Bsf Block 3: Fatty Acid Synthesis (Bondarenko)

Front 1

Where do sharks store fat?

Back 1

liver

Front 2

What kind of protein is expressed in the brown adipose in mammals?

Back 2

mitochondrial uncoupling protein

Front 3

What is brown adipose mainly used for?

Back 3

thermogenesis

Front 4

Where does fatty acid synthesis occur?

Back 4

Mainly in the liver but also in adipose tissue

Front 5

Are carbohydrates the only source of carbons for fatty acid synthesis?

Back 5

amino acids and TCA cycle intermediates

Front 6

Structural lipids and triglycerides contain fatty acids of at least __ carbons.

Back 6

16

Front 7

The introduction of double bonds _____________ fatty acid melting point.

Back 7

decreases (double bond makes the fat unsaturated and it will no longer be tightly packed = easier to melt)

Front 8

What are 2 essential fatty acids?

Back 8

1. linoleic acid
2. linolenic acid

"LIFE LINES"

Front 9

What becomes essential if linoleic acid is deficient in the diet?

Back 9

linoleic acid makes ARACHIDONIC ACID (which is necessary to create prostaglandins)

Front 10

Decreased vision and altered learning behaviors are all symptoms of a deficiency in what essential fatty acid?

Back 10

linolenic acid

Front 11

(Lipogenesis/lipolysis) is inhibited in type 1 diabetes.

Back 11

LIPOGENESIS (fats get metabolized in response to the lack of glucose uptake by cells...lipolysis upregulated and lipogenesis inhibited)

Front 12

What process provides carbons for fatty acid synthesis?

Back 12

malate shuttle

Front 13

What is the committed step in fatty acid synthesis?

Back 13

synthesis of malonyl-CoA by acteyl-CoA carboxylase

Front 14

Although fatty acid synthesis occurs in the cytoplasm, where does the acetyl-CoA + oxaloacetate (OAA) --> citrate precursor come from?

Back 14

mitochondria

Front 15

Once citrate leaves the mitochondria, what happens to it before it can be incorporated into the fatty acid synthesis pathway?

Back 15

it turns back into acetyl-CoA and OAA

Front 16

What enzyme catalyzes fatty acid chain elongation?

Back 16

fatty acid synthase

Front 17

Regulation of acetyl CoA carboxylase: Acetyl CoA carboxylase, the enzyme catalyzing the conversion of acetyl CoA to malonyl CoA (committed step), is dependent on ______ and ______.

Back 17

biotin, CO2 and ATP

Front 18

Regulation of acetyl CoA carboxylase: What is responsible for allosteric activation and inhibition of acetyl CoA carboxylase?

Back 18

1. activation: high citrate levels
2. inhibition: high palmitoyl CoA levels

Front 19

Regulation of acetyl CoA carboxylase: Does insulin activate or deactivate acetyl CoA carboxylase? How?

Back 19

activates through dephosphorylation (insulin secretion indicates high glucose level --> fats will be stored as a result)

Front 20

Regulation of acetyl CoA carboxylase: Acetyl CoA carboxylase is inhibited by (phosphorylation/dephosphorylation).

Back 20

phosphorylation

Front 21

Regulation of acetyl CoA carboxylase: what does AMPK do in skeletal and cardiac muscles?

Back 21

phosphorylates acetyl CoA carboxylase, decreasing its malonyl CoA product. Malonyl CoA is an inhibitor of fatty acid oxidation. Thus, AMPK causes increased ATP production as a result of increased fatty acid oxidation

Front 22

Regulation of acetyl CoA carboxylase: AMPK is activated when there is...

Back 22

low ATP (AMPK stands for "AMP activated kinase"...high AMP means low ATP)

Front 23

Regulation of acetyl CoA carboxylase: a high carb/low fat diet (increases/decreases) the expression of acetyl CoA carboxylase.

Back 23

increases

Front 24

Regulation of acetyl CoA carboxylase: starvation or a low carb/high fat diet (increases/decreases) the expression of acetyl CoA carboxylase.

Back 24

decreases

Front 25

The fatty acid synthase enzyme has a acyl carrier protein (ACP) domain. _________________ is covalently linked to this domain and has a long, flexible arm that allows it to move from one active site to another within the fatty acid synthase complex.

Back 25

Phosphopantetheine (Pant)

Front 26

Once the acyl group of Acetyl CoA gets transferred onto the ACP domian, it gets transferred onto ___________________, allowing malonyl CoA to be transferred onto the vacant ACP site.

Back 26

beta-ketoacyl synthase

Front 27

What are the 2 sources of NADPH for fatty acid synthesis?

Back 27

1. pentose phosphate pathway (main source)
2. conversion of malate to pyruvate

Front 28

Oxidation of palmitate yields _____ ATP.

Back 28

131

Front 29

Oxidation of fatty acid yields _____ ATP.

Back 29

9

Front 30

Malonyl CoA inhibits _________, which transports long chain fatty acids into the mitochondria for beta oxidation.

Back 30

CPT1. You will want to inhibit oxidation because high malonyl CoA means high fatty acid synthesis

Front 31

Does glucagon inhibit or stimulate fatty acid synthesis?

Back 31

inhibits (it's released when you have no blood glucose so it would promote degradation, not synthesis, of fatty acids)

Front 32

Fatty acid elongation occurs where?

Back 32

mitochondria and endoplasmic reticulum

Front 33

__________ is a substrate for fatty acid elongase.

Back 33

Palmitoyl CoA

Front 34

Very long fatty acids (24 carbons) are found where?

Back 34

brain

Front 35

Desaturation of fatty acids (adding double bonds) occurs where? What enzyme is used?

Back 35

endoplasmic reticulum

mixed-function oxidases

Front 36

Humans lack the ability to introduce a double bond at what carbon of a fatty acid chain?

Back 36

carbon 10 from the omega end

Front 37

Triglycerides (triacylglycerols) are formed by the __________ of fatty acids.

Back 37

esterification

Front 38

The initial acceptor of fatty acids in triglyceride synthesis is ____________.

Back 38

glycerol phosphate (GP)

Front 39

What are the 2 sources of glycerol phosphate in the body?

Back 39

1. Glycolysis
2. glycerol kinase creates GP from glucose, only in the liver. ADIPOCYTES DO NOT HAVE GLYCEROL KINASE

Front 40

What converts fatty acids into their activated form?

Back 40

a family fatty acyl CoA synthetases

Front 41

After a meal (high insulin levels), adipocytes secrete ____________, which digests the triglycerides of chylomicrons and VLDL to form free fatty acids, which then enter adipocytes, become activated and form triglycerides.

Back 41

lipoprotein lipase (LPL)

Front 42

What hormone stimulates glucose metabolism and its conversion to fatty acids in adipocytes?

Back 42

insulin

Front 43

With low insulin due to fasting, lipolysis is initiated due to high levels of _________ in the adipocyte.

Back 43

cAMP

Front 44

Lipolysis: cAMP activates _____, which phosphorylates _______________.

Back 44

-PKA
-hormone sensitive lipase

Front 45

Glyceroneogenesis: _________ are used to resynthesize triglycerides using what 2 things?

Back 45

-fatty acids are used to resynthesize triglycerides using
1. lactate/pyruvate/amino acids
2. phosphoenolpyruvate carboxykinase (PEPCK)

Front 46

Glyceroneogenesis: what is the purpose of PEPCK?

Back 46

key enzyme that is induced by elevated [cAMP] in response to insulin or epinepherine, converting OAA to PEP and eventually into G3P

Front 47

When glycerol is produced in the adipocyte, can it be phosphorylated immediately to produce glycerol phosphate?

Back 47

No. It must first go to the liver because adipocytes lack glycerol kinase

Front 48

Can plasma fatty acids, be used by erythrocytes or the brain?

Back 48

No

Front 49

What lipid is found in blood lipoproteins, bile, lung surfactant, and is the source of polyunsaturated fatty acids (arachidonic acid)?

Back 49

glycerophospholipids

Front 50

What lipid is a component of the myelin sheath and serves in intracellular communication and antigens of the ABO blood groups?

Back 50

sphingolipids

Front 51

What 2 pathways can make glycerolphospholipid from phosphatidic acid?

Back 51

1. removal of phosphate > DAG
2. addition of CTP > CDP-DAG

Front 52

The phosphatidyl-somethings and cardiolipin are all...

Back 52

glycerophospholipids

Front 53

Synthesis of glycerophospholipids: DAG interacts with what to make PEA?

Back 53

CDP-ethanolamine to produce phosphatidylethanolamine (PEA)

Front 54

phosphatidylethanolamine (PEA) can be converted to phosphatidylcholine (PC) by an __________ reaction.

Back 54

methylation

Front 55

phosphatidylethanolamine (PEA) can be converted to phosphatidylserine (PS) by an ___________ reaction.

Back 55

exchange

Front 56

Phosphatidylserine (PS) can be converted to PEA by a _________________ reaction.

Back 56

decarboxylation

Front 57

CDP-DAG reacts with ___________ to form cardiolipin, a component of the mitochondrial membrane.

Back 57

phosphatidylglycerol

Front 58

PIP (phosphatidylinositol) can be to PIP2 by _________. PIP2 is a source of the DAG and IP3 second messengers.

Back 58

phosphorylation

Front 59

Synthesis of plasmalogen: plasmalogens are produced from _________ with the formation of an _______ linkage.

Back 59

-DHAP
-ether

Front 60

Ethanolamine plasmalogen is found in __________.

Back 60

myelin

Front 61

Choline plasmalogen is found in _______.

Back 61

heart muscle

Front 62

Plasmalogen synthesis occurs in _________.

Back 62

peroxisomes

Front 63

Plasmalogen synthesis, because it occurs in peroxisomes, is affected in individuals with ____________.

Back 63

Zellweger syndrome

Front 64

Lung surfactant is made of what lipid?

Back 64

phosphatidylcholine

Front 65

Phosphatidylcholine (which makes lung surfactant) is produced and secreted by what cells?

Back 65

granular pneumocytes

Front 66

Degradation of glycerophospholipids: ___________________ produces the second messengers DAG and IP3 from the degradation of PIP2.

Back 66

phospholipase C

Front 67

Degradation of glycerophospholipids: what enzyme is activated in repair of lipids damaged by oxidative free-radical reactions?

Back 67

phospholipase A2

Front 68

Sphingomyelin is synthesized by the reaction of ____________ with phosphatidylcholine.

Back 68

ceramide

Front 69

Deficiency of ______________ in lysosomes results in Neimann-Pick disease.

Back 69

sphingomyelinase

Front 70

Tay-Sachs disease lacks __________.

Back 70

hexosaminnidase (Tay-SaX laX heosaminnidase)

Front 71

Niemann-Pick disease is an accumulation of ______________.

Back 71

sphingomyelin (No man picks his nose with his sphinger)

Front 72

Fabry disease mainly occurs in (males/females).

Back 72

males (FabriX)

Front 73

What is considered the normal BMI range?

Back 73

18.5 to 24.9 kg/m2

Front 74

What are the 3 functions of leptin?

Back 74

1. suppresses appetite
2. promotes lipolysis
3. inhibits fatty acid synthesis

Front 75

Low body fat content = high or low leptin levels?

Back 75

high leptin levels. Low leptin levels = obese

Front 76

When adipocytes become larger, they secrete reduced amounts of ______________. This hormone normally activates AMPK (AMP-activated protein kinase) and nuclear transcription factor--leading to FA oxidation. That means it is harder for an obese person to use circulating fatty acids and glucose for energy.

Back 76

adiponectin