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Biochemistry-Exam 2 > Lipids (general) > Flashcards

Lipids (general) Flashcards

0
Q

5 types of lipids

A

Fatty acids, neutral glycerides, phospholipids, sphingolipids, cholesterol and derivatives

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1
Q

Five functions of lipids

A

Energy storage, membranes, messenger, hormone building blocks, covalent modification of proteins

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2
Q

What type of lipids do we eat?

A

Neutral glycerides (e.g. triglycerides)

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3
Q

Fatty acids come in three forms:

A

Saturated, unsaturated, and unusual (branched/plants)

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4
Q

What does saturated mean in terms of a FA?

A

No double bonds

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5
Q

What are the functional components of a FA?

A

Hydrocarbon chain and a carboxylic acid group

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6
Q

Fatty acids in humans have the following characteristics?

A

Even numbered (made by 2 carbons at a time), 12-24 carbons long, saturated or unsaturated, all double bonds are in cis configuration, DB in FA are separated by at least one CH2 group, unbranched.

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7
Q

T or F: Natural human FA can be trans and odd numbered

A

False to both counts

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8
Q

How do we notate FAs?

A

Number of carbons:Number of double bonds

If unsaturated: Delta(number of first atom from carboxyl group):N of Carbons: Number of bonds

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9
Q

What are alpha, beta…omega carbons?

A

1 Carbon is in the carboxyl group, alpha is first carbon attached to that an so on. Omega is always the last carbon

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10
Q

Beta oxidation happens on what carbon?

A

Beta carbon (second from the carboxyl carbon)

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11
Q

What is an omega-3 FA?

A

Double bond is on the third to last C (between 3 and 4) i.e. double bond starts on the 3rd carbon from the end (same nomenclature for omega-6)

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12
Q

For a human FA, what are the only possibilities for an additional double bond on a unsaturated FA?

A

+/- 3 from the first one e.g. 12 and 9 or 12 and 15 and so on

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13
Q

Longer the chain, the ________ the melting point and is more ________

A

higher, solid

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14
Q

The more cis double bonds, the __________ the melting point and more _________ property

A

Lower, more fluid

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15
Q

Unsaturated bonds lead to _________ increased rate of oxidation

A

Increased

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16
Q

What is the basic structure of neutral glycerides?

A

Glycerol that is esterified with FA up to three times

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17
Q

What determines the property of neutral glyceride?

A

The FAs attached

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18
Q

What is the structure of a phospholipid?

A

Same as FA except one of the FA is replaced with a phosphate group attached to an alcohol group (determines name)

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19
Q

What is the structure of a phospholipid?

A

2 fatty acids, glycerol, phosphate, and alcohol group

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20
Q

Where is cardiolipin found?

A

In inner mitochondrial membrane

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21
Q

What hydrophobicity do phospholipids have?

A

Amphipathic

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22
Q

What is the heiracrhcy of sphingolipids?

A

Sphingosine to ceramide to sphingomyelin and glycosphingolipids

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23
Q

Sphingosine is made into?

A

Ceramide

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24
Q

Ceramide is made into?

A

Sphingomyelin and glycoshingolipids

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25
Q

Where are glycosphingolipids found?

A

Blood cell antigens

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26
Q

What is the structural difference between sphingosine and ceramide?

A

FA added to sphingosine to make ceraminde

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27
Q

Sphingosine is a type of?

A

Long chain amino alcohol

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28
Q

Adding phosphotidylcholine to ceramide gives oyu?

A

Sphingomyelin

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29
Q

T or F: Glycosphingolipids are important for cell cell contact

A

T

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30
Q

What are the four general functions of cholesterol?

A

Essential membrane component, bile salts, steroid hormones, vitamin D

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31
Q

What is an apolipoprotein?

A

Lipoproteins on the outside of miscelles that direct the internal contents

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32
Q

How are triacylglycerols and cholesteryl esters transferred in the blood?

A

In phospholipid enclosed micelles

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33
Q

What are the four major types of lipoprotein carriers?

A

Chylomicrons, LDL, VLDL, and HDL

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34
Q

What is the size order largest to smallest of lipoprotein carriers?

A

Chylomicrons, VLDL, LDL, HDL

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35
Q

What do chylomicrons primarily transport?

A

Triglycerides

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36
Q

What do VLDLs mainly carry?

A

Triglycerides

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37
Q

What do LDL mainly transport?

A

Cholesterol

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38
Q

What do HDLs mainly transfer?

A

Protein

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39
Q

T or F: High LDL is bad prognosis for heart disease

A

T

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40
Q

LDL has only one type of apoprotein:

A

B-100

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41
Q

Mutation of B-100 leads to issues with what?

A

LDL

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42
Q

Mutation in B-48 apoprotein leads to issues with potentially?

A

Chylomicron

43
Q

Triglycerides in the diet are primarily transported by?

A

Chylomicrons

44
Q

VLDL carry fat from where?

A

The liver to tissue

45
Q

What tissues primarily need FA?

A

Adipose, lung, muscle

46
Q

What is the percentage composition of triglycerides from highest to lowest for lipoproteins?

A

Chylomicron, VLDL, LDL, HDL

47
Q

What is the percentage composition of cholesterol from highest to lowest for lipoproteins?

A

LDL, HDL, VLDL, CM

48
Q

Liver AND intestine make this type of Lipoprotein

A

HDL, deliver from tissues to liver for elimination

49
Q

VLDL generates?

A

LDL to deliver cholesterol to tissues and liver

50
Q

Liver generates?

A

VLDL to deliver endogenous FA to peripheral tissue

51
Q

Intestine generates?

A

CM to deliver dietary FA to peripheral tissues

52
Q

Endogenous FA is transported by? Exogenous FA?

A

VLDL, CM

53
Q

What is the function of bile salts?

A

Emulsification of lipid droplets in small gut

54
Q

Bile salts are made in?

A

The liver

55
Q

Bile salts are stored in?

A

Gall bladder

56
Q

How much bile salt is used each day? Lost?

A

15-30 g and 0.5 g/day

57
Q

What is bile made from?

A

Cholesterol

58
Q

What is PTL?

A

Panceratic triglyceride lipase. Released from pancreas to hydrolyze a TAG into a monoacylglyceride and 2 free FA salts

59
Q

What happens to the FA salts and monoacylglyceride from PTL?

A

Rejoined in the intestinal mucosal cells and pushed into lymphatic vessel and to the blood stream

60
Q

What transporter is responsible for bringing fat derivatives from the intestinal lumen into the enterocytes in the mucosa?

A

FATP4 transporters

61
Q

What apoproteins cover chylomicrons?

A

B-48, C, and E

62
Q

CM carry what in addition to TAGS?

A

Fat soluble vitamins

63
Q

What is the function of LPL?

A

In all tissue, cleaves FA off and makes 3 FA and glycerol. Glycerol is water soluble and FA is used by tissue

64
Q

What is steatorrhea?

A

Fat in stool due to absorption issues

65
Q

What is abetalipoproteinamia?

A

B-100 defect causing no FA or ADEK vitamin absorption

66
Q

What are the five main functions of adipose?

A

Energy storage, protection of organs, insulation, soluble fat vitamin storage (ADEK), synthesis of adipokines (hormones from fat, usually peptide hormones)

67
Q

Two body shapes, two types of fat, worse for disease?

A

Apple, Pear. Subcutaneous, Visceral. Visceral is worse.

68
Q

T or F: Adipose cells grow in volume not in number

A

T (generally)

69
Q

When does adipose number typically stabilize?

A

Early 20s

70
Q

What happens in the fed state in regards to fat?

A

High insulin. Glucose taken to glycerol-P for TAG. Glucose to Acetyl-CoA to FA to TAG. CM and VLDL deliver to FA which is taken to TAG

71
Q

What happens in the fasting state for adipose?

A

TAG acted upon by Hormone Sensitive Lipase (HSL, only in adipose) and made into FA and glycerol. FA is carried by albumin in serum to where needed

72
Q

What is HSL?

A

Hormone sensitive lipase which breaks down TAG in adipose during fasting state (only in adipose)

73
Q

In adipose, what happens when glucagon/epinephrine is conjugated to receptor?

A

cAMP to PKA activation. Phosphorylates HSL to make it active.

74
Q

In adipose, what happens when insulin is conjugated to receptor?

A

Activates PDE (phosphodiesterase) to take cAMP to AMP which causes HSL to become dephosphorylated to become inactive

75
Q

What is leptin?

A

An adipokine that inhibits hunger and increases metabolic rate

76
Q

Where is leptin made? Effects? Long or short?

A

Adipose, dec. appetite, inc. caloric expenditure, long term effect

77
Q

What is ghrelin? Where is it made? Effects?

A

Produced by stomach, increases appetite, short and long effects.

78
Q

T or F: Bile salts decrease weight gain

A

T (by increasing energy expenditure via brown fat)

79
Q

What are beige/brown fat cells?

A

Adipose cells that undergo thermogenesis to waste energy

80
Q

What are phospholipases?

A

Break down phospholipids.

81
Q

What bond in phospholipids is important to know?

A

C site (between the glycerol and phosphate group). Important for signal transduction

82
Q

Where does Degredation of sphinosines occur?

A

In the lysosome

83
Q

What is sphingolipodosis?

A

Failure to break down sphigosines leading normally to CNS issues

84
Q

What is Tay-Sachs diesease?

A

Failure to break down ganglioside GM2 which is a glycosphingolipid due to an enzyme deficiency in the lysosome

85
Q

What can cross the lipid bilayer?

A

Small uncharged polar molecules, gases, and urea. Ions, large molecules, water, charged molecules cannot

86
Q

What is endocytosis?

A

Eating of external particles. Autophagy is a special type of endocytosis

87
Q

What are coated pits usually rich in?

A

Receptors in order to endocytose molecules specifically

88
Q

T or F: Endosomes are low in pH?

A

True to release contents from receptors

89
Q

What is transferrin?

A

An important receptor for ion. Apo-transferrin is attached to two irons and brought in in receptors. Acidified to release from receptor the iron

90
Q

T or F: LDL is taken up by cells

A

T (all other lipoproteins are not taken up, LDL has a receptor)

91
Q

Name the four functions of cholesterol

A

Essential membrane component, bile salts, steroid hormones, vitamin D

92
Q

T or F: Plasma levels of cholesterol are linked to death rate

A

T

93
Q

T or F: Dietary cholesterol has a major effect on plasma cholesterol levels

A

F

94
Q

How is cholesterol degraded?

A

Trick question. There is no degradation pathway. It is excreted as bile salts

95
Q

What precursor molecule is cholesterol synthesized from?

A

Acetyl CoA

96
Q

What is the cholesterol production/intake rate for body?

A

0.5 g/d from diet and 0.5 g/d from synthesis

97
Q

What is the rate limiting step for cholesterol synthesis?

A

HMG-CoA Reductase

98
Q

What do statins do?

A

Block HMG-CoA reductase step in synthesis

99
Q

LDL-Receptors are rich in what apoprotein?

A

B-100

100
Q

What is familial hypercholesteremia?

A

Disorder of high plasma cholesterol, typically a mutation in apoB100, autosomal dominant

101
Q

When is cholesterol made de novo?

A

When there is no LDL in the blood serum

102
Q

What is SRE?

A

Sterol Receptor Element in nucleus

103
Q

How is cholesterol synthesis controlled on cellular level?

A

SREBP is activated (SRE-binding protein) which activates BOTH LDL receptor synthesis and HMG CoA reductase synthesis

104
Q

T or F: LDLR and HMGCR are co-regulated? By what?

A

T (Sterol Receptor elements)

105
Q

How does high LDL lead to plaque in bloodstream?

A

LDL gets oxidized and is consumed by macrophage which becomes a foam cell if too many are eaten. Builds up plaque on the endothelial cells.

Biochemistry-Exam 2 (14 decks)

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