Theme 3: Lecture 5 - Introduction to lipids Flashcards
1
Q
What are the functions of lipids
A
- Phospholipids & cholesterol: cell membranes
- Triglyceride is a key energy store
- Steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids
2
Q
How does creatine phosphate store energy
A
Creatine takes the high energy phosphate bond from ATP and stores it to rephosphorylate ADP at a later time when the cell needs the extra energy
3
Q
What can Acetyl CoA be turned into
A
- Cholesterol (blocked by statins)
- Citric acid cycle to produce ATP
- Fatty acids, stored energy (fatty acids can also be converted back into acetyl CoA)
4
Q
Fatty acid synthesis equation
A
Acetly-CoA + ATP + e- (ATP) -> fatty acid + CO2 + CoA
5
Q
Describe fatty acid synthesis
A
Leads to fatty acids with even-number of carbons
Consumes ATP
6
Q
Beta oxidation equation
A
fatty acid -> Acetyl CoA + e- (ATP)
7
Q
Describe beta oxidation
A
- Fat Mobilization: Shortens fatty acid by 2 carbons at a time
- Produces ATP + Acetyl-CoA
8
Q
Describe the structure of fatty acids
A
- Simple straight carbon chains + COOH
- In humans, most are 16-20 carbons long
9
Q
What does it mean if it’s an essential fatty acid
A
It can’t be made in the body, has to be taken in by the diet
10
Q
What is a triglyceride’s official name
A
Triacyl-glyceride
11
Q
What is cholesterol an essential component of
A
cell membranes
12
Q
What is cholesterol a precursor to
A
- Bile acids
- Steroid hormones
- Vitamin D
13
Q
Sources of cholesterol
A
- Diet
- Made in liver (with a big emphasis on recycling)
14
Q
How are cholesterol esters made
A
A cholesterol molecule is esterified by a long chain fatty acid
15
Q
What are cholesterol esters broken down by
A
by lipases to free cholesterol and fatty acids
16
Q
State cholesterol esters’ interaction with water
A
Hydrophobic
17
Q
State cholesterol’s interaction with water
A
Amphipathic
18
Q
What is cortisol
A
hormone secreted by the adrenal cortex
19
Q
Structure of acetate
A
CH3COO-
20
Q
Describe acetate
A
- Main energy production precursor for everything that happens in citrate cycle
- Can’t be transported in the plasma in this form so is transported by co enzyme A
21
Q
What are ketone bodies
A
- Soluble chemicals
- Major energy source during fasting esp for brain and heart
22
Q
How are ketone bodies made
A
-Made from acetyl-CoaA during fasting by the liver
-
23
Q
How long do ketone bodies last
A
5 hours
24
Q
Name the 3 ketone bodies
A
- Acetoacetic acid
- Beta-hydroxybutyric acid
- Acetone
25
Which ketone bodies are useful
Acetoacetic acid & beta-hydroxybutyric acid
26
Which ketone body is the waste product
Acetone
27
How is acetone made
spontaneously by decarboxylation
28
How is acetone eliminated
by the kidney
29
Are most naturally occurring unsaturated fatty acids cis or trans
cis
30
Describe unsaturated fatty acids
- have a lower boiling point so more liquid at body temperature
- increase fluidity of cell membranes
31
Why do molecules that have a cis carbon carbon double bond have a lower melting point
- The cis double bond creates a kink that saturated and trans unsaturated fat slack
- This kink lowers melting point by interfering with stacking and solidification
32
What are the two naming systems for unsaturated fatty acids
- Omega classification
| - Alpha classification
33
Describe the omega naming system for unsaturated fatty acids
- Start at the methyl end and count the position of the double bonds in relation to that end
- Linoleic acid would be omega 6, 9
34
Describe the alpha naming system for unsaturated fatty acids
- State the number of carbons
- State the number of double bonds
- Start at the carboxyl end and count the position of the double bonds in relation to that end
- Linoleic acid would be 18:2 delta 9, 12
35
What do saturated fats increase
LDL
36
Which fats are bad for you
- Saturated fats
| - Trans unsaturated fats
37
Why are cis unsaturated fats not bad for you
- They have a lower melting point because of the kink
| - Therefore less likely to form a big globular fat and solidify
38
Where do the 4 lipid transport pathways transport lipids to
-From gut (digestive tract) to liver & periphery
Periphery for lipids = muscle and adipose tissue
-From liver to periphery
-From periphery to liver
-From liver into digestive tract
39
What is the exogenous pathway
Transport from the gut to the liver (and periphery)
40
What are exogenous lipids
Lipids from the diet i.e. outside the body
41
How are lipids transported by the exogenous pathway
- Lipids from diet packaged by small intestine into “chylomicrons”
- increased lipids in plasma after a fatty meal
- Chylomicrons taken up by liver (or by periphery)
42
What is the endogenous pathway
Transport from the liver to the periphery
43
Where are peripheral lipids stored
in muscle and adipose tissue
44
What are endogenous lipids
Lipids made by the body i.e. from inside
45
How are lipids transported by the endogenous pathway
Lipids from liver are packaged into VLDLs
46
What is the reverse cholesterol transport pathway
Transport from periphery to the liver
47
What is the reverse cholesterol transport pathway important in
recycling of lipids
48
When does the reverse cholesterol transport pathway occur
When lipid supplies in the liver are being exhausted
49
What indicates reverse path activity
HDL in blood
50
Which transport pathway is bile production in
Transport from liver into gut (and gall bladder)
51
How does cholesterol help with bile production
It is converted into bile acids
52
Where do bile acids go after being deposited in the gut
Most are reabsorbed by the gut and returned to the liver and recycled
53
Why are enzymes and receptors needed in the lipid transport pathways
to move fats in and out of blood vessels
54
Give an example of an enzyme used in lipid transport pathways
lipoprotein lipase
55
What does lipoprotein lipase do
- It is a cell surface-linked enzyme in capillary walls
- Metabolises TG to fatty acids + glycerol because TG cannot go through cell membranes
- In order to remove triglycerides from VLDL and to move the TG across the capillary membrane, TG must first be metabolised via lipoprotein lipase
56
What are lipoprotein particles
plasma soluble particles which can carry lipids
57
Why do lipids need to be packaged to be transported in the body
They aren't plasma soluble
58
What are apolipoprotein particles
Proteins in lipoprotein particles that can hold lipids
59
What are apolipoprotein particles' relationship with water
They are amphipathic
60
Example of a apolipoprotein particle
Apolipoprotein E (apoE)
61
What density are triglycerides
very low density
62
What density is cholesterol
midway between TGs and proteins
63
Are bigger lipoprotein particles lower or higher in density
lower in density
64
Why is LDL the most dangerous lipoprotein
- LDL contents get incorporated into atheromas
- LDL in blood may be “storage” for cholesterol that “cannot be stored elsewhere”
- Excess LDL accumulates in atheromas
65
Where does LDL come from
LDL is eventually “left-over” after periphery absorbs endogenous TG from VLDL from liver
66
When does HDL appear
when cholesterol is being used up
67
What does HDL do
lipid transport from fat cells to liver (reverse cholesterol transport)
68
What does VLDL signify
risk of atheroma
69
What does VLDL do
Used to transport endogenous cholesterol and TG from Liver to adipose and muscle
70
What is left after TG is removed by periphery from VLDL
IDL
71
What is IDL
- Intermediate density lipoprotein
- IDL is intermediate step in pathway where VLDL becomes LDL
- Results from VLDL losing TG to periphery
- IDL will become LDL
72
What is IDL a sign of
CV risk
73
When are chylomicron levels high
after fat containing meals
74
Are chylomicrons associated with CV risk
no
75
What do chylomicrons do
carry lipids from gut to periphery (for exogenous lipids)
76
Which cells release insulin
Beta cells in pancreas
77
Which cells release glucagon
alpha cells in pancreas
78
What causes type 1 diabetes
no insulin made
79
What causes type 2 diabetes
absent or decreased response to insulin by target cells but insulin is still being made
80
What causes type 2 diabetes mellitus
obesity and genetic predisposition
81
What is hypercholesterolaemia
- Too much cholesterol in the blood
- A subclass of hyperlipidaemias
- High fasting levels of plasma cholesterol
82
What is hyperlipidaemia
Too much lipid in the blood
83
Example of hypercholesterolaemia
familial hypercholesterolaemia
84
What does hypercholesterolaemia cause
increased risk of arteriosclerosis
85
What is arteriosclerosis
arteries become thick and stiff, sometimes restricting blood flow
86
What causes hypercholesterolaemia
combination of environmental and genetic factors
87
What are statins
Drugs used to treat hypercholesterolaemia
88
How do statins work
Block endogenous cholesterol synthesis by blocking HMG-CoA Reductase (the entry step into cholesterol synthesis)
89
Give and example of a statin
simvastatin
90
What are statins prescribed for
CAD prophylaxis
91
What is metabolic syndrome
a group of risk factors that occur together, leading to increased risk for CAD, stroke, and type 2 diabetes
92
What are the causes for metabolic syndrome
- Insulin resistance
- Central obesity (waist circumference)
- high blood pressure
93
What does increased HDL mean
- More recycling of cholesterol
| - Lower CV risk
