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Terms in this set (45)
Fatty acids used for energy production are stored in the body in the form of ___________________
where are triglycerides stored?
what are Triacylglycerols are composed of?
three fatty acid chains in ester linkage with a single glycerol molecule
= fat cells
store large amounts of triacylglycerols as fat droplets
what is Lipolysis?
= the breakdown lipids to release fatty acids (from adipose tissues)
how are Triacylglycerols stored? (in what form?)
stored in a non-hydrated form, they are hydro-phobic
what is the purpose of the Oxidation of fatty acids?
it is a central energy-yielding pathway in many organisms and tissues.
uses of fatty acid oxidation
In mammalian heart and liver, fatty acids provide up to 80% of the energy needs.
Brain and other tissues can also use products of fatty acid oxidation (ketone bodies) as fuels during starvation.
Muscles burn fats during extended exertion.
During hibernation, animals rely almost exclusively on fatty acid oxidation.
why are fatty acids more suitable for long-term energy storage than carbohydrates?
The carbon atoms of fatty acids are more reduced and hydrophobic
fatty acids can be stored in adipose cells w/o water... they do not have to kept hydrated which keeps them light in weight
Adipose tissue contains a high amount of stored energy and is relatively light-weight.
Lipolysis: In the fat cells (adipose), triacylglycerols are broken down into ___________ and ___________
glycerol and fatty acids
these are released into the blood
where does glycerol go?
it goes to the liver to be used in glycolysis or gluconeo
where do the fatty acids go?
they go to the cells of tissues throughout the body
they enter the mito of cells and then they are broken down by fatty acid oxidation
fatty-acid binding proteins
fatty acids are not soluble, so they need to be carried in the blood via fatty-acid binding proteins.
these proteins bring the fatty acids to other tissues
Lipolysis uses the action of which type of enzyme?
The substrate (Glucagon or epinephrine) will bind to ____________
a g-protein coupled receptor (GPCR)
which molecule serves as a main activator of Lipolysis?
PKA (protein kinase A)
When PKA is activated, it has 2 targets:
1) perilipin (a protein)
2) HSL (hormone-sensitive lipase)
The result of PKA leads to ...........
the release of 3 fatty acids
PKA indirectly activates the first enzyme of the pathway. what is the first enzyme?
first enzyme in the lipolysis pathway = adipose triacyl glycerol lipase (ATGL)
one of the main carriers of fatty acids in the bloodstream
has 7 binding sites for fatty acids
ATGL: enzyme function?
it activates the process of going from a triacylglycerol to a diacylglycerol
activators of Lipolysis
Glucagon and epinephrine
inhibitors of Lipolysis
Insulin antagonizes the effect of glucagon and epinephrine, and blocks lipolysis by destroying cAMP (the second messenger)
what is fatty acid oxdiation?
The breakdown of fatty acids in the mitochondria
benefits of fatty acid oxidation
you get energy from breaking down the fatty acids
You also get acetyl coA which can be fed into the TCA cycle which gives you more ATP
before fatty acids undergo β oxidation in the mitochondria, what has to happen?
Fatty acids must be "primed" or activated in the cytosol
how are fatty acids activated?
the Activation is catalyzed by acyl-CoA synthetase
involves conversion of a free fatty acid into an fatty acyl-CoA (a thioester).
once fatty acyl-CoA is made in the cytosol, how does it get into the mito (where oxidation happens)?
This is accomplished through the carnitine shuttle.
In the cytosol, the fatty acid is transferred to carnitine. A transporter brings in acylcarnitine and exports carnitine. In the mitochondrial matrix, the acyl group is transferred back to CoA .
4 steps of beta oxidation
4. Thiolysis (cleavage)
Complete oxidation of palmitic acid (C16) produces......
8 acetyl- CoA
7 molecules of FADH2 and NADH
Energy Yeild from Complete Oxidation of Palmitic Acid
Total = 106 atp
β-oxidation of odd-chain fatty acids results in the production of _______________
propionyl-CoA (which is metabolized to succinyl-CoA)
Oxidation of Unsaturated Fatty Acids: Enoyl-CoA isomerase
the isomerase flips the problematic double bond
Oxidation of Unsaturated Fatty Acids: NADPH-dependent 2,4-dienoyl CoA reductase
this is used to reduce a Δ4 double bond. then, the isomerase enzyme is used.
Oxidation of Unsaturated Fatty Acids: Propionyl-CoA carboxylase
this enzyme is used in the first step of the conversion of propionyl-CoA to succinyl-CoA
does the carboxylation of propionyl-CoA at C2 to form D-methylmalonyl-CoA
Propionyl-CoA carboxylase uses which type of cofactor?
Propionyl-CoA Carboxylase uses a biotin cofactor
Biotin is a B vitamin (vitamin B7).
the biotin = a co2 carrier
Oxidation of Unsaturated Fatty Acids: methylmalonyl-CoA mutase
used in the 3rd and final step of the conversion of propionyl-CoA to succinyl-CoA
Methylmalonyl-CoA mutase catalyzes an usual carbon skeleton rearrangement reaction.
final product = succinyl-CoA
what is the cofactor of methylmalonyl-CoA mutase?
It is one of the only two enzymes in human that uses cobalamin cofactor
Reaction Mechanism of Methymalonyl-CoA Mutase
uses a free radical & uses its cobalt atom
In humans, acetyl-CoA formed in the liver mitochondria during fatty acid oxidation has two fates:
1) enter the citric acid cycle
2) convert to ketone bodies (ketogenesis)
purpose of ketone body formation
Ketone body formation is a way for the liver to continue generating coA so that it can keep doing B oxidation
coA must be liberated in order to keep breaking down fats
Ketone bodies helps to liberate coA
2 common ketone bodies
Ketone bodies are derived from __________________
Utilization of ketone bodies as fuel
In tissues utilizing ketone bodies, D-β-hydroxybutyrate and acetoacetate are converted back to acetyl-CoA to enter the citric acid cycle.
ketone bodies + diabetes
Diabetes can lead to dangerous overproduction of ketone bodies
what happens in the body w/ diabetes?
Gluconeogenesis is activated
Large amounts of acetyl CoA is produced (because fatty acid release from adipose tissue is activated), but they cannot enter the citric acid cycle.
Therefore, liver releases large amounts of ketone bodies into the blood stream.
Overproduction of ketone bodies lowers blood pH, causing a dangerous condition called acidosis (acidification of the blood)
Recommended textbook explanations
Chemistry: The Central Science
Bruce Edward Bursten, Catherine J. Murphy, H. Eugene Lemay, Matthew E. Stoltzfus, Patrick Woodward, Theodore Brown
Matta, Staley, Waterman, Wilbraham
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