Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

2.2 Metabolism Biochem > Fat Digestion, Storage, Cholesterol > Flashcards

Fat Digestion, Storage, Cholesterol Flashcards

1
Q

Where does triglyceride metabolism start in the digestive tract?

A

-intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What products initially begin breakdown of lipids?

A
  • liver makes bile for emulsification (micelle formation)

- Pancreas secretes LIPASE and COLIPASE to break down TGs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of Colipase?

A
  • binds Lipase, shifts pH optimum to ~6, allows it to work better
  • also prevents denaturing in bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the function of pancreatic lipase.

A
  • Clips 2 FA off a TG @ positions 1 and 3
  • leaves 2-Monoacylglyerol

-these 2 forms can now cross the intestinal brush border, where they re-form TG in the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the function of Chylomicrons.

A
  • secreted from INTESTINAL EPITHELIUM
  • goes into lymph, enters blood thru thoracic duct
  • carries DIETARY TGs to peripheral tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the causes of steatorrhea and the stool findings?

A
  • decreased bile (TG in shit)
  • decreased pancreatic function (TG in shit)
  • malabsorption (FA in shit)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the GENERAL path of hi glucose to adipose deposition.

A
  • (IN LIVER)
  • hi glucose, hi acetyl CoA
  • excess Acetyl CoA made to FA
  • FA made to TG
  • TG moved in VLDLs to adipose tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What enzyme is key in regulation of FA synthesis?

A

-Acetyl CoA Carboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the requirements for the key enzyme in FA synthesis?

A
  • ATP, Biotin, CO2

- (its 1 of 3 ABC carboxylases!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 enzymes that are ABC carboxylases?

A
  • Pyruvate Carboxylase (gluconeogenesis; pyruvate–>OAA)
  • Acetyl CoA Carboxylase
  • 3rd one, look up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What reaction is key to regulation of FA synthesis?

A

-Acetyl CoA into Malonyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The conversion of Malonyl CoA into FA is regulated by what, and requires what cofactors?

A
  • FA Synthase (no shit!)

- needs NADPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the ONLY fatty acid that can be synthesized by the body from scratch?

A

-Palmitate (16 C, no double bonds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do other fatty acids form from palmitate in the liver?

A

-they are modified by enzymes in the ER that add dbl bonds, or add/delete C’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What two signals stimulate FA synthesis by activating its key enzyme?

A
  • INSULIN induces trascription of Acetyl CoA Carboxylase

- cytoplasmic CITRATE will allosterically activate Acetyl CoA Carboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What product of the TCA cycle must move from the matrix, across the inner mitochondrial membrane, and into the cytosol for FA synthesis to occur?

A

-Citrate!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the pathogenesis of fatty liver in alcoholics.

A

EtOH disrupt assembly of VLDLs in the liver, which results in fatty deposition of TGs+cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lipases and Phospholipases cleave what type of bond on what molecules

A

-cleave ESTER bonds of TGs and phospholipids, respectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Differentiate between Phospholipase A1, A2, and C

A
  • A1 cleaves 1st FA
  • A2 cleaves 2nd FA
  • C cleaves btw DAG and IP3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the difference in cholesterol and cholesterol esters.

A
  • cholesterol (able to be absorbed into mucosa)
  • cholesterol esterases have a FA attached, must be cleaved by PANCREATIC ESTERASE to be absorbed
  • gut cell will reform them into CEs for shipping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What apolipoprotein is essetial for carrying cholesterol ESTERS and TGs from the diet and into the blood?

A
  • Apo B-48

- needed for Chylomicron assembly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What pathology is associated with the essential apolipoprotein for dietary TG and cholesterol transport?

A
  • Abetalipoproteinemia (no B-48)

- AR mutation in MTP gene; failure to thrive, lipid accumulation in enterocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When the chylomicron exits the lymph and enters the blood, what key process occurs?

A
  • the chylomicron gets a gift from HDL

- HDL donates Apo-E and Apo-C to the chylomicron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the process of Chylomicron emptying.

A
  • Apo-C is the trigger for activation of LPL (lipoprotein lipase)
  • chylomicron dumps its passengers into the Adipose tissue via LPL
  • chylomicron re-gifts the Apo-C to HDL
  • now we have a teeny little CHYLOMICRON REMNANT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What apolipoprotein is involved in chylomicron remnant degredation?
-ApoE's function is to allow chylomicron remnant uptake into liver (apoE=EXIT from blood)
26
Describe the process of chylomicron remnant degredation in the liver.
- endocytosis of remnant - endosome+primary lysosome fusion=2 lysosome - enzymes in secondary lysosome break down the little bit of TG and cholesterol esterase left inside
27
For all practical purposes, where do dietary TGs and cholesterol end up?
- dietary TGs to the adipose tissue | - dietary cholesterol to liver
28
What the heck does the liver do with all the FA it made from extra glucose and the cholesterol it got from breaking down chylomicrons?
-it ships it as a VLDL
29
What apolipoprotein is found immediately on a VLDL?
-Apo-B100
30
What apolipoproteins are gifts from HDL to VLDL?
-ApoC and E | just like the gifts from HDL to chylomicrons
31
Chylomicron is to B-48 as VLDL is to?
B-100
32
VLDL is the liver as Chylomicron is to?
-Enterocyte
33
Chylomicron is to Cholesterol Esterase as VLDL is to?
Cholesterol | not esterified to a FA since it comes from liver
34
VLDL is to IDL as chylomicron is to?
chylomicron remnant
35
Describe the 2 fates of IDL.
- can enter liver for degredation (via Apo-E; exit) | - can lose Apo-E and become an LDL
36
How does IDL get cholesterol esterase?
- IDL gives cholesterol to HDL - HDL has Apo-A, which calls LCAT over - LCAT converts cholesterol to CE - CE is given back to IDL - now IDL drops its ApoE and becomes LDL
37
LDL's primary function is what?
-to deliver its cholesterol esterase contents to peripheral tissues
38
Describe the process of LDL dropping off its cholesterol esterases.
- LDL-R binds to SINGLE COPY of Apo-B100 of LDL - endocytosis, clathrin coated pits - lo pH dissoctiates R and LDL, R is recycled - esterase cleaves CE into cholesterol - now cell has higher levels of cholesterol!
39
Cholesterol inside a cell can really screw with the membrane fluidity, so its tightly regulated. What is cholesterol synthesized from (de novo), and what is the key enzyme?
- from Acetyl CoA (from glucose) | - HMG CoA Reductase
40
What 3 processes are affected by hi levels of intracellular cholesterol to prevent accumulation inside the cell?
- inhibit HMG CoA Reductase (block de novo synthesis) - activation of ACAT (esterifies chol with FA, ability to be stored) - inhibition of LDL-R expression (downregulation)
41
What is the difference between LCAT and ACAT?
- LCAT circulates in the blood; interacts with Apo-A on HDL so it can create CE from cholesterol - ACAT is INTRACELLULAR; it creates CE from cholesterol so it can be stored away and do no harm to the cell membrane
42
What familial hyperlipidemia involves a screwed up copy of the LDL receptor?
- Type IIa familial hypercholesterolemia | - no cholesterol in cells, so they start to make it themselves (this exacerbates the hypercholesterolemia!)
43
How does LDL become oxidized LDL (oxLDL)?
- free radicals in the blood from oxygen are floating around looking for electrons - they can grab some e from Apo-B100 on LDL molecules
44
What is the pathological manifestation of oxLDL?
- oxLDL is NOT RECOGNIZED by the LDL-R | - now there is excess LDL in the blood
45
Describe the pathogenesis of a atherosclerotic plaque.
- oxLDL gets into tunica intima via endothelial dmg - scavenger R on Macrophage eats oxLDL since its recognized as foreign - macrophages keep eating oxLDL, become FOAM CELLS - foam cells die, spill out oxLDL, which deposits - get inflammation, process continues (fatty streak)
46
Describe how HDL is a scavenger of cholesterol from peripheral tissue.
- HDL can pick up peripheral cholesterol - will be esterified (due to Apo-A and LCAT in circulation) - CE is then either transferred to IDL, or given back to liver
47
How do antioxidants prevent plaque formation?
- Antioxidants (Vit E, beta carotene) will prevent the oxidation of LDL to oxLDL - no oxLDL=no plaques!
48
Type I familial hyperlipidemia is a defect of what PROCESS?
-defect in Clearing out the Chylomicron/VLDL of their lipid components @ the peripheral tissues
49
Type I familial hyperlipidemia can be a defect in what 2 genes?
- either LPL - or Apo-C -both involved in CLEARING out contents
50
How will a patient present if they have no ability to Clear out their chylomicrons/VLDL @ peripheral tissues?
- red/orange eruptive XANTHOMAS all over body - pancreatitis - fatty liver (hepatosplenomegaly) - hi Chylomicrons, and VLDL (after hi carb meal) - hi blood TG
51
Type IIa familial hyperlipidemia is defect in what gene, and how is it inherited?
- defective LDL receptor | - AD (homozygotes=very bad, hetero=bad)
52
The two big ticket symptoms for a patient presenting with Type IIa hyperlipidemia (aka familial hypercholesterolemia) are?
- Xanthomas of the Achilles tendon (et al) | - Corneal arcus (grey ring around cornea)
53
What apolipoprotein and lipid are elevated in familial hypercholesterolemia, and why?
- hi LDL (duh, no LDL-R) | - hi cholesterol (duh, LDL carries cholesterol esters)
54
The #1 enzyme of cholesterol synthesis is ____________ and where in the cell is it located?
- HMG CoA Reductase | - ER of cell
55
HMG CoA Reductase, along with most reductases, require what?
- NADPH | - this is the source of electrons (reduce=gain of e)
56
What reaction does HMG CoA reductase catalyze?
HMG-CoA --> Mevalonate (aka mevalonic acid)
57
Name some products that come from Farnesyl Pyrophosphate (part of the cholesterol synthesis after HMGCoAR)
- cholesterol (duh) - synthesis of CoQ (ETC) - synthesis of Dolichol PPi (N-glycosylation)
58
Describe Dolichol PPi and its involvement in N-glycosylation.
- proteins being made in ER network - sugars are placed on the N group of Asparagine (hence N glycosylation) - Dolichol PPi is what brings the sugar from the cytosol in the lumen of the ER
59
What are the fates of cholesterol in the body, since it can't be burned to CO2 and water?
- steroid hormone synthesis - membrane component - synthesis of Vit D - bile acid component
60
What is the key enzyme to know in bile acid synthesis (post-cholesterol)?
-7a-hydroxylase
61
Describe the enterohepatic circulation of bile acids and the effects on bile synthesis.
- most bile acids are reabsorbed in the gut - albumin carries them back into the liver - there they inhibit 7a-hydroxylase, which prevents synthesis of extra bile acids
62
What are three substances that negatively influence HMG CoA Reductase?
- cholesterol (via allosteric) - Glucagon (via Pi and reduced gene expression) - Statins
63
What stimulates activity of HMG CoA Reductase?
-Insulin (thru chopping of a Pi)
64
Statin drugs are ___________ inhibitors of HMG CoA R; __________ changes and __________ stays the same
- Competitive - Km changes - Vmax does not change
65
Connect HMG CoA Reductase side effects with its biochemistry.
- Recall: choesterol, CoQ, and Dolichol PPi are all reduced with statins - CoQ is in the ETC (mitochondria); what has tons of mitochondria? MUSCLE AND LIVER -therefore, can get rhabdomyolysis+hi liver enzymes
66
Liver 7a-hydroxylase (invovled in bile acid synthesis) will increase in activity with the administration of what drug?
- Bile acid sequestrants (ex: cholestyramine) | - reduced levels of enterohepatic circulating bile
67
What malabsorptive pathology is associated with the inability to absorb chylomicrons into the lymphatics of the intestinal villi?
Whipple's disease

2.2 Metabolism Biochem (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions