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Block 3; Week 4 Michelle > Mastick Lipids > Flashcards

Mastick Lipids Flashcards

1
Q

What are 3 predominant chronic diseases of our time? What is their common thread?

A

Obesity
Heart Disease
Type II Diabetes
**common thread: insulin resistance

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2
Q

What are diabetic complications caused by high lipids?

A

heart disease & stroke

high blood pressure

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3
Q

What was Mastick’s good, hopeful news for us?

A

If blood glucose & lipid levels are kept in check, all of these complications & diseases we have been talking about are preventable!!

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4
Q

When do we normally see life-threatening hypoglycemia?

A

Type I Diabetics w/o insulin injections

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5
Q

Which tissues don’t have glucagon receptors?

A

muscles & adipocytes

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6
Q

What happens to glucagon & insulin after a high protein meal?

A

They both rise.

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7
Q

There are four major forms of familial hypercholesterolemia. They are all single gene causes. What are they?

A

LDLR
APOB
PCSK9
LDLRAP1

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8
Q

Which of the 4 FH mutations is autosomal recessive? Note: the rest are all autosomal dominant

A

LDLRAP1 is the only one that is autosomal recessive

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9
Q

What’s the deal with LDLR?

A

This stands for low density lipoprotein receptor
loss of function mutation
prevents the LDL receptors from doing their thing–or they are just absent.

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10
Q

What’s the deal w/ APOB?

A

The ApoB-100 apolipoprotein is defective on LDL. This prevents it from binding the LDLR properly.
this is considered a receptor binding site mutation

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11
Q

What’s the deal w/ PCSK9?

A

gain of function mutation
this has the fcn of down regulating the LDL receptors
*this mutation enhances that activity

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12
Q

What’s the deal w/ LDLRAP1?

A

loss of fcn mutation
this is a mutation of the adaptor proteins
these adaptor proteins are supposed to bind to the cytosolic side of the LDLR to create a Clathrin coat. The Clathrin coat is necessary for the endocytosis of LDL.
**with this mutation–>that can’t happen

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13
Q

What is the definition of general familial hypercholesterolemia?

A

disorder that causes severe elevations in total cholesterol & LDL

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14
Q

Describe the LDL receptor.

A

it is transmembrane
internalizes LDL via endocytosis
primary way to deal w/ cholesterol
the LDL goes to lysosomes & is degraded into AA & cholesterol

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15
Q

Describe how PCSK9 works.

A

This down regulates LDLR. So it binds LDLR & then degrades it in lysosomes…
When highly active, like in the mutated form, there just aren’t LDLR at the cell surface.

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16
Q

What are the 4 main types of lipid-lowering drugs?

A

Statins
Fibrates
Niacin
Ezetimibe

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17
Q

How do statins work?

A

Statins inhibit HMG CoA reductase. This reduces the levels of cholesterol in hepatocytes. With the low cholesterol, the hepatocytes up regulate their LDL receptors. This has the overall effect of lowering lipid levels.

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18
Q

How do fibrates work?

A

they bind to transcription factor PPAR alpha. This alters the gene expression in cells so that TAG is decreased & HDL is increased. Decreased VLDL & LDL…It does this by increasing Apo proteins & Acyl CoA Synthase

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19
Q

How does niacin/nicotinic acid work?

A

At high doses (higher than in vitamin B complex), it increases HDL & decreases LDL & TAG. It inhibits an enzyme in TAG synthesis & inhibits HDL breakdown. It is the most effective drug for raising HDL levels.

20
Q

How does ezetimibe work?

A

It inhibits cholesterol absorption in the small intestine. It decreases biliary cholesterol secretion. This also increases cholesterol excretion. It effectively lowers LDL levels. May not help prevent heart disease, tho.

21
Q

When the cholesterol binds to SRBPs in the RER…what happens?

A

Less HMG CoA Reductase
More ACAT
Fewer LDL receptors

22
Q

When there is less cholesterol in the cell what happens?

A

More HMG CoA Reductase
Less ACAT
More LDL receptors

23
Q

T/F Statins end up causing an increase in LDL receptors.

A

TRUE

24
Q

Low cholesterol actually activates SREBPs…what happens next?

A

This activates the transcription of HMG CoA Reductase & LDL receptors, among other things. Statins start this pathway of low cholesterol & SREBP activation…
the bad part is the increase in HMG CoA Reductase
the good apart is the increase in LDL receptors.

25
Q

Would Statins help LDLR form of FH? APOB form? PCSK9? LDLRAP1?

A

LDLR–yes b/c that problem is caused by a lack of receptors
APOB wouldn’t be helped by statins.
I don’t think PCSK9 or LDLRAP1 would be helped by statins either.

26
Q

What is multiple lipoprotein-type hyperlipidemia?

A

a disorder of high cholesterol & high triglycerides
it is inherited
higher risk of early heart attacks

27
Q

What conditions make multiple lipoprotein-type hyperlipidemia?

A

diabetes
alcoholism
hypothyroidism

28
Q

What is lipodystrophy?

A

adipose tissue deficiency

29
Q

What does obesity do with fat cells?

A

It sort of kills them & so other tissues are exposed to excess fatty acids & TAG…then there is lipid accumulation in weird places…this interferes with insulin sensitivity in skeletal muscle & liver…and it interferes with insulin secretion from the pancreas

30
Q

What are some of the factors that contribute to ectopic fat deposition & insulin resistance?

A 
Enlarged adipocytes
impaired adipose tissue blood flow
adipose tissue hypoxia
local inflammation & macrophage infiltration
disturbed adipokine secretion
31
Q

What’s the deal with macrophages & fat cells?

A

Dead fat cells bring macrophages into the tissue. They produce foam cells in the fat (macrophages full of fat). They become active & secrete cytokines. This makes the fat cells insulin resistant.

32
Q

What do the oral hypoglycemics, thiazolidinediones, do to fat cells?

A

It is a transcription factor for PPAR gamma. This is an insulin sensitizer. It differentiates the stem cells into active adipocytes. It increases the number of at cells in the patient, but it also improves the insulin resistance in the individual.

33
Q

Describe the structure of fat cells.

A

It has all of the normal organelles inside of them. It just has a teeny tiny cytoplasm & a huge lipid droplet.

34
Q

Normally you have enough insulin that _____ is inhibited.

A

lipolysis

35
Q

In a patient with Type I Diabetes, when they have low insulin levels–>what happens?

A

Fat cells are broken down & ketoacidosis results.

36
Q

What is a way to bypass insulin resistance in muscle?

A

Exercise.

37
Q

Glucose transport increases 30-50 fold in fat cells, but only 3-4 fold in muscle, when both are presented with glucose. Why is that?

A

b/c muscle always has glucose uptake

fat only has glucose uptake when there is excess…takes advantage of it

38
Q

What limits the rate of glucose transport in fat & muscle?

A

the amount of GLUT4 receptors.

39
Q

Do adipocytes take up very much glucose during fasting?

A

NO

40
Q

What is the major site of lipid disposal after a meal?

A

adipose tissue

41
Q

What is the rate limiting step of creating triglycerides in adipocytes?

A

the creation of the backbone of triglycerides b/c adipocytes lack glycerol kinase

42
Q

What’s the deal with LPLs on skeletal muscle, heart muscle & fat surfaces in a fed & fasting state?

A

Fed State: LPL activity is high everywhere, including adipose tissue
Fasting State: LPL activity in adipocytes is low; LPL on heart is always high & has a high affinity for substrate

43
Q

What determines whether VLDL is metabolized in fat or muscle?

A

the insulin/glucagon ratio

44
Q

Which LPL is insulin dependent? Which is insulin independent? Fat & Muscle…

A

Fat: insulin dependent
Muscle: insulin independent

45
Q

What is the effect of a low insulin/glucagon ratio on lipid uptake to fat.

A

With low insulin or insulin resistance…low lipid uptake in fat.
Low insulin down regulates the Glut4 receptors on the adipose surface. Less glucose gets in–>harder to make TAGs.
The fatty acids that are available are bound to albumin & utilized for beta oxidation.

Block 3; Week 4 Michelle (9 decks)

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