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Biochemistry > Lipid, Cholesterol and Bile Acid Synthesis > Flashcards

Lipid, Cholesterol and Bile Acid Synthesis Flashcards

Contains 1/2 Week 6 Material

1
Q

What is the most fundamental structure of lipids?

A

Fatty Acids

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2
Q

Which kinds of fatty acids have double bonds?

A

Unsaturated

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3
Q

What is the nomenclature for unsaturated fatty acids?

A

Total# of carbons : (# of double bonds) △ ^ (# carbon where double bond starts INCLUDING C from carboxyl carbon)

If the fatty acid is poly-unsaturated, we add commas to indicate the starting point of additional double bonds.

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4
Q

What is an omega carbon?

A

The last carbon in the chain

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5
Q

How can we use omega carbons to describe fatty acid nomenclature?

A

Omega________

_____ will be number of carbons from omega carbon that starts the double bond closest to the terminal carbon

Include omega carbon when countin

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6
Q

What are the three essential fatty acids?

A
  1. Linoleic Acid (Omega-6)
  2. Alpha- linoleic acid (Omega 3)
  3. Arachidonic Acid (Omega 6)
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7
Q

What happens if you lack the three essential fatty acids?

A
  1. Skin and kidney damage
  2. Cataracts
  3. Increased membrane permeability of water
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8
Q

All double bonds in naturally occurring polyunsaturated fatty acids are in _____ configuration.

A

cis

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9
Q

Arachidonic Acid is a major precursor of _______.

What are they?

How many carbons?

A

Eicosanoids

Prostaglandins, thromboxane, leukotrienes are 20 carbon fatty acids and powerful physiological regulators

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10
Q

How does arachidonic acid play a role in our bodies?

A

Arachidonic acid is ingested from the diet and combines with a phospholipid to enter the cell membrane of a tissue cell.

Phospholipase A2 will cleave the ester bond in the second fatty acyl chain to release AA from the cell membrane into the cytosol of the cell. AA is now able to become

  1. Epoxides
  2. Leukotrines
  3. Thrombonxane
  4. Prostaglandins

which are all 20 carbon fatty acids called Eicosanoids

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11
Q

Eicosanoids come from _________. Examples include __________ and their function is to _______.

A

Arachidonic Acid

  1. Epoxides
  2. Leukotrines
  3. Thrombonxane
  4. Prostaglandins

Regulate BP
Muscle Contraction
Bronchodilation and constriction
Water/Sodium Excretion
Inflammatory Response

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12
Q

Thromboxine is responsible for stopping ______.

A

Bleeding

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13
Q

Prostaglandins and Thromboxane have precursors of ________ and ________.

A

Arachidonic Acid and Linoeic Acid

(Eicosanoids have precursors of the ^^)

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14
Q

Essential fatty acids come from ______.

A

Our diet

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15
Q

Where can you find trans-fatty acids?

A

Food products, especially processed ones and baked goods!

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16
Q

Trans-fats occur naturally.

True or false?

A

FALSE

It is made by food corporation.

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17
Q

How much trans-fat does an Oreo have?

A

2.5g

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18
Q

How are trans-fatty acids made?

A

Transfer acids are formed during hydrogenation a process that solidifies liquid vegetable oil by adding hydrogen atoms to the double bonds of unsaturated fatty acids.

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19
Q

What is hydrogenation?

A

The addition of hydrogen. In the case of fatty acids hydrogenation is the process that takes cis-unsaturated fatty acids and makes them trans- fats

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20
Q

Linoieic Acid when hydrogenated becomes _________ which has _____ double-bond.

A

Elaidic Acid

Trans-double bond

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21
Q

What types of unsaturated fatty acids make membrane packing loose ?

What types of unsaturated fatty acids make membrane packing tight?

A

Cis-fatty acids

Trans-fatty acids

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22
Q

What occurs in cis-unsaturated fatty acid stacking that causes it to pack _____ ?

A

loosely

the cis-configuration of the double bond causes a 120 degree kink in the chain creating spaces between chains that creates the membrane fluidity.

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23
Q

Why is it important for our membrane to be able to pack loosely?

A

Membrane fluidity allows for entrance of molecules into the cell (aka plasma membrane)

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24
Q

Trans fatty acids increase __________
Trans fatty acids decrease ___________

They can lead to ______

A

LDL
Triacylglycerol
Platelet Aggregation

HDL

Growth retardation in newborns

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25
Q

Fish oil is rich in _______ fatty acids which can decrease ___________.

A

Cis Omega-3 polyunsaturated fatty acids

Cardiovascular mortality

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26
Q

What other food item can contain lots of Omega-3?

A

Eggs

(Probably modified tho)

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27
Q

What is the structure of a triacylglycerol?

A

Carbon with 1 Hydrogen + 3 Variable hydrocarbon chains with a variable number of carbons and double bonds

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28
Q

Where are triacylglycerols stored?

A

Adipose Tissue

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29
Q

What acylglcerols are abundant in mammal cell membranes?

A

Phosphosacylglycerol
Sphingolipids
Cholesterol

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30
Q

Phosphosacylglycerols is also called ___________.

Describe the structure

A

Glycerophospholipids

Glycerol Backbone
C1- Fatty Acid
C2- Fatty Acid
C3-Phosphate moiety + Head group

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31
Q

Phosphatic acid is ________ with _________ on the C3 of the ______.

A

Phosphoacylglycerol with one phosphate acid on the C3 of glycerol

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32
Q

If a choline moeity group is attached to the _______ on the C3 of acylglycerol, what is the compound called

A

Phosphatidylcholine

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33
Q

At ph=7, the amine group of Phosphatidylcholine is _________, the phosphate is _______.

Net charge is :

What is another name?

A

Postitive

Negative

0

Lecithin

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34
Q

The ________ attached to the C3 carbon of glycerol is ________ and will face the _______ of a compound.

A

Phosphate + head group

Polar

Outside (facing water)

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35
Q

What charges will exist on the SURFACE of cell membrane and why?

A

Neutral or Negative

Think about Phosphatidylcholine and Phosphatidic Acid

Phosphates are negatively charged = -

Phosphate + The addition of a polar head group = Neutral

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36
Q

Phosphatidylinositol 4,5 - bisphosphate (PIP2) carries what charge?

Why is it important?

A

Negative or no charge

It is a degradation product that serves as important signaling molecules.

Phosphoacylglycerol

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37
Q

If a lipid only has one fatty acid chain, what is it called?

A

Lysolecithin or Lyso-PC

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38
Q

Lyso means ________.

A

One fatty acid chain on the glycerol molecule

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39
Q

Phosphoacylglycerols are important for _________

A
  1. Cell membrane Structure
  2. Signal Transduction
  3. Metabolic Pathway
  4. Membrane fluidity and lateral organization
  5. Cell membrane function
  6. Lung Surfectants
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40
Q

What makes lung surfectants?

A

Phosphoacylglycerols

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41
Q

All sphingolipids are derived from ________.

What is the backbone of sphingolipids?

A

Ceramide

An 18-carbon structure made of sphingosine + fatty acyl chain

Ceramide is the compound when the amino group of sphingosine is linked to an acyl chain

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42
Q

Sphingosine is a major/minor part of _______.

What is on C1 ,C2 and C3 of the ceramide

A

Major part of ceramide- it IS the backbone

C1- OH or some variable group
C2- Amino group with hydrocarbon chain
C3- OH with long hydrocarbon chain

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43
Q

Sphingomyelins can be split into two groups. What are they?

A

Sphingomyelin and Sphingoglycolipid

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44
Q

All sphingolipids come from _________.

The first carbon of ceramide is attached to a _________.

What happens if that group is replaced with

  1. Phosphorylcholine
    2.Galactose
    3.Oligosaccharide
A

Ceramide

-OH

  1. Sphingomyelin
  2. Galactocerebroside
  3. Ganglioside
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45
Q

How are sphingomyelins made?

Sphingomyelin is a type of sphingo___

A

Addition of phosphorylcholine to C1 of ceramide

Sphingolipid

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46
Q

What are the similarities between Sphingolipids and Phosphoacylglycerols?

A
  1. Polar moiety on first Carbon
  2. Second Carbon has long hydrocarbon chain
  3. Long hydrocarbon chain on 3rd carbon.

ASKKKK

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47
Q

In phosphoacylglycerols, fatty acids are attached to glycerol via _____ linkages, whereas in sphingolipids, a fatty acid is attached to sphingosine via an ____ linkage

A

ester

amide

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48
Q

Sphingolipids are key components of _______ and regulators in ________.

What are two key sphingolipid metabolites ?

A

Cell membranes;particulary nerve cell membrane

regulators in cell death/survival, toxin binding, cell-cell recognition

S1P
Ceraminde

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49
Q

What is S1P?

A

SphingoSINE 1- Phosphate that develops from sphingolipid degradation

Stimulates cell proliferation and survival, regulates cell motility and cytoskeletal reorganization

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50
Q

What is ceramide?

A

Apoptosis regulator

When sphingolipid is degrades, they regenerate ceramide.

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51
Q

Cholesterol is non-soluble in water and therefore _____. It’s signature feature is a ________.

Can humans degrade this structure?

A

non-polar

Tetracycline Ring

NO

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52
Q

Free cholesterol can be converted to ________.

A

Cholesterol esters

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53
Q

Cholesterol is a major component of cell membrane and is embedded into the membrane.

True or False

A

FALSE

Located INSIDE cell as part of oily droplets or located in blood lipoprotein particles

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54
Q

Cholesterol can insert itself into the _________ formed by ________.

A

Bilayer

Sphingolipids and phosphoacylglycerols

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55
Q

Can cholesteryl esters enter the cell membrane?

A

NO

They aggregate with triacylglycerols to transfer themselves into the cell membrane.

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56
Q

What is the component in cell membranes that keeps it stable?

A

Cholesterol

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57
Q

What makes up the hydrophilic head of phosphoacyl glycerols?

A

Phosphate + Moiety on Carbon 3

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58
Q

Integral proteins insert themselves ___________ the membrane while peripheral proteins ________ the membrane.

A

All the way through

Half-way

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59
Q

Most dietary lipids are _______.

A

Triacylglycerols

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60
Q

Dietary TGs are digested by _________ produced by glands in the _________ and _______.

When they reach the _____, they can be digested by _______.

Both of these substances have pH of _______.

What do TG’s break down into?

A

Lingual Lipase, Tongue and Soft Palate

Stomach, Gastric Lipase

4-5

Fatty acids and DIacylglycerol

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61
Q

Lingual lipase and gastric lipase prefer to hydrolyze what kind of triacylglycerols?

Why is this important for BABIES?

A

short-chain and medium-chain ( less than 12 carbons on acyl chains)

SCTGs and MFTGs are abundant in milk

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62
Q

Major part of digestion occurs in the _________.

What does digestion of lipids (TGs) require along with ______and _______ ?

A

Lumen of Small Intestine
Lingual and Gastric

  1. Bile Salts
  2. Pancreatic Lipase
  3. Co-Lipase
  4. Bicarbonate (HCO3-)

These are after breakdown by lingual and gastric lipase

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63
Q

Bile acid is produced from _________ in the _______ and thus has a _________.

A

Cholesterol in the liver

Tetracycline Ring

64
Q

Bile can exist at two different forms. What are they and when do they exists?

A

Bile Acid which is the protonated form COOH

Bile Salt which is the anionic deprotonated form COO-

65
Q

Which form of bile exhibits detergent properties and why?

A

Anionic Form (COO-) BILE SALT

66
Q

Which bile form is most abundant at neutral body ph?

A

Anionic Bile Salt

67
Q

Digestion uses bile _____.

A

SALT

Anionic
Deprotonated COO-

68
Q

Emulsion particles are ______, about _____ micrometers.

Mixed micelles are _____, about ______micrometers

A

Large , 1-20 micrometers

Small, 4-7 micrometers

69
Q

Cholesterol will be present on the _______ of the emulsion droplet while cholesterol esters will be present _______.

A

Outside

Inside

70
Q

TAGs will be present __________ emulsion droplet

A

inside

71
Q

Monoacylglycerols will be present ________ emulsion droplet

A

Outside

72
Q

When bile enters the small intestine, bile salts break down ___________into_________ through a process called emulsification.

A

When bile enters the small intestine, bile salts break down large fat globules into smaller micelles through a process called emulsification.

73
Q

Pancreatic lipase is attracted and anchored to the ________ by _______.

A

Emulsion particles by CO-lipase

74
Q

Pancreatic lipase cleaves the _______ bond of the TAG to remove a ________ creating a ______. This process occurs once more until ___________ is made.

A

Ester bond

Fatty acid to create a diacylglycerol

This process continues to until a 2-monoacylglycerol is made.

75
Q

The final product after pancreatic lipase hydrolyzes the ester bonds of triacylglycerol is _________.

A

2- Monoglycerol

76
Q

Bile salts create __________ that are recognized by _______ and broken down by _________.

A

emulsion particles that are recognized by co-lipases and are broken down by lipases.

77
Q

What does HCO3- do?

A

Bicarbonate reduces the pH of the small intestine and increases anionic species. This promotes lipid digestion and absorption by increasing enzyme activity.

78
Q

What are the final degradation products of lipid metabolism and where are they located?

A

Fatty Acid and 2-Monoacylglycerol in lumen of small intestine.

79
Q

How do the products of dietary TG’s get to the rest of the body from the small intestine lumen?

A
  1. Dietary TGs have been hydrolyzed to 2-monoacylglycerol and fatty acids
  2. Mixed micelles formed by many lipid soluble materials including FA, 2-MG and Bile salts are taken up by intestinal epithelium via endocytosis.
  3. TG’s are re-synthesized in intestinal epithelial cells and combine with other lipid-soluble materials and apo-proteins to form chylomicrons.
  4. Chylomicrons are lipoprotein molecules released into lymph and eventually to blood for other organs to take up.
80
Q

What are cholymicrons?

A

The name for the lipoprotein resynthesized TAGs that have been transported from the intestinal epithelial cells to lymph for transport to the blood.

81
Q

Lipid Malabsorption can be caused by __________

A

deficiency in pancreatic lipase or bile acid

Steatorrhea or lipid accumulation in feces could occur

LOSS of important fuels, weight loss and vitamin loss, fatty acid deficiency

82
Q

What are the 4 fat-soluble vitamins?

A

ADEK

83
Q

What is the major organ that synthesizes fatty acids?

A

Liver

84
Q

What is the most abundant fatty acid in the body?

A

Palmitate

85
Q

Describe the general flow from glucose to fatty acids.

A

Glucose goes through glycolysis and pyruvate dehydrogenase to made Aceytl CoA.

Aceytl CoA will go into fatty acid synthesis to generate a LCFA, such as palmitate, which can be made to Fatty Acid CoA.

This Fatty Acid CoA will combine with glycerol 3 phosphate to make a TAG.

TAG will combine with other lipids to make VLFCA and enter the blood.

86
Q

Starting material for fatty acids is ______ which contains ______ carbons.

A

Acetyl-CoA

2

87
Q

Palmitate has _____carbons.

A

16

88
Q

Fatty acid synthesis from carbohydrates starts with the _____________.

A

Conversion of glucose to mitochondrial Acetyl-CoA.

In order for Acetyl-CoA to be produced from pyruvate. The pyruvate dehydrogenase enzyme is required.

89
Q

_________ is present only in the _______ and is required to catalyze the conversion of ____________ into Acetyl-CoA.

The reaction as a _________ delta G and is __________.

A

Pyruvate dehydrogenase is present only in the mitochondria and is required to catalyze the conversion of pyruvate to acetyl-CoA.

Negative delta G and is irreversible

90
Q

Pyruvate dehydrogenation in the mitochondria is reversible. True or False.

A

FALSE

91
Q

Acetyl CoA is very ______ and has ________ charges at neutral pH.

It cannot pass through the ___________.

What happens next?

A

large, 4 negative

mitochondrial membrane

Pyruvate carboxylase converts pyruvate to oxaloacetate. This combines with Acetyl CoA to make citrate which is transported to the cytosol via tricarboxylate translocation.

Citrate will break down into OAA and AcetylCoA

92
Q

Pyruvate has been dehydrogenated in the ______________ by ________ to ____________.

____________ cannot exit the ___________membrane

_________ will turn ________ into __________. _______ will combine with _________ to make _________.

___________ will leave the __________ via ___________ and break off into _______.

A

mitochondria, pyruvate dehydrogenase to Acetyl CoA

Acetyl CoA cannot exit the mitochondrial membrane

Pyruvate carboxylase will turn Pyruvate into oxaloacetate. OAA will combine with AcetylCoA to make Citrate

Citrate will leave the mitochondrial membrane via tricarboxylate translocase to enter the cytosol and break off into the OAA and AcetylCoA

93
Q

What two compounds are required to synthesize long-chain fatty acids?

A

NADPH and Acetyl CoA

94
Q

What generates NADPH necessary for the synthesis of long-chain fatty acids?

A

The Malic Enzyme Pathway and The Pentose-Phosphate Pathway

95
Q

When NADPH is high, what rate-limiting enzyme of the pentose phosphate pathway is regulated?

A

Glucose 6 Phosphate Dehydrogenase

96
Q

What is the rate-limiting enzyme in the pentose phosphate pathway?

A

Glucose 6-Phosphate dehydrogenase

which converts Glucose 6-Phosphate to 6-Phosphoglucono-lactone

NADP+ is converted to NADPH

97
Q

NADPH is mainly for ___________

NADH is mainly for _________.

A

Reductive biosynthesis such as synthesis of cholesterol and fatty acids

ATP generation

98
Q

Remember in fatty acid transport, __________ inhibits the __________ that is required to shuttle fatty acids across the mitochondrial membrane.

Why is this important?

A

Malonyl CoA, Carnitine

Fatty acid synthesis and beta-oxidation both occur in the mitochondria! When one is occuring we don’t want the other to happen! So the production of Malonyl CoA inhibits fatty acids from entering the mitochondria for breakdown when synthesis is needed instead.

99
Q

What is the rate-limiting step in fatty acid synthesis?

Where does it occur?

A

Carboxylation of Acetyl-CoA to form Malonyl CoA by Acetyl CoA Carboxylase

100
Q

What is the most important enzyme in fatty acid synthesis ?

What does it do ?

A

Acetyl CoA Carboxylase

Add a CO2 to Acetyl CoA to create Malonyl CoA

101
Q

What key component is required for the carboxylation of Acetyl CoA to Malonyl CoA via ________ ?

Describe the interaction

A

Acetyl CoA Carboxylase

Biotin is required!

The lysine residue of Acetyl CoA Carboxylase will covalently link to the carboxyl group of biotin to make Enz-biotin complex

The nitrogen on the cyclic portion of biotin becomes very reactive and will bind a CO2 to make an enzyme intermediate that is very unstable that has a HIGH tendency to loose the CO2 to a substrate such as ACoA.

102
Q

Why is biotin key?

A

Biotin incorporates with Acetyl CoA Carboxylase to make Malonyl CoA by serving as a CO2 carrier for Acetyl CoA.

103
Q

The fatty acid synthase complex contains monomers made of __________ in the polypeptide chain.

These monomers are arranged as a ________.

A

8 components

7 enzymes + Acyl Carrier Protein

HOMODIMER. There are 2 monomers that are exactly the same.

104
Q

Describe the monomers of the fatty acid synthase complex and how they form a homodimer.

A

Monomer 1 and 2

Cysteine with SH ——— SH- PPT

7 enzymes

Phosphopanthertheine with SH ———SH Cysteine

The SH of the Cysteine residue on Monomor 1 and the SH of the Phosphopantherteine residue on Monomer 2 will align and form bonds.

105
Q

Where are the elongation centers in the fatty acid synthase complex?

A

Where the Monomer residues align in the homodimer.

At the SH-SH bonds!

106
Q

Why is the SH group on phosphopantetheine important ?

A

PPT is attached to the Acyl Carrier Protein. PPT is covalently linked to a serine residue to the acyl carrier protein segment of the enzyme.

The SH group on phosphopantethiene covalently binds with malonyl-CoA to form a thioester during fatty acid synthesis.

107
Q

The SH group on phosphopantethiene, which is associated with a ______ residue on ________, covalently binds with ________ to form a _______ during fatty acid synthesis.

A

The SH group on phosphopantethiene , which is associated with a serine residue on ACP, covalently binds with malonyl-CoA to form a thioester during fatty acid synthesis.

108
Q

The cysteine residue with ____ is associated with ______ on the opposite end from __________.

A

Ketoacyl synthethase

SH

Phosphopanethine +ACP complex

109
Q

Describes the steps of fatty acid synthesis now that we have formed the fatty acid synthase complex

A
  1. Acetyl CoA will bind to the SH on the PPT+ACP complex. It can shift over to the Cystein-Ketoacyl synthetase complex as well.
  2. Malonyl CoA formed from Acetyl CoA by acetyl CoA carboxylase will attach the SH group on the PPT+ACP complex (it is empty now that the Acetyl CoA group has shifted to the other elongation site)
  3. Acetyl Co-A and Malonyl Co-A combine and undergo a decarboxylation reaction.
  4. NADPH is oxidized twice to complete an elongation cycle which pushes the reduction of the compound until the wanted fatty acid is formed.
110
Q

How many carbons is the molecule that yields after 1 round of elongation by fatty acid synthase?

A
  1. Acetyl-CoA add 2 Carbons
  2. Malonyl Co-A adds 3 Carbons
  3. The decarboxylation when Acetyl CoA and Malonyl CoA combine results in a loss of one Carbon Dioxide

Final : 4 Carbon molecule

111
Q

How much NAPH is used in one cycle of fatty acid elongation?

A

2!

NADPH is OXIDIzed and serve as a reducing agen

  1. Carbonyl to hydroxyl
  2. Reduce double bond to single bond
112
Q

In the first chain elongation cycle

Malonyl CoA provides ______ carbon units.

NADPH serves as ______.

A

2 carbon units

Reducing Agent (NADPH itself gets oxidized)

113
Q

What happens in the second elongation cycle?

A

Exactly same thing as first!

114
Q

How do we release fatty acid from the fatty acid synthase complex?

A

Thioesterase cleaves the thioester bond between the fatty acid and the synthetase complex.

115
Q

Can the body synthesize fatty acids with a chain length shorter than 16Cs?

A

Yes!

Thioesterase can cleave the fatty acid chain at different points during the synthesis cycle but prefers to have 16 carbonds as palmitate.

116
Q

Can we synthesize fatty acyl chains LONGER than 16 carbons?

A

Yes!

Convert palmitate to Palmitoyl CoA.

Use Malonyl CoA to insert 2 carbons into the chain and use NADPH

117
Q

How does the body synthesize fatty acids containing double bonds?

A

There system of 3 proteins embedded in the Endoplasmic Reticular Membrane that adds electrons to single carbon-carbon bonds to make it a double carbon-carbon bond.

118
Q

We know that the ER membrane has a system that can turn saturated fatty acids into a monounsaturated fatty acids by adding double bonds via ___________. How can we generate polyunsaturated fatty acids?

A

fatty acyl CoA desaturase

different kinds of desaturases

119
Q

Humans lack enzymes to introduce double bonds between ________ and ________.

What can add double bonds at these points?

A

Carbon 10 and the terminal carbon

PLANTS

120
Q

Why are essential fatty acids important?

A

Linoleic, Alpha-linoleic and Arachidonic acid are all fatty acids which have double bonds past the 10 carbon.

Humans cannot synthesize double bonds between C10 and the terminal carbon so we need to eat these fatty acids instead.

121
Q

Free fatty acids are safe for our cells. True or False?

A

False!

We need to covert Free Fatty Acid to Fatty Acid CoA. This also makes the compound high energy?

122
Q

Free fatty acids get converted to _________ and react with ________ to form __________.

These combine with other lipids and proteins to form _________.

A

Fatty acyl CoA and react with Glycerol-3-P to form triacyl glycerols.

These combine with other lipids and proteins to form VLDLs.

123
Q

Triclosan is found in ________.

Why is it important?

A

Toothpaste, Laundry Soap, Cosmetics, Mouthwash, Antimicrobial Soap

Kills bacteria and yeast by inhibiting an Acyl Carrier Protein Reductase which is necessary for fatty acid synthesis in germs.

124
Q

Triclosan can cause _________ resistance.

A

Antibacterial

125
Q

What is a triclosan alternative?

A

Stannous Flouride

126
Q

Acetyl CoA carboxylase is active in the ________ state catalyzed by ___________.

Therefore, fatty acid synthesis is active in the _______.

A

dephosphorylated, insulin-stimulated phosphatase

fed state

127
Q

Low energy levels cause ________ to be rendered inactive via _________ by _______.

A

Acetyl CoA Decarboxylase to be rendered inactive via phosphorylation by AMP-activated protein kinase.

128
Q

When insulin is high, _________ is active which allows __________ of __________.

A

Phosphatase, phosphorylation of Acetyl CoA Carboxylase

129
Q

Which enzymes are induced after a high-carb diet?

A
  1. Pyruvate Dehydrogenase
  2. Acetyl CoA Carboxylase
  3. Fatty Acid Synthase
  4. Citrate Lyase
  5. G-6-P Dehydrogenase (Pentose Phosphate Path)
130
Q

Cholesterol synthesis occurs in the _________ particularly on the ___________ of the __________.

Which organs?

A

cytosol, cytoplasmic face of the Endoplasmic Reticulum

Liver and Intestinal Cells

131
Q

What is the rate limiting step in cholesterol synthesis?

What is the rate limiting enzyme in cholesterol synthesis?

A
  1. HMG-CoA to mevalonate is the rate limiting STEP
  2. Its enzyme, HMG-CoA reductase is the rate limiting enzyme
132
Q

HMG-CoA reductase is associated with _______.

A

Cholesterol synthesis

133
Q

The _______ domain of HMG-CoA faces the _________ while the rest of the molecule is embedded in _________.

A

N-terminal , cytoplasm

Endoplasmic Reticulum Membrane

134
Q

What is the first step of cholesterol synthesis?

A

Acetyl CoA is converted to AcAcCoA

AcAcCoa is converted to HMG Co-A via HMG Co-A synthase

HMG Co-A is converted to Mevalonate via HMG Co-A reductase. NADPH is also oxidized to NADP+

135
Q

What are the products of the first step of cholesterol synthesis?

A
  1. NADP+
  2. Mevalonate
136
Q

HMG Co-A synthase is found in the _________.

A

ER membrane with N-terminus facing cytoplasm

137
Q

What is the second step of cholesterol synthesis?

A

Formation of activated isoprene units

Condensation of SIX 5-carbon isoprenes from the 30-square squalene

Isoprenes are made from mevalonate

(Mevalonate to 30 square squalene)

138
Q

What is stage three of cholesterol synthesis?

A

30 carbon squalene to cholesterol involving another oxidation of NADPH.

139
Q

What are the generic steps of cholesterol synthesis?

A
  1. Acetyl CoA to Mevalonate via HMG CoA reductase and NADPH oxidation
  2. Mevalonate to 30-carbon squalene
  3. Conversion of squalene to cholesterol.
140
Q

HMG Co-A Reductase Regulation

How is transcriptional control done?

A

There are two key proteins

  1. SREBPs - Sterol Regulatory Element Binding Proteins
  2. SCAP - SREBP cleavage activating protein

When cholesterol is high, these proteins will transfer to the golgi membrane. The DNA binding domain of SREBP will be cleaved after exposure to two proteases in golgi. This promotes transcription of HMG CoA reductase.

141
Q

When cholesterol content in cell is high, how is transcription of HMG CoA affected?

A

HMG CoA reductase will be degraded

142
Q

How does insulin affect cholesterol synthesis?

A

Insulin will remove a phosphate group from HMG-CoA reductase to render it inactive.

Remember if we have insulin, we have been FED!

143
Q

Where is cholesterol synthesized?

A

Liver

144
Q

Bile Salt synthesis occurs only in the ______.

A

Liver

145
Q

What is the rate limiting enzyme of bile salt synthesis from cholesterol?

A

7alpha- hydroxylase

145
Q

What are the two bile acids made in the liver?

A

Chenodeoxycholic Acid

Cholic Acid

146
Q

Bile acid can conjugate _______ and ______ to reduce the ________. This makes them ________.

A

Taurine and Glycine

pKA

better emulsifying agents

147
Q

Conjugated bile acids are important for __________. They are stored in the ______ and secreted into the _______ to aid in _________.

A

Serving as good emulsifying agents due to their low pkA

They are stored in the gallbladder and secreted into the intesting to aid in digestion

148
Q

Bacteria in the _________ does what to bile salts?

A

Large Intestine

Deconjugate
Dehydroxylate

As a result, bile acid may become so non-polar that it cannot enter back to the liver. Instead they are excreted by the body.

149
Q

What is a common secondary bile salt?

What is a secondary bile salt?

A

These are bile salts that bacteria have deconjugated or dehydroxylated rendering them too non-polar to enter the liver.

Lithocholic Acid

150
Q

Conjugated bile acids are ________.

A

Primary Bile Acids

151
Q

Why is it important to have secondary bile acids?

A

They help remove cholesterol from our bodies!

152
Q

Lipid degradation is particularly important for ___________ which are derived from condensation of ________ and ______.

A

Sphingolipids

Palmitoyl CoA and Serine

153
Q

Niemann-Pick Disease

What is the key enzyme?

A

Patients are unable to digest sphingolipids causing a buildup of fats.

Sphingomyelinase is the key enzyme.

154
Q

What diseases can be caused by the lack of ability to digest sphingolipids?

A
  1. Tay-Sachs
  2. Gauchers
  3. Neimann Pick

Biochemistry (18 decks)

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