endosomes/lysosomes
3) Degradation in endo/lysosomes
4) apo-B100 degraded –> amino acids
cholesteryl esters degraded –> Free cholesterol + FAs
5) The free cholesterol moves either to the plasma membrane for membrane synthesis or to the ER to help out with regulation.
6) How does it do this? It downregulates SREBP and increases ACAT1
In this disease, pts do not have functional LDL(R)
familial hypercholesteremia
How can we regulate HMG-CoA-reductase?
1) Sterol-dependent transcriptional regulation:
low cholesterol –> high SREBP2 –> high HMG-CoA-Reductase –> Synthesize more cholesterol and Activate LDL(r) gene
2) Dihydrolanosterol (aka 27-hydroxycholesterol) -> decreases stability of HMG CoA Reductase –> Less cholesterol
3) Sterol-indep phosphorylation –> phosphorylation makes HMGR INACTIVE
4) Hormones –> high insulin = high activity HMGR
5) Drugs –> statins –> inhibit HMGCR
tell me what happens w/statins.
Statins inhibit HMG-CoA Reductase
So low cholesterol –> high SREBP –> increase activity of LDL(R) b/c body thinks more cholesterol is coming –> more cholesterol is taken up –> less cholesterol in the blood
