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103 theme 3 > Introduction to lipids > Flashcards

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

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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

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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

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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

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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

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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

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7
Q

what is the citric acid cycle

A

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

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8
Q

What is fatty acid synthesis

A

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

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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

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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

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11
Q

what is the difference between mono and poly unsaturated

A

one DB monounsaturated, two DB polyunsaturated

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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)

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13
Q

how are fatty acids stored

A

as triglycerides (a glycerol and 3 fatty acids)

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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

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15
Q

where is cholesterol found

A

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

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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

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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
Q

how do double bonds link to atherogenesis

A

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
Q

how are lipids transported (4 ways)

A

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
Q

what is the exogenous pathway

A

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
Q

what is the endogenous pathway

A

From liver to periphery (peripheral lipids stored in adipose and muscle0
Lipid from liver packaged into VLDL

29
Q

what is reverse cholesterol transport

A

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
Q

what is bile production

A

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
Q

why are enzymes and receptors needed in lipid transport

A

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
Q

what are lipoprotein particles

A

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
Q

how can lipids be identified

A 
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
Q

what is LDL

A

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
Q

What is HDL

A

The good lipoprotein (lower cv risk)

Lipid transport from fat cells to liver (reverse cholesterol transport, appears when cholesterol is being used up)

36
Q

What is VLDL

A

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
Q

What are chylomicrons

A

Not usually ass with CV risk (high after fatty meal)

Carry lipids from gut to periphery (for exogenous lipids)

38
Q

what do pancreatic cells do

A

B cells release insulin and a release glucagon

39
Q

what is type II diabetes mellitus

A

Adult onset
High blood glucose and poor plasma glucose control
Insulin resistance
Relative insulin deficiency
Cause: obesity and genetic predisposition

40
Q

what is hypercholesterolaemia

A

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
Q

what are statins

A 
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
Q

what is metabolic syndrome

A

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

103 theme 3 (20 decks)

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