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BIOCHEM Y2S2 > lipid metabolism > Flashcards

lipid metabolism Flashcards

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1
Q

what is fatty acid function?

A

-Major reserve and are esterified in form of TRIGLYCERIDES to be stored in adipose tissue

-Most cells can oxidize fatty acids to produce energy

-Source of ketone bodies ( in liver )

-Structural component to membrane lipids and membrane proteins

-Precursor for hormones like PROSTAGLANDINS

-Alteration in FFA ( free fatty acids ) metabolism are associated with obesity and diabetes

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2
Q

what is the fatty acid structure ?

A

2 ESSENTIAL FEATURES

1- Long hydrocarbon chain

2- A carboxylic acid group ( carbon 1 )

Either saturated or unsaturated

Unsaturated fatty acids exist in cis or trans and can be classified as monounsaturated or polyunsaturated

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3
Q

describe the long hydrocarbon chain?

A

chain length range from 4 to 30 carbons

12-24 is most common

The chain is typically linear and usually contain an even number of carbons

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4
Q

describe the carboxylic acid group ?

A

at carbon 1

give fatty acid at their AMPHIPHATIC NATURE

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5
Q

How does FFA tranpsort ?

A

either bound to:

Albumin

or

Lipoproteins

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6
Q

describe fatty acid forms and SOURCES?

A

DIET –> essential FA ( like linoleic and linolenic FA )

Carbohydrates and proteins obtained from diet can be converted to FA –> TAGS –> Storage

Proteins –> Ketogenic AA –> Fatty acids –> TAGS

Glucose ( carb ) —> Glycolysis —> Acetyl CoA —> Excess ATP —> FATTY ACID synthesis —> THEN CAN BE SOURCE OF ACETYL COA for energy

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7
Q

what are the forms of FA present in our body?

A

Free

TAGs

Cholesterol esters

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8
Q

describe fatty acids transport after eating ( FED)

A

-Triglycerides in chylomicrons ( Lipoprotein in small intestine )

-Cleared by LIPOPROTEIN LIPASE at endothelial surface of capillaries

  • Free FA can then be stored as fat in adipose tissue as TAGS or for energy generation

-In the liver :

Re-esterified FAs into TAGs will result in Latter to be transported to the peripheral tissue by VLDL

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9
Q

what is the effect of insulin of FATTY ACIDS?

A

Stimulates LIPOPROTEIN LIPASE at the capillaries

Stimulates —> FATTY ACID AND TAG synthesis in liver and adipose tissue

INHIBITS LIPASE IN ADIPOSE TISSUE ( HORMONE SENSITIVE LIPASE )

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10
Q

what happens in well fed states?

A

Occurs after carbohydrate , fat and protein rich meal

High insulin

Low glucagon

DEPHOSPHORYLATION

ANABOLISM

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11
Q

what happens in starvation/fasting state?

A

Low insulin

High glucagon

Posphorylation

catabolism

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12
Q

when is lipoprotein lipase activated?

A

when DEPHOSPHRYLATED

( Well fed state / insulin )

active when we have high energy and need to store more

its the enzyme found in endothelial surface

inhibited by glucagon cuz we need to use not store

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13
Q

when is hormone sensitive lipase activated?

A

WHEN POSPHORYLAYED

( STARVING STATE = glucagon )

active when we have low energy and we need to break down for energy

found in adipose tissue

inhibited by insulin cuz we need to use not to store

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14
Q

describe fatty acid synthesis?

A

Occurs in LIVER and ADIPOCYTES and in mammary gland during lactation

Mainly occur in CYTOPLASM

When glucose is plentiful, large amounts of ACETLY COA are produced by glycolysis and can be used for fatty acid synthesis

high ACETLY COA promotes denovo fatty acid synthesis ( from glycolysis or FA oxidation, ketogenic amino acid catabolism )

Fatty acid is not degraded to produce acetyl COA cuz Acetly coa is used for lipid formation

Acetyl Coa is produced in mitochondria matrix while FA synthesis in CYTOPLASM

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15
Q

what are the 3 stages of FA synthesis ?

A

1-Transport of Acetyl Coa into CYTOSOL ( cuz occurs in cytoplasm

2- Carboxylation of acetyl Coa

3- ASSEMBLY OF FA CHAIN

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16
Q

describe transport of acetyl Coa into Cytosol ?

A

1- Mitochondrial acetyl Coa produced by Pyruvate and form AA ketogenesis

2- Coa cannot pass the inner mitochondrial membrane

3- Acetyl Coa is COMBINED with oxaloacetate (OAA) to PRODUCE CITRATE by CONDENSATION reaction ( Coa + Oxaloacetate = citrate by citrate synthase )

4- Citrate now can pass and leave to go to cytosol and then there degrade back to Coa

5- Fatty acid transport requires ATP thats why INCREASE IN ATP AND CITRATE –> BOTH STIMULATE FA synthesis

this process is part of citrate acid cycle

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17
Q

can fatty acids be converted back to carbohydrates? ( glucose )

A

No

cuz pyruvate –> Acetyl Coa is IRREVERISBLE REACTION

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18
Q

why is Acetyl Coa is NOT considered by gluconeogenic ?

A

Although OAA is gluconeogenic

the 2 carbons from acetyl Coa

Doesnt directly contribute to the OAA that enter gluconeogenesis

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19
Q

describe Co Carboxylation ?

A

Acetyl Coa Carboxylase ( ACC )

Catalyzes the 2 step reaction by which Acetyl Coa is CARBOXYLATED

to form MALONYL - COA

Committed step in fatty acid synthesis

Acetyl Coa ——-> Malonly -COA by ACC

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20
Q

what does acetly coa carboxylase require?

A

CO2

ATP

Biotin cofactor

all carboxylaes require biotin

CO2 bind to biotin forming unstable intermediate which reacts with acetyl-Coa to form MALONYL COA

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21
Q

what activates ACC ?

A

activated when we need fatty acid synthesis

like in well fed state ( High insulin, low glucagon )

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22
Q

what is the regulation of acetly Coa carboxylase? ACC?

A

Its the committed step of fatty acid synthesis

1- Phosphorylation / dephosphorylation ( dephosphorylation is ACTIVE FORM in high and well fed energy by insulin )

2- Activated by high citrate and ATP and insulin ( citrate is allosteric activator )

3- Inhibited by Glucagon and epinephrine

High calorie diet , especially high carbohydrate diet—> High insulin and low glucagon —> DEPHOSPHORYLATION –> ACTIVE ENZYME

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23
Q

what enzyme responsible for Fatty acid elongation ?

Study These Flashcards
A

Fatty acid synthase

24
Q

describe fatty acid synthase ?

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A

Multifunctional

Dimeric enzyme

Each enzyme monomer has 7 different enzymes ( CONSIST 2 POLYPEPTIDES THAT CARRY SEVEN STEP REACTION)

TRANSICRPTIONALLY REGULATED ( MEANS FORMED WHEN ENEDED and upregulated during fatty acid synthesis )

25
what does elongation of fatty acid result in ?
Palmitic acid 16 carbon atoms fully saturated long chain fatty acid
26
what does fatty acid synthase require ?
NADPH ( pentose phosphate pathway or from malate conversion into pyruvate by malic enzyme ) for reductive biosyntehsis of fatty acid
27
what fatty acid synthase regulation in liver?
Fatty acid synthase expression is stimulated by INSULIN ( high energy so need to store) Thus excess glucose is stored as fat Polyunsaturated fatty acids DIMINISHES Transcription of fatty acid synthase gene in liver cells BY SUPRRESING PRODUCTION OF STEROL RESPONSE ELEMENT BINDING PROTEIN ( SREBPS ( transcription factor )
28
fatty acid Synthase regulation in FAT CELLS ?
Leptin ( high energy indicator ) ---> INHIBIT SREBP1 expression and FA SYNTHASE Leptin = hormone that has a role in regulating food intake and fat metabolism Leptin is produced by fat cells in response to EXCESS fat storage Leptin regulates body weight by DECREASING FOOD INTAKE , INCREASING ENERGY EXPENDITURE , INHIBITORY FATTY ACID SYNTHESIS Obese individuals have LEPTIN resistance ( cuz it wont inhibit food intake and wont inhibit fat acid synthesis )
29
describe triglyceride synthesis ?
occurs in liver and adipose tissue TG in adipose tissue are primarily stored for energy reserves TG in liver --> Packed into VLDL and released into the bloodstream An imbalance between TG synthesis and release in the liver can lead to FATTY LIVER DSIEASE accumulation of TAGs in tissue other than adipose = pathological state like NAFLD
30
describe the process of TG formation?
Combination of glycerol and fatty acids Glycerol ( Glycerol 3 phosphate )---> Essential for TG synthesis is derived from GLYCOLYSIS in both LIVER AND ADIPOSE tissue Dihydroxyacetone phosphate ( DHAP from glycolysis ) will be CONVERTED to Glycerol 3 phopshpate In the liveR : Glycerol 3 phopshate can be sourced from glycerol which is either derived from DIET or produced through the action of LIPOPROTEIN LIPASE which breaks down triglycerides in lipoproteins
31
what happens in well fed state?
these process of formation of TG are regulated to ensure that energy is stored efficiently and triglyceride are EITHER UTILIZED OR STORED APPROPRIATELY
32
what happens in Fast state?
Lipolysis of TAGS in response to hypoglycemia and STRESS Hormonal sensitive lipase (HSL ) break down fat for energy During times of stress or fasting , triglycerides TGs in adipose tissue are broken down to release FFA for energy production with the exception of BRAIN and RBCS ( cannot utilize FFA) Glycerol released from TG degradation in adipose tissue is transported to LIVER where its used to form GLUCOSE through GLUCONEOGENESIS The glycerol 3 phosphate formed can serve for another purpose depending on the need In fasting state - Glycerol 3 phosphate is exclusively directed toward GLUCONEOGENESIS to produce glucose which is ESSENTIAL FOR MAINTAING BLOOD SUGAR Under normal circumstances Glycerol 3 phopshate can be used in GLYCOLYSIS or incorpated into backbone of new triglycerides depending on need Fasting state - we dont use glycerol for glycolysis cuz the brain and RBC cant use glycerol as energy source so body uses them to make glucose
33
what stimulates gluconegensis in liver?
Glucagon Cortisol Glycerol ---> Glucose
34
what stimulates glycerol formation and Triglyceride breakdown ?
Epinephrine Cortisol High glucagon/insulin RATO ( glucagon ) Tags ----> Glycerol ( then moved to liver) by hormone sensitive lipase
35
describe oxidation of fatty acids?
Oxidation of palmotyl Coa ( 16 carbons ) Results in : CO2, H2O , NADH , FADH2 129 ATP (should be 131 but we use 2 atp for activation of the FA )
36
what are the steps of oxidation of fatty acids ?
4 steps in cycle 1- Oxidation 2- Hydration 3- Oxidation 4- Cleavage each cycle reduces the chain by 2 carbons From the CARBOXYL END OF FA
37
where does oxidation of FA occurs?
Very long FA 22C oxidation occur in : Peroxisomes ( MITOCHONDRIA ) ( a membrane- bound organelle a type of microbody found in cytoplasm of virtually all eukaryotic cells ) Peroxisomes are oxidative organelle )
38
How is FA transportation occur?
Require transportation of fatty acid to the mitochondria matrix by carrier CALLED CARNITINE ( carnitine shuttle ) Source of CARNITINE : meat, endogeneous synthesis by liver from methionine
39
what happens in CARNITINE deficiency?
Reduction in the ability to use a long chain fatty acids It could primary or secondary to liver disease and secondary to take VALPROIC ACID ( anti seizure drug ) cuz it decreases renal reabsorption This can lead to SEVERE HYPOGLYCEMIA and in severe CASES MIGHT LEAD TO DEATH
40
what enzyme activate Fatty acid for oxidation ?
Fatty acyl synthetase at outer mitochondrial membrane Fatty acid ---> Fatty acyl Coa
41
what enzyme binds FA to Carnitine ?
Carnitine acyltransferase 1 transfers the fatty acyl group to carnitine ( leaves the Coa to move alone inside ) AT OUTER MITOCHONDRIAL MEMBRANE Then Fatty acyl carnitine is shuttled across the inner mitochondria via A TRANSPORTER
42
what is the function of carnitine acyltransferase 2 ?
Once inside the inner membrane it will take the Fatty acyl from carnitine and add it back to Coa at the mitochondrial matrix
43
what is the use of L- carnitine and Acetyl L carnitine ?
Supplements are known to provide Cardiovascular and neuorlogical beneifts
44
how do short and medium chain fatty acid transport ?
Diffuse freely to the mitochondria ( no need for carnitine )
45
what is the most common genetics deficiencies in fatty acid oxidation ?
Medium chain acyl Coa dehydrogenase Specifically causes HYPOKEOTIC HYPOGLYCEMIA
46
describe the activation of fatty acid ?
only step in the complete degradation of fatty acid that require energy from ATP (2 atp ) by FATty acyl synthetase accomplished in two steps fatty acid ---> fatty acyl coa
47
result of beta oxidation ?
Produce NADH and FADH ( used in electron transport chain ) Results in 2 acetly Coa as final product ( UNLESS ODD NUMBER ) 129 ATP
48
describe oxidation of odd number carbon atoms?
( most of the FA are even number ) The final round of B oxidation of odd number yeilds : ACETLY -COA and PROPIONYL -COA Propionyl -COA is converted to the KREB cycle intermediate SUCCINYL-COA by a pathway involving vitamin B12 ( catabolism of some AA also yields propionyl COA )
49
describe cholesterol synthesis ?
Synthesized in all body cells BUT LIVER, INTESTINE, ADRENAL , CORTEX AND REPRO ORGANS CONTRIBUTE TO MAXIMUM CHOLESTEROL POOL Function of cholesterol? : Steroid hormones Plasma membrane Bile acids Vit D synthesis PRECURSOR FOR CHOLESTEROL = Acetyl - Coa
50
sources of cholesterol ?
Dietary cholesterol Endogenous synthesis : Tightly controlled cuz excess will lead to atherosclerotic plaque formation First molecules to be synthesis made by HMG COA SYNTHASE --> gives six carbon compound B hydroxy b methylgutarly COA ( HMG - COA ) Then it goes to Reduction by HMG COA reductase to form mevalonate ( RATE LIMITING STEP ) BY HMG COA REDUCTASE ( targeted by statins )
51
what control cholesterol synthesis ?
Insulin and glucagon Insulin stimulates it cuz we need to store Insulin stimulates ACC , FAS, HMG coa reductase
52
describe regulation of HMG COA reductase ?
1- Sterol lvls are low in the cell = increases the transcription of HMG Coa reductase ( cuz we need cholesterol ) 2- Increase in AMP ( less ATP ) ---> AMP kinase will PHOSPHORYLATE HMG COA reductase will INACTIVE it 3- High cholesterol will also MEDIATE THE PROTESOMAL DEGRDATION OF HMH COA REDUCTASE 4- Hormonal regulation
53
relation between obesity and NAFLD?
Obesity is associated with an increased risk of non alcoholic fatty liver disease Steatoisis is the hall mark feature of NAFLD occurs when : Rate of hepatic fatty acid uptake from plasma and denovo synthesis is GREATER than the rate of fatty acid oxidation and EXPORT ( as VLDL ) Presence of steatosis is associated with a group of adverse alteration in glucose , fatty acid and lipoprotein metabolism in case of alcoholic disease = alcohol become aldehydes which is converted to acetyl COA which is produces FATTY ACIDS
54
what happens to Adiponectin in obesity?
Adiponectin : Protein hormone that modulates a number of metabolic process, including glucose regulation and fatty acid oxidation LVLS FALL IN OBESITY --> CUZ REDUCED FATTY ACID OXIDATION
55
What happens to leptin levels in obesity ?
Leptin : Hormone made by adipose cells and enterocytes in the small intestines that help regulate energy balance by inhibiting hunger and in turn dminishes fat storage in adipocytes LVL INCREASES IN OBESITY BUT BECOME RESISTANCE
56
What happens to perilipins in obesity ?
Perilipin : essential protein for mobilization of fat in adipose tissue INCREASE IN NON ESTERIFIED FATTY ACID LEVELS ( NEFA ) BECAUSE INSULIN RESISTANCE

BIOCHEM Y2S2 (8 decks)

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