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Block 3 Week 4 Meg > Mastick: Genetics of Dyslipidemia > Flashcards

Mastick: Genetics of Dyslipidemia Flashcards

1
Q

Blood glucose AND lipid levels are regulated by (blank).

A

insulin

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2
Q

When would you see life threatening hypoglycemia?

A

When a type I diabetic is using insulin injections

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3
Q

A high protein meal causes both (blank) and (blank) to be secreted simultaneously.

A

insulin and glucagon

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4
Q

4 major forms of single gene causes of familial hypercholesterolemia: (blank) loss of function mutations, (blank) receptor binding site mutations, (blank) gain of function mutations, and (blank) loss of function mutations.

A

LDLR; APOB; PCSK9; LDLRAP1

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5
Q

Loss of LDLR, mutations in APOB, and gain of functions in PCSK9 mutations are all inherited in an autosomal (blank) manner

A

dominant

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6
Q

LDLRAP1 is a mutation inherited in an autosomal (blank) manner

A

recessive

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7
Q

An autosomal dominant disorder that causes severe elevations in total cholesterol and low-density lipoprotein cholesterol

A

familial hypercholesterolemia

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8
Q

Trans-membrane protein

Primary pathway for removal of cholesterol from circulation

A

LDL receptor

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9
Q

LDLR internalizes LDL via (blank) and cholesterol is released into the cell due to the low pH of the endosome. The LDL receptor then goes back to the membrane.

A

endocytosis

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10
Q 
Different LDLR mutations:
Class 1
Class 2
Class 3
Class 4
Class 5
A

Class 1: null alleles–>no LDL receptors
Class 2: defective transport alleles–>mutated receptors
Class 3: affect binding of LDL
Class 4: affect concentration of normal receptors
Class 5: defective recycling of LDLR

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11
Q

What do statins block?

A

HMG-CoA reductase (committed step for synthesis of cholesterol)

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12
Q

blindness
kidney disease
nervous system disease
amputation

A

Diabetic complications caused by elevated blood glucose

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13
Q

Heart disease and stroke

High blood pressure

A

Diabetic complication causes by elevated blood lipid

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14
Q

The diabetes epidemic is due to insulin (blank).

A

resistance

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15
Q

ApoB is a (blank) mutation, so LDL particles cannot bind to LDL receptor.

A

binding

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16
Q

PCSK9 gain-of-function mutation is a mutation that down-regulates (blank) by causing their degradation in lysosomes. Thus, they are not recycled to the surface, and LDL cannot be efficiently absorbed.

A

LDL receptors

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17
Q

LDLRAP1 loss-of-function mutations cause a defect in the LDL receptor (blank) required for LDL receptor to bind to clathrin.

A

adaptor protein

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18
Q

Bind to the nuclear receptor PPAR-alpha, which works as a transcription factor to alter gene expression in target cells. These increase HDL levels and decrease triglyceride levels

A

Fibrates

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19
Q

Increases HDL levels and decreases triglyceride and LDL levels through a poorly understood mechanism

A

Niacin

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20
Q

Inhibits cholesterol absorption in the small intestine, and promotes cholesterol excretion, since biliary cholesterol accounts for some of the cholesterol that passes through the small intestine

A

Ezetimibe

21
Q

Statins block HMG-CoA and cause a (blank) in LDL receptors

A

increase

22
Q

When HMG-CoA is inhibited, this decreases intracellular cholesterol, which activates (blank).

A

SREBP

23
Q

What do SREBPs activate the transcription of?

A

HMG CoA reductase

LDL receptors

24
Q

Fibrates bind to a transcription factor directly and increase (blank) production, decrease (blank) production, increase (blank) clearance, and decrease (blank) particles.

A

HDL; VLDL; VLDL; LDL

25
Q

Niacin decreases mobilization of free fatty acids, so decreases triglyceride synthesis, and (blank) secretion.

A

VLDL

26
Q

Ezetimibe blocks this transporter, which leads to reduced biliary cholesterol secretion

A

NPC1L1

27
Q

a disorder of high cholesterol and high blood triglycerides that is inherited

A

Familial combined hyperlipidemia

28
Q

The most common genetic disorder of increased blood fats that causes early heart attacks

A

Familial combined hyperlipidemia

29
Q

T/F: Most cases of high cholesterol are not caused by a single inherited condition, but result from a combination of lifestyle choices and the effects of variations in many genes

A

True

30
Q

Normal function of adipose tissue

A

buffer the daily influx of dietary fat

31
Q

When fat cells are not functioning properly, other tissues are exposed to excess (blank) and (blank) which interferes with insulin sensitivity and secretion

A

fatty acids; TAGs

32
Q

In patients with diabetes, many of their adipocytes are dead. This brings (blank) into the tissue to eat up the fat, and causes the release of inflammatory intermediates that cause surrounding healthy adipocytes to become insulin resistant.

A

macrophages

33
Q

Oral hypoglycemic which induces the differentiation of preadipocytes (stem cells) into small, young, active adipocytes

A

thiazolidinediones

34
Q

Thiazolidinediones is considered an insulin (blank)

A

sensitizer

35
Q

Healthy adipocytes are highly (blank) and (blank) in response to insulin

A

sensitive; responsive

36
Q

If very little glucose enters adipose tissue after a meal, why does glucose transport increase 20-50 fold in fat cells?

A

Under normal circumstances, glucose transport is MINIMAL to adipocytes. So when you eat, and insulin is increased, a lot more glucose enters the cell RELATIVE to the basal level.

37
Q

Glucose transport in fat and muscle is rate limited by what?

A

the number of transport proteins in the plasma membrane

38
Q

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

A

Adipose tissue

39
Q

Discuss the fate of dietary lipids from intestinal cell to the liver

A

intestinal cell–>chylomicrons–>capillaries (lipoprotein lipase)–>chylomicron remnants–>LDL receptors on liver

40
Q

As the chylomicron is headed to the liver, it encounters (blank) and triglycerides are removed, which reduces the size of the chylomicron

A

lipoprotein lipase

41
Q

As the chylomicron loses TG, (blank) will then disassociate from the particle and lipoprotein lipase activity will no longer be supported. This particle is now called a (blank) and is destined for the liver

A

CII; chylomicron remnant

42
Q

In the fed state, chylomicron synthesis is (blank). LPL activity is (blank). Storage of FFA as TG in adipose is (blank).

A

high; high; high

43
Q

In the fasted state, chylomicron synthesis is (blank), LPL activity in adipose is (blank). LPL activity in heart and other muscle remains steady.

A

low; low

44
Q

Once free fatty acids are deposited in the fat cell, glucose enters through the (blank) transporter and generates the (blank) necessary to form triglycerides.

A

glucose; G3P

45
Q

Two components of triglyceride

A

Free fatty acids (fatty acyl CoA)

G3P (backbone)

46
Q

In high protein, low carb diets, fatty acids will be used primarily for (blank) due to a shortage of G3P from glucose

A

Beta-oxidation

47
Q

Insulin regulates both of these two things; if there is low insulin, there will be very little uptake of lipid into fat cells.

A

LPL; glucose transport

48
Q

Is lipoprotein lipase insulin dependent in fat?

In muscle?

A

YES; no

Block 3 Week 4 Meg (6 decks)

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