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NTR 521- Macro Metab > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

TG digestion in stomach

A

Not a lot
Gastric lipase cleaves 1 FA from sn-3 end
End product: DAG

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2
Q

What 3 components in bile?

A

Bile acids
Cholesterol ester: has fat attached that will be pulled off to digest and make free cholesterol
Phospholipid

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3
Q

TG digestion in Small Intestine

A

CCK stimulates Gb to release bile acids/salts
Pancreatic Lipase- cuts sn-1 and sn3 FAs to make MAG
PL needs colipase and trypsin enzyme needed to make CL

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4
Q

End products/enzyme of phospholipid digestion

A

Lysophospholipid and one FA

Phospholipase A2 is enzyme activated by trypsin and cleaves at an-2

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5
Q

Cholesterol digestion

A

Free cholesterol- none needed

Cholesterol esters broken by cholesterol esterase to make cholesterol and FFA

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6
Q

What structure is formed to get fat through unstirred water layer?

A

Micelles take from lumen to intestinal cells

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7
Q

How are lipids absorbed?

A

Concentration gradient

Esterification in GI happens fast to keep gradient high

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8
Q

What does MTP do?

A

Allows B48 to be lipidated and get into ER to make a CM

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9
Q

What does MGAT do? (ER surface)

A

Attaches a FA to MAG

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10
Q

What does DGAT do? (ER surface)

A

Attaches the 3rd FA onto DAG

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11
Q

What does ACAT do?

A

Attaches FA to cholesterol to make cholesterol ester once inside ER

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12
Q

What does cholesterol/bile acids need to get into GI cell?

A

NPC1L1 and ABST

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13
Q

What is a CM and what is required to form it?

A

It’s a lipid and protein.

You need apoB48, fatty acid, MTP (on the ER surface)
MTP allows B48 and fatty acid to join

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14
Q

What is the difference between MCT and micelle absorption?

A

MCT- direct through GI cell and into hepatic portal vein

Micelle- absorption, esterification in ER, out vescicle, and into lymph

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15
Q

How much fat goes through lymph system and what ones can?

A

About 30% do and only the shorter (up to 12C) can.

95% of fats make it to circulation. It’s bad if they don’t because that means steathorrea.

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16
Q

What are 2 causes of fat being absorbed poorly?

A

Pancreatic insufficiency so need a low fat diet, eat pancreatic enzymes, and take MCT

Abetalipoproteinemia means a MTP mutation so TG buildup at GI and apoB not used so degraded.

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17
Q

What does Orlistat (Xenical and Alli) do?

A

Makes people eat less fat because it stops lipases from working. Only 30% lipids absorbed, wt loss, fatty stools, and liver failure

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18
Q

Where does fat go after small intestine when fed?

A

Small intestine makes TG and CM.
Glucose goes to liver which makes de novo fats, TAG, and VLDL
CM go to lymph then blood and carry the TG in CM and deliver to adipose and muscle, just like VLDL

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19
Q

What do adipose and skeletal muscle do with delivered TG?

A

Muscle- oxidizes for energy, make into TG again and storage
Adipose- reesterify FFA into
tAG and store them.

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20
Q

Where happens to Fat in liver In Fasted state?

A

VLDL made, make TAG, and make ketone bodies.
All 3 carried to skeletal muscle which uses FFA and ketones (oxidized)
Lipolysis of stored IMTG

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21
Q

Where does lipogenesis occur? What is the substrate?

A

Adipose and liver in the cytosol
Does high fat diets make it go less?
The substrate is Acetyl CoA (mitochondria makes pyruvate to Acetyl CoA to Citrate)

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22
Q

What is the link between glycolysis and lipogenesis?

A

Glycolysis makes pyruvate which enters TCA to make citrate which can get into lipid cells and turn into Acetyl CoA and make fats

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23
Q

What are the three main lipogenesis enzymes?

A

Acetyl CoA Carboxylase (ACC)
Fatty Acid Synthase (FAS)
Stearoyl CoA Desaturase (SCD)

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24
Q

What is substrate and end product and regulators of ACC?

A

Stimulated by citrate and insulin high CHO and fat diet (more glycolysis- need more fat storage)
Inhibited by long chain dietary FA and glucagon
End product is Malonyl CoA and regulates B oxidation

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25
What does insulin stimulate that is related to ACC?
It stimulates the transcription factor SREBP that increases ACC then lipogenesis
26
What is the "end product" of lipogenesis?
16:0 | Palmitic acid
27
What is the substrate, job, end product and regulators of FAS?
Malonyl CoA is substrate, end product is 16:0 (then turned into 18:0 by SCD) CHO stimulates and PUFA inhibit Regulated by SREBP (makes Malonyl CoA)
28
What is the regulation, job, and substrate of SCD-1?
If there is more of SCD, then there is a faster reaction Mostly in the liver and adipose Changes stearic to oleic The first double bond goes to the delta 9 position
29
After SCD, what happens to the end product?
``` SCD elongates (16 to 18) and desaturates to 18:1. The 18:1 (9) goes to 18:2 omega 6 or 18:3 omega 3. Desaturases can turn them into EPA and some DHA ```
30
What is the ratio for EPA:DHA and what sources do they come from?
Between 2:1 and 1:2 EPA is only animal sources (salmon, seabass, trout) DHA is only plant foods (algae)
31
Was there a difference when flax and chia were milled versus whole?
Yes, 58% higher ALA and 39% higher EPA in ground chia. | Can't guarantee that the ALA can be turned into EPA so recommend fish for that.
32
What is a general opinion on omega 6 and omega 3 ratio?
Omega 6's are less inflammatory than saturated fat | Omega 3 is still super anti-inflammatory so maybe done worry about those two ratios
33
How do we know the type of fat is important?
Figure shows low fat diets and high fat omega 3 FA diets are insulin sensitive people High fat diet with low omega 3 FA showed insulin resistant people (How the fat hides the receptors)
34
What is one way to tell what FA you're eating in your diet?
Phospholipid membranes shows the diet. The different types can impact cell signaling.
35
Why is shape important?
Unsaturated are rounded so fluid | Saturated are linear so the clump up
36
List the FA synthesis steps and enzymes. What is the main TF regulator?
``` Acetyl CoA (ACC) Malonyl CoA (FAS) Palmitic Acid (SCD) Oleic Acid SREBP-1 is main regulator ```
37
How to SREBPs regulate the lipogenesis enzymes?
SREBP binds SRE on the genes of the enzymes. Binding increases the expression. SREBP stimulated by less fatty acids in the cell.
38
How to ChREBP and SREBP overlap?
C is glucose sensitive and turns CHO in liver to fat. Targets L-PK, ACC, FAS, and SCD. S is fat sensitive (when they are low) and causes liver to make fats. Targets ACC, FAS, SCD. It also can be sensitive to insulin!
39
How do TFs react with high CHO and low fat diet?
Glucose signals ChREBP which upregulates enzymes and lipogenesis. Glucose causes insulin which stimulates SREBP which stimulates glucokinase and makes ChREBP to more lipogenesis. Low fat diet stimulates more SREBP.
40
What happened to pts with 1000 extra kcals from simple CHO for 3 weeks?
27% increase liver fat. | 40 mg/dL TG increase
41
What is the cause of NAFLD?
Too many TG are made in liver (high CHO) but they cannot be exported.
42
What was seen in the low CHO group of the Bazzano study?
They could not stay with 8% CHO Lost some weight Ate more fat and protein
43
What is the primary way to lower high TGs?
Omega-3s because PUFA can block pathways to ChREBP and STEBP so less lipogenesis.
44
How and where does a FA leave the liver?
Leaves in a VLDL and goes into blood then peripheral tissues for energy.
45
What does LPL do?
Hydrolyzes TG to glycerol and FFA. FFA then taken to store in adipocytes or oxidized in ms for energy (Glycerol goes to liver)
46
Where is LPL and when does it work?
Works in a fed state when insulin is present. On the luminal side of GI cell. LPL is high during fasting the the muscle because it still needs energy.
47
When and where does HSL work?
During fasting (glucagon present) to mobilize fat from adipose. HSL is inside the cell and works when insulin isn't present. Break FA to put into circulation.
48
Why can't LPL and HSL work at the same time.
LPL is anabolic and HSL is catabolic. Insulin stimulates one and inhibits the other. (LPL does work in muscle for fasted though)
49
Where and when does Beta oxidation happen. What's the end product?
Mitochondria with 3 enzymes. 2 step process. End of step one is Acetyl CoA.
50
What is step 2 of beta oxidation after Acetyl CoA gets to mitochondria?
3 enzymes take CoA from FA and add carnitine. Then remove carnitine and get to Mito matrix membrane then add CoA back to FA so it can be used for energy.
51
What are the 3 enzymes in beta ox step 2?
CPT 1 Carnitine palmitic carnitine translocase CPT 2
52
What does carnitine supplementation claim to do?
Lowers muscle glycolysis and increase muscle glycogen storage and fat oxidation Allows for fuel selection (use more fat) Ketogenic diet only eat fat so might need to restore carnitine.
53
How is B ox regulated?
Malonyl CoA (produced by ACC in lipogenesis) inhibits by not letting fatty acid CoA enter mito (stops CPT1) Fed state inhibits B ox PPAR increases B ox
54
Why are ketones produced (for what organs) and by what enzyme?
When glucose is not available they are made by HMG CoA synthase for brain and muscle to use.
55
Where are ketones made and where are they used?
Made in the liver but oxidized by brain/muscle. Acetyl CoA is end product and ketones highest in starved state.
56
Why do people with DM have high ketones?
Insulin doesn't work so glucose isn't let into cell and ketones are made for energy.
57
How are MCT absorbed and how does that relate to coconut?
They bypass B ox so metabolized quickly and not stored as fat. It is 6:0-12:0 but coconut is not totally medium (some 14:0).
58
Major downfalls of coconut oil and how to substitute?
Increases LDL worse than PUFA but not as. Ad as butter. | Need to sub for PUFA plant sources (corn, soy, flax)
59
What happens to LPL in adipose and muscle in fed state?
LPL is high km in adipose when fed. Can take up a lot. | LPL is high (low km) in muscle when fasted so that fat can be broken down and used for energy.
60
What can we look at to prove that we eat a lot of omega 6?
Phospholipids. 22.94 percent are linoleic
61
What are the 2 steps of competition between omega 3 and 6?
Esterification and metabolism by COX, LOX, and CYP to become eicosanoids.
62
If you sub PUFA for SFA, what happens?
Lower LDL and lower CVD
63
What is the order of cholesterol intake and packaging?
Eat, made to C, to SI made to CE and pack as CM (B48), to liver made into CE and pack as VLDL (B100), eventually to adrenal cortex/testes/ovaries in LDL
64
How much cholesterol does body make? How is cholesterol output?
1000-1500mg day | Output as bile acids or cholesterol.
65
What is the primary protein that takes up cholesterol from lumen to enterocyte? Protein that excretes into lumen?
NPC1L1 takes up cholesterol. ABCG5/ABCG8 excretes
66
What do lipoproteins have that define their specific identity? Name the kinds on CM, VLDL, LDL and HDL
``` Apolipoproteins woven into surface ApoB48 and E ApoB100 and apoE Only ApoB100 Some have apoA1 ```
67
4 ways cholesterol is made/comes to liver (input)
Biosynthesis (HMG CoA reductase) (statins blocks) Input from CM (GI input) LDL back into circulation HDL back to liver
68
Why is ApoB100 important? (Or ApoE)
It allows binding to LDLR so it can be recycled in liver.
69
What are the steps to LDL uptake in cell?
Endocytosis, vescicle, LDL and LDLR separate, LDLR back to cell surface, LDL fuse with lysosomes, apo and CE degraded, FC and FA made, C made into CE
70
3 main outputs of cholesterol?
Export through ABCG5/G8 Make bile acids (with cholesterol 7a-hydroxylase enzyme) Cholesterol esters made into VLDL or into lipid pool
71
How are bile acids and salts different?
Conjugated (add taurine or glycine) acids become salts.
72
What types of fats increase LDLR activity?
18: 1 oleic 18: 2 corn

NTR 521- Macro Metab (3 decks)

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