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Lipids Flashcards

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1
Q

What acids are the building blocks of lipids?

A

fatty acids

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2
Q

What are fatty acids formed of?

A

polar (soluable) carboxylic head and non-polar (insoluble) hydrocarbon chain tail

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3
Q

What number of carbon atoms do most common fatty acids have?

A

even, between 12-24

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4
Q

Are fatty acid chains typically branched or unbranched?

A

unbranched

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5
Q

What is the furthest carbon from the carboxyl group called?

A

the omega carbon

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6
Q

What number is the omega carbon given?

A

1

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7
Q

What two forms can the hydrocarbon tail of a fatty acid be in?

A

saturated or unsaturated

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8
Q

What does it mean if a hydrocarbon tail is unsaturated?

A

double bonds are found between carbon atoms

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9
Q

what does it mean if a hydrocarbon tail is saturated?

A

there are no double bonds between carbon atoms

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10
Q

What is an unsaturated fatty acid known as if they only have one double bond in the hydrocarbon chain?

A

monounsaturated fatty acids (MUFAs)

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11
Q

What is a polyunsaturated fatty acid?

A

have multiple double bonds in the hydrocarbon chain

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12
Q

How can unsaturated fatty acids be classified?

A

according to the position of the first double bond from the omega end

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13
Q

What is the stability of fatty acid aggregates dependent on?

A

the length and degree of saturation

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14
Q

What consistency will an aggregate of saturated fatty acids have?

A

waxy texture

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15
Q

What texture will a mix of saturated and unsaturated fatty acids have?

A

oily texture

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16
Q

What are the two conformations of double bonds in unsaturated hydrocarbons?

A

cis and trans

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17
Q

What is the cis conformation of double bonds?

A

two hydrogens are on the same plane

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18
Q

What is the trans conformation of double bonds?

A

two hydrogens are on opposite planes

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19
Q

What conformation are most fatty acid double bonds in?

A

cis conformation

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20
Q

What do lipids form from?

A

fatty acids

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21
Q

What does the structure of a lipid determine?

A

its function

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22
Q

Name the primary storage lipid

A

triacylglycerol

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23
Q

What is triacylglycerol formed of?

A

three fatty acid chains joined in a glycerol backbone by ester bonds

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24
Q

Storage lipids are neutral, what does this mean?

A

they do not carry a charge and are soluble in water

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25
Q

How can membrane lipids be categorised?

A

by the non fatty acids components of their structures

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26
Q

What way are membrane proteins initially categorized?

A

into phospholipids which have a phosphate group and glycolipids which have a sugar (saccharide) chain

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27
Q

Once membrane lipids have been split into phospholipids and glycolipids how can they be further categorised?

A

by the backbone group and any other additional ‘head group substituent attached to the phosphate or sugar groups

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28
Q

What are the two types of backbone group?

A

glycerol or sphingosine

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29
Q

What could be included as a ‘head’ group substituent?

A

alcohol or sulphate

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30
Q

What is a property of all membrane lipids?

A

they are polar

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31
Q

What part of the membrane lipid forms the hydrophobic portion?

A

fatty acid chains

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32
Q

What part of the membrane lipid forms the hydrophilic polar head?

A

the backbone and head group substituent

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33
Q

What does the dual nature of hydrophobic and hydrophilic parts of the same molecule mean they are classed as?

A

amphipathic

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34
Q

What does the amphipathic properties of membrane proteins allow them to form?

A

bilayers

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35
Q

How do membrane lipids arrange themselves to form bilayers?

A

so that their polar heads contact the aqueous environment

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36
Q

What are the 2 main categories of hormones?

A

eicosanoids and steroids

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37
Q

What are all eicosanoids formed from?

A

arachidonate

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38
Q

What are steroid hormones formed of?

A

cholesterol

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39
Q

What type of lipid is cholesterol?

A

a sterol

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40
Q

What structures do sterols form?

A

ring structures rather than straight chains

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41
Q

What further classifications can steroid hormones be placed into?

A

sex hormones, glucocorticoids, mineralocorticoids and synthetic steroids

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42
Q

What is the starting molecule for the synthesis of fatty acids?

A

Acytel-CoA

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43
Q

What enzyme is involved in the conversion of acetyl-CoA and carbon dioxide into malonyl-CoA?

A

acetyl-CoA carboxylase

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44
Q

What does the conversion of acetyl-CoA and carbon dioxide into malonyl-CoA require as well as an enzyme?

A

ATP and biotin

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45
Q

How many carbons does fatty acid synthase donate from malonyl-CoA to acetyl-CoA?

A

2

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46
Q

What else is added to malonyl-CoA?

A

4 hydrogen and 4 electrons

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47
Q

When does the reaction sequence of acetyl-CoA to malonyl-CoA end?

A

when enough carbons have been donated that palmitate is formed

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48
Q

How many carbons is palmitate formed of?

A

16

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49
Q

What is palmitate the precursor of?

A

other long chain fatty acids

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50
Q

What can palmitate be lengthened to form?

A

stearate (18 carbons)

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51
Q

How can longer fatty acids than stearate be formed?

A

with the addition of more acetyl groups

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52
Q

Where does the formation of fatty acid take place in the cell?

A

smooth endoplasmic reticulum or the mitochondria

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53
Q

What MUFAs are pamitate and stearate precursors for?

A

the two most common MUFAs in animal tissues palmitoleate and oleate

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54
Q

What type of bond do palmitoleate and oleate have beetween C9 and C10?

A

cis double bond

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55
Q

How is a double bond introduced into the fatty acid chain?

A

by an oxidative reaction catalysed by fatty acid acetyl-caA desaturase

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56
Q

What mammalian cells can introduce double bonds to the C9 position of fatty acids?

A

hepatocytes

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57
Q

What are essential fatty acids?

A

those that must be obtained from the diet

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58
Q

What does the fact that mammalian hepatocyte cells an only introduce double bonds at C9 mean?

A

cannot synthesise linoleate

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59
Q

What are eicosanoids made from?

A

arachnidonate

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60
Q

what enzyme releases arachnidonate from phospholipids?

A

phospholipase A2

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61
Q

What are triacylglycerols?

A

the energy storage molecules for the mammalian body.

62
Q

What are the 2 precursors of triacylglycerols?

A

fatty acyl-CoA and glycerol 3-phosphate

63
Q

What enzymes are involved in the formation of fatty acyl-CoA?

A

acyl-CoA synthetases.

64
Q

What is the structure of phosphatidic acid?

A

Phosphatidic acid has a glycerol backbone with 2 fatty acids and a phosphate group attached.

65
Q

In Triacylgylcerols how many fatty acid chains are joined to the glycerol head group?

A

3

66
Q

What is the name of the bond between fatty acid chains and the glycerol head group of Triacylgylcerols?

A

phosphodiester bonds

67
Q

In what amounts is Phosphatidic acid present in cells?

A

trace amounts

68
Q

What happens to phosphatidic acid in the the pathway to triacylglycerols (TAGS)?

A

phosphatidic acids is hydrolysed by phosphatidic acid phosphatase to form a 1,2-diacylglycerol. Diacylglycerols are then converted to triacylglycerols by transesterificationwith a third fatty acyl-CoA.

69
Q

How is the production of TAGS regulated?

A

This production of TAGs is regulated by hormones to keep the amount of body fatty relatively constant

70
Q

What hormone promotes the conversion of dietary carbohydrates and proteins to TAGs?

A

insulin

71
Q

How does the synthesis of glycerophospholipids compare to the synthesis of TAGs?

A

follows are very similar pathway to that of TAGs, but the precursor phosphatidic acid has a head group attached to the phosphate group rather than being hydrolysed to diacylglycerol.

72
Q

What is involved in the synthesis of sphingolipids?

A

Synthesis of the backbone molecule (glycerol or sphingosine). Attachment of fatty acid(s) to the backbone through an ester or amide linkage. Addition of a hydrophilic head group to the backbone through a phosphodiester linkage. Alteration or exchange of the head group to yield the final phospholipid product (in some cases)

73
Q

In eukaryotic cells where does phospholipid synthesis primarily occur?

A

surface of the smooth ER

74
Q

Where do newly formed phospholipids move to?

A

Some newly formed phospholipids stay at the site of synthesis, but others travel to their intracellular destinations via transport vesicles or specific proteins.

75
Q

Why is cholesterol not required in the diet?

A

can be synthesised from acetate

76
Q

What does the first stage of cholesterol biosynthesis create?

A

mevalonate from three acetate molecules

77
Q

What happens in the second stage of cholesterol biosynthesis?

A

converts mevalonate to two activated isoprenes.

78
Q

What do 6 activated isoprene units then condense to form during cholesterol synthesis?

A

squalene

79
Q

What is squalene converted into during cholesterol biosynthesis?

A

four-ring steroid nucleus

80
Q

What does ring closure generate in mammals?

A

lanosterol

81
Q

How is lanosterol finally converted into cholesterol?

A

in a series of about 20 reactions that include the migration of some methyl groups and the removal of others

82
Q

where does digestion and absorption of dietary lipids occur?

A

in the small intestine

83
Q

Where are packaged fatty acids delivered to once they are released from TAGs?

A

muscle and andipose tissue

84
Q

How much more energy can TAGs yield than glycogen, gram for gram?

A

2.5 times as much

85
Q

When fatty acids need to be used for energy where are they released from?

A

TAGs

86
Q

What enzyme action releases fatty acids from TAGs when they are needed for energy?

A

lipase

87
Q

what is lipolysis?

A

releasing fatty acids from TAGs with lipase

88
Q

During lipolysis what is released from TAGs?

A

3 fatty acid chains and a glycerol molecule

89
Q

What happens to the 3 fatty acid chains and glycerol molecule released by lipolysis?

A

released into the blood stream and bound to serum albumin to be carried to the tissues

90
Q

When fatty acids bound to serum albumin reach the tissues what happens to them?

A

undergo oxididation to release acetyl-CoA

91
Q

In what tissues does oxidation not occur?

A

the brain

92
Q

What are lipases activated by?

A

adrenaline, noradrenaline, ghrelin, growth hormone, testosterone and cortisol

93
Q

Where does 95% of the biologically available energy of TAGs reside?

A

in the 3 long-chain fatty acids

94
Q

where does 5% of the biologically available energy of TAGs reside?

A

glycerol

95
Q

what happens to approximately 75% of all fatty acids released by lipolysis?

A

re-esterified to form TAGs rather than being used for fuel.

96
Q

does re-esterifiying of TAGs persist under starvation conditions?

A

yes - even when energy metabolism is shunted from the use of carbohydrate to oxidation of fatty acids

97
Q

what happens to some fatty acids released into the blood stream?

A

taken up by the liver an resynthesised into triglycerol. This is then transported back to adipose tissue where fatty acid is released by extracellular lipoprotein lipase, taken up by adipocytes and re-esterified into TAG

98
Q

where are enzymes of fatty acid oxidation found in animals?

A

mitochondrial matrix

99
Q

what fatty acids can enter the mitochondria directly?

A

those with 12 or fewer carbons

100
Q

what must happen to fatty acids with 14 or more carbons in order to enter the mitochondrial matrix?

A

undergo a number of enzymatic reactions

101
Q

describe the enzymatic reactions that take place so that fatty acids with 14 or more carbons can enter the mitochondrial matrix?

A

acyl-CoA synthases on the surface of the mitochondria convert free fatty acids to acyl-CoA using 2 molecules of ATP
this can then enter the mitochondria

102
Q

describe the reactions of the carnitine shuttle

A

fatty acyl-CoA is attached to carnitine to form fatty-acyl carnitine by the action of carnitine acyltransfurase 1
this then enters mitochondrial matrix by facilitated diffusion through acyl-carnitine translocase
acyl-cartinine is converted back to acyl-CoA by carnitine transfurase 2. It is released into the matrix along with free carnitine

103
Q

what is the carnitine shuttle used for?

A

Acyl-CoA crossing mitochondrial matrix

104
Q

where does fatty acyl-CoA attachment to carnitine to form fatty-acyl carnitine by the action of carnitine acyltransfurase 1 occur?

A

outer mitochondrial membrane

105
Q

where is acyl-carnitine translocase located?

A

inner mitochondrial membrane

106
Q

where is carnitine acyl-transfurase 2 located?

A

inner face of inner mitochondrial membrane

107
Q

what happens during beta oxidation of fatty acyl-CoA?

A

undergoes the oxidative removal of successive 2 carbon units in the form of acetyl-CoA. The sequence is repeated until the acyl-CoA has been completely broken down to acetyl-CoA

108
Q

what is produced as well as acetyl-CoA during beta oxidation of fatty acyl-CoA?

A

FADH2 and NADH

109
Q

what are FADH2 and NADH presented to?

A

mitochondrial respiratory chain causing production of ATP and water

110
Q

what regulates beta oxidation?

A

controlling rate of carnitine shuttle

111
Q

what are the 2 main categories of lipid hormones?

A

eicosanoids and steroid

112
Q

what are the 3 eicosanoid classes?

A

prostaglandins
thromboxanes
leukotrienes

113
Q

what are the functions of prostaglandins?

A

inflammation, blood flow, clot formation and control of smooth muscle contraction

114
Q

what is the role of thromboxanes?

A

blood clotting

115
Q

what is the role of leukotrienes?

A

immune response

116
Q

what type of hormone action do eicosanoids have?

A

paracrine

117
Q

what are the 4 main steroid hormone classes?

A

glucocorticoids
sex hormones
mineralocorticoids
synthetic steroids

118
Q

what are the roles of glucocorticoids?

A

metabolism and immune system

119
Q

what are the roles of mineralocorticoids?

A

electrolyte balance

120
Q

what are synthetic steroids used for?

A

medications used to treat various disorders

121
Q

what type of hormone action do steroids have?

A

endocrine

122
Q

what are the main vitamins formed by lipids?

A 
vitamin A - visual pigments
vitamin D3 - calcium and phosphate homestasis
vitamin E - antioxidant
vitamin K - blood clotting
Ubiquinone - electron carrier co-factor
123
Q

how is vitamin K obtained?

A

the diet via the intestine

124
Q

what is vitamin K converted to?

A

vitamin K hydroquinone (KH)

125
Q

what is the role of KH?

A

cofactor for adding the carboxylic acid functional group (-COOH) to inactive clotting factors - activating them

126
Q

how is -COOH added and removed?

A

oxidation of KH to vitamin K epoxide (VKO)

recycled back to KH by VKO reductase

127
Q

what happens if animals are vitamin K deficient?

A 
bruising
petechiae
prolonged bleeding from minor wounds
spontaneous haematoma formation 
haemorrhage
128
Q

how may animals become vitamin K deficient?

A

vitamin K absorption deficits in the gut preventing entry into blood stream
vitamin K recycling defects where VKO is not converted back into KH so unable to be used to create clotting factors - can be blacked by rodenticides

129
Q

what are COX enzymes responsible for?

A

prostaglandin synthesis

130
Q

what are the 2 mammalian COX enzymes?

A

COX 1 - synthesises prostaglandins that regulate secretion of gastric mucus
COX 2 - synthesises prostaglandins that mediate inflammation, fever and pain

131
Q

what can be used to reduce pain?

A

COX 2 inhibiting drugs

132
Q

what are the problems with COX 2 inhibiting drugs?

A

also inhibit COX 1 which can lead to gastric side effects such as stomach irritation, ulceration and gastric bleeding

133
Q

how does asprin reduce risk of stroke/heart attack?

A

inhibits formation of thromboxane platelets

134
Q

what is fatty acid metabolism disorder?

A

broad group of genetic disorders where the body is unable to produce/use enzymes required for fatty acid oxidation. Body is unable to gain any energy from them

135
Q

what are 2 types of fatty acid metabolism disorder?

A

defects in oxidation of fatty acids to acyl-CoA - fatty acids unable to enter mitochondria to be oxidised
defects in carnitine shuttle - acyl-CoA is unable to enter mitochondria to be oxidised

136
Q

what does fatty acid metabolism disorder lead to?

A

TAG are still sent from adipose tissues to liver to be broken down to fatty acids and used as energy
inability to use fatty acids for energy - weakness and lethargy
excessive use of glucose as the primary energy source can lead to hypoglycaemia

137
Q

what does TAG are still sent from adipose tissues to liver to be broken down to fatty acids and used as energy cause?

A

fatty acid build up in liver

138
Q

how is fatty acid metabolism disorder treated?

A

no possible to cure but can be managed with high-fibre low-fat) diets that involve frequent meals to avoid use of fat stores rather than usual 1-2 meals a day

139
Q

what are lipomas?

A

adipocytes which grow abnormally and form benign masses

140
Q

how to tell if a mass is a lipoma?

A 
usually in the skin and mobile
usually slow growing
should not cause pain when manipulated
usually squishy
on fine needle aspirate there will be cells with large lipid vacuoles
141
Q

how should lipomas be treated?

A

do not always require treatment as non-cancerous. May cause discomfort/reduce mobility due to location and look unsightly so can be surgically removed
dietary changes can help as they are formed of adipocytes. Most often seen in obese dogs which means they may reduce if weight is lost

142
Q

when are ketone bodies released?

A

from liver into blood along with glucose after liver glycogen stores have been depleted (~24hrs starvation/low glucose)

143
Q

what are ketone bodies used as?

A

energy sources by heart, skeletal muscle, kidneys and the brain

144
Q

what are ketone bodies?

A

some acetyl-CoA diverted from fatty acid oxidation

145
Q

what are the 3 main ketone bodies?

A

acetoacetate
b-hydroxybutyrate
acetone

146
Q

what is ketosis?

A

when ketone synthesis exceeds rate of use (constant use by extrahepatic tissues) so blood concentration increases and ketone bodies are secreted in urine

147
Q

what can happen if ketosis continues for a prolonged period of time?

A

ketoacidosis

148
Q

what can cause ketoacidosis?

A

extreme starvation or uncontrolled diabetes

149
Q

what effect does ketoacidosis have on the kidneys?

A

high levels of ketone bodies lower pH of blood plasma triggering kidneys to excrete very acidic urine
glucose and ketone bodies are present in urine
causes increase in urination (osmotic diuresis)

150
Q

what does an increase in urination rate due to ketoacidosis cause?

A

removal of water and electrolytes from the blood causing potentially fatal dehydration

X Pre Clinical Science (17 decks)

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