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Biochemistry-Exam 2 > Lipids (general) > Flashcards

Lipids (general) Flashcards

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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
Ceramide is made into?
Sphingomyelin and glycoshingolipids
25
Where are glycosphingolipids found?
Blood cell antigens
26
What is the structural difference between sphingosine and ceramide?
FA added to sphingosine to make ceraminde
27
Sphingosine is a type of?
Long chain amino alcohol
28
Adding phosphotidylcholine to ceramide gives oyu?
Sphingomyelin
29
T or F: Glycosphingolipids are important for cell cell contact
T
30
What are the four general functions of cholesterol?
Essential membrane component, bile salts, steroid hormones, vitamin D
31
What is an apolipoprotein?
Lipoproteins on the outside of miscelles that direct the internal contents
32
How are triacylglycerols and cholesteryl esters transferred in the blood?
In phospholipid enclosed micelles
33
What are the four major types of lipoprotein carriers?
Chylomicrons, LDL, VLDL, and HDL
34
What is the size order largest to smallest of lipoprotein carriers?
Chylomicrons, VLDL, LDL, HDL
35
What do chylomicrons primarily transport?
Triglycerides
36
What do VLDLs mainly carry?
Triglycerides
37
What do LDL mainly transport?
Cholesterol
38
What do HDLs mainly transfer?
Protein
39
T or F: High LDL is bad prognosis for heart disease
T
40
LDL has only one type of apoprotein:
B-100
41
Mutation of B-100 leads to issues with what?
LDL
42
Mutation in B-48 apoprotein leads to issues with potentially?
Chylomicron
43
Triglycerides in the diet are primarily transported by?
Chylomicrons
44
VLDL carry fat from where?
The liver to tissue
45
What tissues primarily need FA?
Adipose, lung, muscle
46
What is the percentage composition of triglycerides from highest to lowest for lipoproteins?
Chylomicron, VLDL, LDL, HDL
47
What is the percentage composition of cholesterol from highest to lowest for lipoproteins?
LDL, HDL, VLDL, CM
48
Liver AND intestine make this type of Lipoprotein
HDL, deliver from tissues to liver for elimination
49
VLDL generates?
LDL to deliver cholesterol to tissues and liver
50
Liver generates?
VLDL to deliver endogenous FA to peripheral tissue
51
Intestine generates?
CM to deliver dietary FA to peripheral tissues
52
Endogenous FA is transported by? Exogenous FA?
VLDL, CM
53
What is the function of bile salts?
Emulsification of lipid droplets in small gut
54
Bile salts are made in?
The liver
55
Bile salts are stored in?
Gall bladder
56
How much bile salt is used each day? Lost?
15-30 g and 0.5 g/day
57
What is bile made from?
Cholesterol
58
What is PTL?
Panceratic triglyceride lipase. Released from pancreas to hydrolyze a TAG into a monoacylglyceride and 2 free FA salts
59
What happens to the FA salts and monoacylglyceride from PTL?
Rejoined in the intestinal mucosal cells and pushed into lymphatic vessel and to the blood stream
60
What transporter is responsible for bringing fat derivatives from the intestinal lumen into the enterocytes in the mucosa?
FATP4 transporters
61
What apoproteins cover chylomicrons?
B-48, C, and E
62
CM carry what in addition to TAGS?
Fat soluble vitamins
63
What is the function of LPL?
In all tissue, cleaves FA off and makes 3 FA and glycerol. Glycerol is water soluble and FA is used by tissue
64
What is steatorrhea?
Fat in stool due to absorption issues
65
What is abetalipoproteinamia?
B-100 defect causing no FA or ADEK vitamin absorption
66
What are the five main functions of adipose?
Energy storage, protection of organs, insulation, soluble fat vitamin storage (ADEK), synthesis of adipokines (hormones from fat, usually peptide hormones)
67
Two body shapes, two types of fat, worse for disease?
Apple, Pear. Subcutaneous, Visceral. Visceral is worse.
68
T or F: Adipose cells grow in volume not in number
T (generally)
69
When does adipose number typically stabilize?
Early 20s
70
What happens in the fed state in regards to fat?
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
What happens in the fasting state for adipose?
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
What is HSL?
Hormone sensitive lipase which breaks down TAG in adipose during fasting state (only in adipose)
73
In adipose, what happens when glucagon/epinephrine is conjugated to receptor?
cAMP to PKA activation. Phosphorylates HSL to make it active.
74
In adipose, what happens when insulin is conjugated to receptor?
Activates PDE (phosphodiesterase) to take cAMP to AMP which causes HSL to become dephosphorylated to become inactive
75
What is leptin?
An adipokine that inhibits hunger and increases metabolic rate
76
Where is leptin made? Effects? Long or short?
Adipose, dec. appetite, inc. caloric expenditure, long term effect
77
What is ghrelin? Where is it made? Effects?
Produced by stomach, increases appetite, short and long effects.
78
T or F: Bile salts decrease weight gain
T (by increasing energy expenditure via brown fat)
79
What are beige/brown fat cells?
Adipose cells that undergo thermogenesis to waste energy
80
What are phospholipases?
Break down phospholipids.
81
What bond in phospholipids is important to know?
C site (between the glycerol and phosphate group). Important for signal transduction
82
Where does Degredation of sphinosines occur?
In the lysosome
83
What is sphingolipodosis?
Failure to break down sphigosines leading normally to CNS issues
84
What is Tay-Sachs diesease?
Failure to break down ganglioside GM2 which is a glycosphingolipid due to an enzyme deficiency in the lysosome
85
What can cross the lipid bilayer?
Small uncharged polar molecules, gases, and urea. Ions, large molecules, water, charged molecules cannot
86
What is endocytosis?
Eating of external particles. Autophagy is a special type of endocytosis
87
What are coated pits usually rich in?
Receptors in order to endocytose molecules specifically
88
T or F: Endosomes are low in pH?
True to release contents from receptors
89
What is transferrin?
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
T or F: LDL is taken up by cells
T (all other lipoproteins are not taken up, LDL has a receptor)
91
Name the four functions of cholesterol
Essential membrane component, bile salts, steroid hormones, vitamin D
92
T or F: Plasma levels of cholesterol are linked to death rate
T
93
T or F: Dietary cholesterol has a major effect on plasma cholesterol levels
F
94
How is cholesterol degraded?
Trick question. There is no degradation pathway. It is excreted as bile salts
95
What precursor molecule is cholesterol synthesized from?
Acetyl CoA
96
What is the cholesterol production/intake rate for body?
0.5 g/d from diet and 0.5 g/d from synthesis
97
What is the rate limiting step for cholesterol synthesis?
HMG-CoA Reductase
98
What do statins do?
Block HMG-CoA reductase step in synthesis
99
LDL-Receptors are rich in what apoprotein?
B-100
100
What is familial hypercholesteremia?
Disorder of high plasma cholesterol, typically a mutation in apoB100, autosomal dominant
101
When is cholesterol made de novo?
When there is no LDL in the blood serum
102
What is SRE?
Sterol Receptor Element in nucleus
103
How is cholesterol synthesis controlled on cellular level?
SREBP is activated (SRE-binding protein) which activates BOTH LDL receptor synthesis and HMG CoA reductase synthesis
104
T or F: LDLR and HMGCR are co-regulated? By what?
T (Sterol Receptor elements)
105
How does high LDL lead to plaque in bloodstream?
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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