Introduction to lipids Flashcards

1
Q

what are the functions of lipid molecules

A

Phospholipids and cholesterol: cell membranes
Triglyceride is a key energy store
Steroids and fatty acids play regulatory roles as hormones, vitamins and bile acids

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

how is energy stored in cells (short term)

A

ATP (and other phosphate bonds)
Redox agents (NADH, FADH2)
Ionic transmembrane gradients (H+ across mitochondria membrane, Na+ across plasma membrane)
All are labile

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

how is energy stored in cells long term

A

There is a limit to how much ATP can be stored (some energy is stored intracellularly as creatine phosphate)
Energy stored as large, stable energy efficient precursors eg carbs and fats
Acetyl-CoA as energy mediator

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

what is acetyl-CoA

A

Made from glucose, used to form citric acid + ATP and fatty acids (stored energy) (can be reversed)
Also converted to cholesterol – blocked by statins

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

how can carbs be stored as energy

A

Starch digested into sugars (glucose) in the gut
Sugars absorbed from gut into bloodstream
Sugars absorbed by liver and stored as glycogen (via hepatic portal vein)
Also sugars stored throughout body as glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is glycogen used for

A

Glycogen can be broken down when body needs energy

No glycogen in brain, needs glucose or ketone bodies from plasma constantly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the citric acid cycle

A

Citric Acid (6C) > +O2 > rel CO2+ATP > Oxalo-acetic acid (OAA - 4C) + Acetyl-CoA (2C)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is fatty acid synthesis

A

synthesis leads to fatty acids with even number of carbons, consumes ATP

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

what is beta oxidation

A

fat mobilisation by shortening fatty acids by 2 carbons at a time to produce ATP and acetyl CoA

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

what are fatty acids

A

Simple straight carbon chains + COOH
In humans mostly 16-20 carbons long
50% have double bonds
Esp FA at position 2 (middle) of glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the difference between mono and poly unsaturated

A

one DB monounsaturated, two DB polyunsaturated

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

how are double bonds made in mammals

A

Mammals have limited ability to make double bonds (some types of fatty acids must be in the diet – essential fatty acids)

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

how are fatty acids stored

A

as triglycerides (a glycerol and 3 fatty acids)

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

what is cholesterol

A

Essential components of cell membranes
Precursor of bile acids, steroid hormones and vit D
Ring system so very rigid

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

where is cholesterol found

A

Sources: from diet or made in liver
A major emphasis on recycling
Bile salts
Endogenous pathways

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

what are cholesterol esters used for

A

A large portion of plasma cholesterol is esterified (75%)
Broken down by lipases to free cholesterol and fatty acids
Cholesterol is amphipathic as free alcohol but hydrophobic when esterified

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

what are the steroids (4)

A

Cholesterol
Vit D (produced by skin by action of light on a cholesterol derivative)
Cortisol (hormone secreted by adrenal cortex)
Testosterone (male sex hormone)

18
Q

what does acetyl-coenzyme A do

A

Energy production - oxidises fatty acids

Acetyl-CoA can’t be transported in plasma so is converted to acetate

19
Q

what are ketone bodies

A

3 soluble chemicals, not bodies

Made from acetyl coA during fasting, by liver, only lasts for 5 hours

20
Q

what do ketone bodies do

A

During fasting they’re major energy source (esp heart and brain)
Form Acetoacetic acid and beta hydroxybutic acid
Acetone = waste product
Made spontaneously by decarboxylation and eliminated by kidney

21
Q

how do unsaturated fatty acids compare to saturated

A

have a lower MP (more liquid at body temp so increase fluidity of cell membranes)

22
Q

how are unsaturated fatty acids found

A

Most naturally occurring fatty acids are cis (even no of carbons, 14-22)

23
Q

why are saturated fats popular

A

popular with manufacturers of processed foods as they’re less vulnerable to rancidity and are more solid at room temp

24
Q

how can unsaturated fatty acids be classified

A

2 classifications terminologies
Named from alpha carbon at carboxyl end
Omega (opposite end) counting of double bonds

25
how do double bonds link to atherogenesis
Fatty acids in diet affect plasma cholesterol levels (also triglyceride levels) Saturated fats increase LDL Trans unsaturated fatty acids - bad Cis unsaturated fatty acids are monounsaturated or polyunsaturated – good Lower melting temp because of kink High melting temp = solid and unmobillisable
26
how are lipids transported (4 ways)
From gut (digestive tract) to liver and periphery (muscle and adipose tissue) From liver to periphery From periphery to liver From liver into digestive tract
27
what is the exogenous pathway
From gut to liver and periphery Lipids from diet packaged by small intestine into chylomicrons (lipids in plasma increase after a fatty meal) Chylomicrons taken up by liver (or by periphery)
28
what is the endogenous pathway
From liver to periphery (peripheral lipids stored in adipose and muscle0 Lipid from liver packaged into VLDL
29
what is reverse cholesterol transport
From periphery to liver Occurs when lipid supplies in liver are being exhausted (sign of reduced body lipid) HDL in blood indicates reverse pathway activity
30
what is bile production
From liver into gut (and gall bladder) Bile released into cystic duct Cholesterol converted into bile acids (bile necessary to digest fats in diet, emulsifies fat) Most bile acids are reabsorbed by gut (returned to the liver and recycled)
31
why are enzymes and receptors needed in lipid transport
Needed for pathways to move fats in and out of blood vessels Eg lipoprotein lipase, Cell surface linked enzyme in capillary walls Metabolises TG > Fatty acids and glycerol to remove TG from VLDL and move across capillary membranes, TG must 1st be metabolised as cannot cross CM
32
what are lipoprotein particles
Lipids not soluble in plasma so must be packaged for transport Lipoprotein particles in plasma are soluble and can carry lipids Apolipoproteins are proteins in LPP that can hold lipids (amphipathic eg ApoE)
33
how can lipids be identified
``` Lipids identified by density Lipids much less dense than proteins TG very low density Cholesterol mid way Bigger lipoprotein particles usually carry a lot of lipids (lower in density) ```
34
what is LDL
Most dangerous lipoprotein (incorporated into atheromas, in blood store cholesterol that can’t be elsewhere, excess accumulates) LDL left over after periphery absorbs endogenous TG from VLDL from liver
35
What is HDL
The good lipoprotein (lower cv risk) | Lipid transport from fat cells to liver (reverse cholesterol transport, appears when cholesterol is being used up)
36
What is VLDL
Signifies risk of atheroma Used to transport endogenous cholesterol and TG from liver to adipose and muscle After TG removed by periphery from VLDL to IDL (intermediate step in pathway where VLDL becomes LDL)
37
What are chylomicrons
Not usually ass with CV risk (high after fatty meal) | Carry lipids from gut to periphery (for exogenous lipids)
38
what do pancreatic cells do
B cells release insulin and a release glucagon
39
what is type II diabetes mellitus
Adult onset High blood glucose and poor plasma glucose control Insulin resistance Relative insulin deficiency Cause: obesity and genetic predisposition
40
what is hypercholesterolaemia
High fasting levels of plasma cholesterol (eg familial) Hyperchol is a sub class of hyperlipidaemias Inc risk of atherosclerosis (HDL reduces risk) Due to a combination of environmental and genetic factors
41
what are statins
``` Drugs used to treat hypercholesterolaemia (block endogenous cholesterol synthesis by blocking HMG-CoA reductase (the entry step to it)) Eg simvastatin (one of the most commonly prescribed drugs, esp men over 50, prescribed for CAD prophylaxis ```
42
what is metabolic syndrome
A group of risk factors that occur together Lead to increased risk for CAD, stroke and type 2 diabetes Main causes insulin resistance, central obesity (waist circumference) and high BP