Advanced Nutrition Exam 2
What does nonesterified mean for nonesterified fatty acids?
FREE fatty acids; not bound to anything
what is a free fatty acid? - any type of fatty acid: saturated, unsaturated, monounsaturated, trans-; mentioned in previous ppt
What three components make up/define nonesterified fatty acids?
Carbon chain length, saturation, isomerism
What are the various carbon chain lengths and what are they "classified" as?
Short-chain (less than 6 carbons)
Medium-chain (6 to 10 carbons)
Long-chain (12 or some carbons)
Saturation can be either: ______________ or ______________, and each of these means what?
Isomerism can be either: _________ or _________, and each of these means what?
saturated = no double bonds in carbon chain
unsaturated = double bonds located in the carbon chain (mono-, poly-)
isomerism = the way the molecule "folds" or doesn't "fold"
cis: H (hydrogen) molecules are located on the same side of each other (most predominant position); causes a "kink" in molecule formation
trans: H (hydrogen) molecules are located opposite of each other; straight molecule
in fatty acid nomenclature, there are 4 different ways to name fatty acids
for instance, the trivial name for the above given molecule is linoleic acid
the IUPAC name for this molecule is:
the Delta system name is:
the Omega system is:
IUPAC: 9,12-octadecenoic acid
Delta system: 18:2 Δ9,12 (start counting double bonds from carboxyl end)
Omega system: 18:2 (ω-6 or n-6) (start counting double bonds from methyl/omega end)
why are phospholipids (glycerophospholipids) so important?
cell membranes' phospholipid bilayer
what are phospholipids structurally similar to?
what is the difference makes a phospholipid a phospholipid?
both have the glycerol molecule backbone that holds the fatty acids
in the case of a phospholipid, there is (on the 3rd carbon of the glycerol) a polar head group, which is a phosphate molecule attached to a polar head group, which is what makes the molecule hydrophilic (water loving) on one end and able to react with water
_______________ hormones are types of lipids that circulate throughout the blood and "signal" certain actions to occur
what are steroids considered to be?
what are they mostly made out of?
types of lipids
What are the 5 classes of steroid hormones?
what is TAG? define it.
Triacylglycerols (triglycerides) are synthesized from three fatty acids joined together by one glycerol molecule
lipids present in foods are made up of more than 90% _______________________, and the other 10% is made up of _________________________, ________________, and other lipids
phospholipids, sterols, and other lipids
(the 90% / 10% ratio is basically the same in the body)
_____________ is the form of storage of fatty acids in the body, and in foods it is the same deal (most of the fat that is in foods is in this form)
fats in foods classified as saturated fats contains around 60% of their total fat as ___________________ fatty acids and 5% as ____________________________ fatty acids
some sources of _____________________ fat are: coconut, palm kernel, palm oils
sources of _________________ are: peanut, sesame, safflower oils
sources of _________________ are: flaxseed, canola, soy, walnut oils
sources of ____________ are: olive and avocado oils
MUFAs (monounsaturated fatty acids)
the first site of digestion of TAG is in the stomach by the action of this enzyme:
the substrate of gastric lipase is:
the products are:
1,2-diacylglycerol and a free fatty acid
where does gastric lipase act?
how does it work? (mech. of action)
in the stomach
gastric lipase hydrolyzes the fatty acid at the sn-3 position of the TAG; it can also hydrolyze the fatty acid at the sn-1 position, but prefers sn-3
the substrate of pancreatic lipase is:
the products are:
mostly 2-monoacylglycerols and 2 free fatty acids
where does pancreatic lipase act?
how does it work? (mech. of action)
works in small intestine, but produced in pancreas
mainly hydrolyzes the sn-1 and sn-3 positions of TAGs to release the 2-monoacylglycerols and free fatty acids
what is the role of pancreatic colipase?
pancreatic lipase cannot work without colipase
colipase (an enzyme that contains distinct hydrophobic, lipid-loving regions) binds to the TAG to act as an anchor/ linking point for pancreatic lipase
the substrate of phospholipases are:
the products are:
lysophospholipid and free fatty acids
where do the phospholipases act?
how does it work? (mech. of action)
act in small intestine, but synthesized and secreted by pancreas
pancreatic phospholipase A1 and A2 hydrolyze the fatty acids from the sn-1 and sn-2 positions, while phospholipase C cleaves before the phosphate, releasing the polar head group
the substrate of cholesterol esterase is:
the products are:
cholesterol ester (which is a fatty acid attached to cholesterol)
free cholesterol and free fatty acids
where does esterase act?
how does it work? (mech. of action)
small intestine, made and secreted by pancreas
cleaves the fatty acid to release the free cholesterol and free FAs
_______________________ are highly organized lipid-protein complexes (or particles) that act as lipid transporters in the blood
(the lipids are transported in the blood as components of these highly organized lipid-proteins complexes)
all lipoproteins contain these 5 main components, plus vitamins A and E:
and vitamins A and E
what really changes in the various lipoproteins are the type of (____________)proteins present, and the amount of ____________ and ____________________ present
the ______________ the TAG content, the _______________ the density of the lipoprotein
the least dense lipoprotein is a ______________________, which contains 82% TAG
list the 4 lipoproteins from least dense to most dense
VLDL (very low density lipoprotein)
LDL (low density lipoprotein)
HDL (high density lipoprotein)
the "signature" (apolipo)protein in chylomicrons is: ____________
The "signature" (apolipo)protein in VLDL and LDL is: ____________
the "signature" (apolipo)protein in HDL is: ____________
what are the major (apolipo)proteins present in chylomicrons?
apo B-48, apo A-I, apo A-IV, apo C-II
what is so important about apoC-II ?
apoC-II activates lipoprotein lipase so breakdown of TAG from can occur
what are the major (apolipo)proteins present in VLDL/ LDL?
Apo B-100, Apo C-II, Apo C-III, Apo E
what are the major (apolipo)proteins present in HDL?
Apo A-1, Apo E, Apo C-II, Apo C-III, LCAT
where do chylomicrons go in the body?/ where is their goal site?
where is their creation site?
adipose and muscles = goal site
intestine = creation side
-chylomicron remnant (TAG removed from chylomicron) goes back to the liver
where does VLDL go in the body?/ goal site?
tissues (adipose, muscles) = goal
liver = creation
where does LDL go in the body?/ goal site?
transports cholesterol to tissues (adipose, muscle) to be used for membrane construction or to make steroid hormones
liver = creation
______________ is the major carrier of cholesterol in the body (60% of total serum cholesterol)
where does HDL go in the body?/ goal site?
brings unesterified cholesterol back to the liver to be excreted via bile (reverse cholesterol transport)
creation: liver, intestine
what is LCAT?
what does it do?
lecithin cholesterol acyltransferase
it is an enzyme that can attach to HDL to convert free cholesterol to cholesterol esters; does it by taking a fatty acid from lecithin, which is a phospholipid, and attaching it to free cholesterol that HDL is picking up
what is CEPT?
what does it do?
cholesterol ester transfer protein
cholesterol ester can be transferred to LDL via CEPT or transported directly to the liver by HDL
CETP is the cholesterol ester transfer protein that facilitates the exchange of cholesterol esters and TAG between HDL and the ApoB-containing proteins like VLDL and chylomicrons
what is LPL?
what does it do?
the key enzyme that allows the removal of TAG from the lipoproteins and be put into the cells
in order for the TAGs to be removed from the VLDL and chylomicrons, you need to break down the TAGs so they can be incorporated into the cells (LPL is key to this process)
HDL functions to remove ___________________ cholesterol from cells and other lipoproteins to the ______________ for excretion via bile (primary process) or go to other parts too (reverse cholesterol transport as whole process)
ABCA1 and SR-B1 proteins are important, why?
they transport cholesterol from in the cells into HDL
HDL can bind to LDL receptors through Apo E so the LDL receptor recognizes both Apo B and Apo E... what does this mean?
it is a benefit because when HDL binds to LDL receptors, there is a competition and allows more LDL cholesterol to be removed from cells (since the HDL got into the receptor instead of LDL)
______________ stimulates activity of the enzyme lecithin cholesterol acyltransferase (LCAT)
LCAT forms ____________________ ____________ by transferring fatty acids from sn-2 position of phosphatidylcholine (aka lecithin) to free cholesterol derived from cells or other lipoproteins
CE can be transferred to __________ via cholesteryl ester transfer protein (CETP) or transported directly to the liver by HDL
one of the roles of the liver is to synthesize _____________ and __________ (lipoproteins)
another role of the liver is to take up ___________________ _________________ and _________ lipoproteins to "recycle" it through the liver again and attach to the receptors
cholesterol comes back to the liver by the ___________________ _________________ or through ___________
what possible fates does cholesterol have once it is back into the liver? (3 answers)
mostly used for bile salt synthesis
incorporated into VLDL and HDL
free cholesterol secreted into bile as is
after a carbohydrate-rich meal (especially in simple sugars), TAG synthesis increases in the liver resulting in ____________ overproduction
this is why doctors/dietitians will tell you to decrease ______________ intake if you have high TAGs in the blood
the role of the adipose tissue is to be a storage site of what?
TAG and cholesterol
what enzyme is mainly responsible for storing the TAG and cholesterol?
85% of an adipose cell is __________
TAG is constantly being turned over in ___________________
____________________ _________________ _______________ (found inside adipose cells) hydrolyzes (breaks down) TAG inside the cell
hormone sensitive lipase
why is hormone sensitive lipase named as it is? what hormone stimulates it? what hormone decreases its activity? when is it most active?
glucagon stimulates it, insulin inhibits it?
most active in fasting state so the body can use the TAG as energy
what hormone stimulates the activity of LPL (lipoprotein lipase)? when is LPL most active?
recap the purpose of LPL
most active in fed state
LPL most active after meal because there are all of the chylomicrons and VLDL circulating and the TAG needs to get removed
what is the process called by which lipids are synthesized?
de novo lipogenesis
what specific lipid does de novo lipogenesis create? what is its composition?
16 carbons, completely saturated
where are the sites for fatty acid synthesis (de novo lipogenesis)?
adipose tissue and liver
Western diets suppress this pathway ( ________ __________ _____________________), so it does not contribute greatly to TAG synthesis
why is this pathway suppressed in our Western diet?
de novo lipogenesis
we already have so much fat in our diet, we don't need more (we make more TAG than fatty acids)
how might de novo genesis contribute to glycemic control?
by diverting excess glucose to fat
where does fatty acid synthesis occur in the cell?
in the cytosol
what are the building blocks for fatty acid synthesis?
what are the major enzymes?
building blocks: acetyl CoA, malonyl CoA
enzymes: acetyl CoA carboxylase, fatty acid synthase system (contains several enzymes, not just one)
which enzyme makes malonyl CoA from acetyl CoA?
acetyl CoA carboxylase
acetyl CoA is produced in the mitochondria - how does acetyl CoA get into the cytosol for synthesis of fatty acids?
the PDH reaction (pyruvate dehydrogenase reaction) which converts pyruvate to acetyl CoA in the mitochondria, so how do we get that acetyl CoA to the cytosol?
through citrate (the citrate-malate shuttle)
how does the citrate-malate shuttle work?
The mitochondrial membrane is permeable to both citrate and malate but not to acetyl CoA and oxaloacetate.
Acetyl CoA is shuttled out of the mitochondria via citrate. The enzyme citrate synthase converts acetyl CoA + oxaloacetate into citrate. In the cytosol, the enzyme citrate lyase converts citrate back to acetyl CoA and oxaloacetate in a reaction that uses ATP, CoA and H2O.
The acetyl CoA then gets used for de novo lipogenesis
this enzyme is extremely important in fatty acid synthesis; it is the enzyme that converts acetyl coA into malonyl-coA
acetyl CoA carboxylase
how does acetyl coA carboxylase work?
takes a CO2 molecule and adds it to the Acetyl CoA to make Malonyl CoA
this reaction requires biotin (a vitamin B) and ATP to make Malonyl CoA
in fatty acid synthesis elongation, _______________ _______ always attaches to an ACP (acyl carrier protein)
only one ______________ ________ starts the whole fatty acid synthesis cascade
the 2 reductase enzymes in each elongation uses which reducing equivalent?
in the synthesis of one 16:0 fatty acid molecule, palmitate, what are the substrates?
______ molecule(s) of malonyl CoA
______ acetyl CoA(s)
______ NADPH + ______ H+
what is the major product produced?
note the other products
7 molecules malonyl CoA
1 acetyl CoA
14 NADPH + 14 H+
major product: 1 molecule of palmitate
others: 8 CoA, 7 CO2, 14 NADP, 6 H2O
the adipose tissue is not able to use free glycerol
true or false?
the adipocyte cannot metabolize free glycerol for energy when we are breaking down fat because it lacks the enzyme _________________________
glycerol must be ______________________ so it enters the glycolytic pathway
free glycerol leaves the adipose and goes to other tissues (primary the ___________) to enter the glycolytic pathway or to synthesize glucose
when the adipose needs to make TAG, where does it get the glycerol from?
it removes it from the glycolytic pathway; it is convenient for the TAG synthesis pathway because the the glycerol already has the phosphate group attached to it to start de novo lipogenesis
the liver can use free glycerol because it possesses the glycerolkinase enzyme
true or false?
fatty acids undergo oxidation in the _________________________
fatty acid oxidation requires activation by attaching _________________ _______ to form acyl-CoA, which requires the use of _____ ATPs
(note: ^ no, acyl-CoA is not misspelled)
which enzyme is the one that adds the coenzyme A to fatty acids for their oxidation?
the activation for fatty acid oxidation occurs in the _________________, but actual oxidation occurs inside the ________________________
long chain fatty acids (more than 10 carbons) must be shuttled to the mitochondria by a set of enzymes that utilize ______________________
(side note: people take carnitine to "burn" fat faster)
in the intermembrane space, which enzyme is responsible for taking acyl-CoA plus carnitine, releasing the CoA off of it, and thus making an acylcarnitine?
CPT1 (carnitine palmitoyl-transferase I)
which enzyme shuttles the acylcarnitine from the inter membrane space to the mitochondrial matrix?
carnitine acylcarnitine translocase (CAT)
what enzyme takes the acylcarnitine, attaches the CoA back to it, and removes the carnitine to end back up with the original acyl CoA?
CPTII (carnitine palmitoyl transferase II)
lipid oxidation, fatty acid oxidation, and _____-oxidation all mean the same thing
every time the cycle turns in fatty acid oxidation, how many Acetyl CoA(s) do you get?
unless it is the last 4 carbons of the fatty acid chain, in which you get 2 Acetyl CoAs
each cycle produces 1 NADH2 and 1 FADH - how many ATPs does that equate to per cycle?
4 ATPs every cycle
How many ATPs are produced with this molecule of palmetic acid?
16 carbon chain, so 2 carbons for each Acetyl CoA = 8 Acetyl CoAs
but one Acetyl CoA does not go through the cycle because it is the one at the very end, so in oxidation of palmetic acid, only 7 Acetyl CoAs are made
4 ATPs per cycle from FADH2 and NADH, multiplied by 7 for the number of cycles = 28 ATPs just from cycle
each Acetyl CoA will produce 10 ATPs in the ETC, so 8 Acetyl CoAs multiplied by 8 = 80
28+80 = 108 total ATPS in oxidation of palmetic acid (the net production is 106 ATPs because 2 ATPs are used in activation)
which pathway is upregulated when you are fasting/under starvation or have a low carb intake?
ketogenesis (formation of ketone bodies)
why does a low-carb intake stimulate ketogenesis?
you have a deficit in supply of oxaloacetate for the TCA cycle, which means Acetyl CoA cannot enter the TCA cycle very fast because you lack the oxaloacetate to keep the cycle going
the accumulation of ______________ ________ is what generates ketogenesis/ the formation of ketone bodies
two acetyl coAs combined together make a ______________________
which enzyme makes the acetoacetyl-CoA?
acetoacetyl CoA is made into acetoacetate (the first ketone body) by removal of the _________
acetoacetate can be converted into ________________, which is a second ketone body or it can reversibly be converted into ________________________________, which is the third ketone body
Beta-hydroxybutyrate (can be converted back and forth [reversibly] by 3-hydroxybutyrate dehydrogenase)
where does ketogenesis occur?
liver mitochondria, possibly kidneys if prolonged starvation
one other way the body can get acetoacetate is by the combination of acetoacetyl CoA + acetyl coA, which gives you 3-hydroxyl-3-methylglutaryl CoA (HMG CoA)
the enzyme that can break down HMG CoA to acetyl CoA + acetoacetate is ____________________________
HMG CoA lyase
even though the liver makes ketone bodies is cannot use ketone bodies
true or false?
why can't the liver use ketone bodies? what does it lack?
succinyl-CoA-3-keto acid CoA transferase
what does succinyl-CoA-3-keto acid CoA transferase actually do?
it attaches a coA to acetoacetate
where does the succinyl-CoA-3-keto acid CoA transferase get the coA from that it attaches to the acetoacetate?
from succinyl CoA which is an intermediate enzyme from the TCA cycle (the succinyl CoA gets turned into succinate)
what enzyme breaks the newly formed acetoacetyl CoA with another CoA into 2 acetyl coA molecules?
CoASH (CoA, same thing)
this medication inhibits a specific intracellular lipid-transfer protein from binding to apolipoprotein B in the lumen of the endoplasmic reticulum in order to decrease the lipidation and secretion of triglyceride-rich lipoproteins
decreases production of apolipoprotein B (which causes reduced levels of LDL cholesterol and TAG)
MTP is an intracellular lipid-transfer protein
this medication facilitates the bidirectional transfer of cholesterol esters and triaclyglycerides between HDL and apoliprotein B-containing lipoproteins VLDL, intermediate-density lipoproteins, and LDL
predominant effect: elevation of HDL-cholesterol level
(cholesteryl ester transfer protein inhibitor)
this medication increases HDL-cholesterol levels by stimulating the production of apolipoprotein A-I and apolipoprotein A-II, the two major protein components of HDL
this medication binds to cholesterol-rich bile salts in the small intestine, blocks their enterohepatic recirculation to the liver, and thus increases the cholesterol-rich bile salts excretion; it increases synthesis of "new" bile salts and thus decreases intrahepatic cholesterol levels
bile acid resins
__________________ essential fatty acids are present in much larger amounts in the body than __________________ essential fatty acids, especially in the Western diet
the following chart denotes the percentage of omega-6 versus omega-3 in the typical Westerner diet
the only exception in this Western pattern is the high content of omega-3 PUFAs, especially ____________ in the ______________ and _______________
retina and brain
why are the essential fatty acids so important? what two important physiological processes are they vital in?
1) synthesis of (we have to make) lipid biomediators (arachidonic acid, EPA, DHA)
2) synthesis of membrane phospholipids (for all cells in the body) with optimal structural and signal transduction properties
omega-6 derivatives have 4 major effects in the body:
pro-arrhythmia, pro-inflammation, vasoconstriction, and platelet activation (forming blood clots)
omega-3 derivatives have 4 major effects in the body:
anti-arrhythmic, anti-inflammatory, vasodilators (lower blood pressure), platelet inhibition (lessen blood clots)
the absorption of ethyl alcohol (alcohol in drinks) occurs by __________________ diffusion in the stomach and intestine
alcohol is transported unaltered in the blood and oxidized in the ________________ and other tissues
the three main enzyme systems involved in alcohol metabolism are:
alcohol dehydrogenase (ADH)
microsomal ethanol oxidizing system (MEOS)
catalase (accounts for less than 2%)
the ____________ pathway is the pathway that predominates when only small to moderate amounts of alcohol are consumed
where is ADH present?
cytosol of liver cells
how does the ADH pathway work?
alcohol dehydrogenase converts ethanol to acetaldehyde with production of NADH
note: acetaldehyde - the intermediate (THE component that gives all the side effects of alcohol)
when there is a high amount of alcohol in the system (ADH is saturated), there is an imbalance between _________/___________, which is when a shift occurs to MEOS (higher levels of alcohol in body)
the lack of __________ impairs TCA, cycle, gluconeogensis, and fatty acid oxidation
all of the NAD that you have in your body goes to the alcohol
dehydrogenase because alcohol MUST be metabolized when it is in the
body (foreign things must get out first; alcohol does not get stored
or anything, only metabolized)
gluconeogenesis is also impaired with alcohol b/c the TCA cycle is not working well; fatty acid oxidation cannot occur because it stops at the Acetyl CoA and once again needs the TCA cycle to continue
acetaldehyde toxicity results in metabolic consequences how?
1) damage liver cells (acetaldehyde can bind to certain proteins in the liver cells, disrupt the cell membrane, and damage the cells)
2) substrate competition and induced tolerance (like vitamin A deficiency)
how does alcohol cause a vitamin A deficiency?
retinol dehydrogenase is important to transform retinol into retinal; this dehydrogenase can also be used for alcohol, so when alcohol is high, the retinol dehydrogenase works on the alcohol instead of the retinol; this is why alcoholics often have vitamin A deficiency
how does induced tolerance work?
induction of MEOS accelerates oxidation of retinol and hepatic depletion leads to higher needs
why is a high NADH/NAD ratio dangerous?
- increased levels of reducing equivalents (NADH)
- increased reduction of pyruvate to lactate (lactic acidosis)
- accumulation of citrate which stimulates acetyl CoA carboxylase
- increased activity of glycerophosphate dehydrogenase to make glycerol-3-phosphate, hence increased TAG synthesis
- glutamate dehydrogenase shifts toward production of glutamate from alpha ketoglutarate which impairs gluconeogenesis
ATP production is not the problem, it is a problem with glucose breakdown (increased production of lactate, lactic acidosis can occur, which makes the blood more acidic)
alcoholics have fatty liver because: acetyl coA carboxylase causes built up TAGs from the built up citrate
have less alpha ketoglutamate which further impairs gluconeogenesis
____________ deficiency leads to enlarged fatty liver and hypoketotic hypoglycemia and possibly coma during fasting
*this deficiency means you cannot shuttle LCFAs into the mitochondria matrix for energy
CPT1 (carnitine palmitoyl transferase)
why would hypoketoic hypoglycemia occur in CPT1 deficiency?
hypoketotic hypoglycemia (do cannot produce even ketone bodies; all glucose is going to cells and is being depleted from blood)
where do ketone bodies come from/ how are they made?
when you oxidize LCFAs, you get Acetyl CoA; if you have no LCFAs, then you don’t have Acetyl CoA made, thus ketone bodies cannot be made, so all the glucose in the body is used to get Acetyl CoAs (you constantly have to eat/ make sure there are enough sugars)
what dietary recommendations would you make for patients with CPT1 deficiency?
consume only MCFAs and SCFAs (these fatty acids do not need CPT1 to get into the mitochondrial cells)
this deficiency leads to deficiency of arachidonic acid and docohexanoic acid (DHA)
why is Δ6-desaturase a big deal to be deficient in?
it is one of the enzymes that is in the pathway of elongation for essential fatty acids; if you can'y make DHA, there are quite awful consequences
what are some of the symptoms of Δ6-desaturase deficiency?
-poor growth in children
-scaly skin lesions
remember: DHA in highest amounts in the brain and retina
what do you do if you have Δ6-desaturase deficiency?
what happens in an Apo C-II deficiency?
recall: which lipoproteins normally contain apo C-II?
what is the main function of Apo C-II?
Activates lipoprotein lipase, which helps with removal of TAG from chylomicrons and VLDL
so when you have an Apo C-II deficiency, lipoprotein lipase cant be activated and TAG cannot be removed from chylomicrons or VLDL; thus, hypertriacylglycerolemia occurs (too much TAG in body)
__________________ ______________________________ is a genetic effect in the gene encoding for the LDL-receptor; elevated LDL-cholesterol levels occur in the blood
if you cannot pick up cholesterol from LDL, it will go up in the blood a lotttt
very serious condition; Coronary heart disease develops during childhood in homozygous patients
this is a vascular disease that is characterized by deposition of fatty plaques in the arteries
why is plaque accumulation so dangerous?
it can lead to blockage of blow flow, rapture and precipitation of blood clots within smaller arteries, which leads to heart attacks, stroke, or peripheral arterial disease
the main event that occurs in atherosclerosis is retention of Apo-B containing lipoproteins (mainly ________) in artery walls
true or false
hormone sensitive lipase is stimulated by insulin
hormone sensitive lipase is stimulated by glucagon, inhibited by insulin
phospholipids have hydrophilic and hydrophobic parts
phospholipase A2 hydrolyzes the polar head attached to the second carbon in the glycerol molecule
phospholipase A2 hydrolyzes the second fatty acid attached to the second carbon in the glycerol molecule
polar head = phospholipase C on third carbon
colipase is important for gastric lipase to work b/c it provides a site of attachment for gastric lipase
colipase is important for pancreatic lipase to work b/c it provides a site of attachment for pancreatic lipase
cholesterol synthesis starts with two acetyl CoA molecules being joined together
the fatty acid 20:4 Δ5,8,11,14 has 20 carbons and 4 double bonds with the first double bond starting on carbon 5 from the methyl end
the fatty acid 20:4 Δ5,8,11,14 has 20 carbons and 4 double bonds with the first double bond starting on carbon 5 from the carboxyl end
the trans-configuration of a fatty acid leads to a 45 degree fold on the fatty acid molecule
the cis-configuration of a fatty acid leads to a 45 degree fold on the fatty acid molecule
malonyl CoA decarboxylase is more active in the fed state
malonyl CoA decarboxylase is more active in the fasting state
the primary apolipoprotein in LDL is apo B-100
VLDL carries cholesterol from the liver to the other tissues in the body
VLDL carries TAG from the liver to the other tissues in the body
LCAT is responsible for making cholesterol esters in the intestinal cell before transport by chylomicrons
LCAT (lecithin cholesterol acyl transferase) is responsible for making cholesterol esters in the blood before transport by HDL
CEPT is key to exchange of cholesterol esters and TAG between HDL and other lipoproteins
CEPT (cholesterol ester transport protein)
reverse cholesterol transport refers to moving cholesterol from the tissues and blood to the liver by HDL
the lipoprotein with the lowest density is the chylomicron
omega-6 fatty acids can increase inflammation in the body when ingested in high amounts
omega-3 fatty acids function as vasoconstrictors
omega-6 fatty acids function as vasoconstrictors
arachidonic acid is an important lipid mediator that can be synthesized in the body from linoleic acid
fatty acyl CoA synthetase activates fatty acids prior to TAG synthesis
*fatty acid synthesis does not need activation
fatty acyl CoA syntheses activates fatty acids prior to fatty acid oxidation
de novo lipogenesis requires one acetyl CoA and seven malonyl CoAs
CPT2 is responsible for moving a fatty acyl carnitine from the inter membrane space to the matrix of the mitochondria
translocase is responsible for moving a fatty acyl carnitine from the inter membrane space to the matrix of the mitochondria
short and medium chain fatty acids do not require carnation to enter the mitochondrial matrix
complete oxidation of a 10 carbon saturated fatty acid would yield a total of 56 ATPs
complete oxidation of a 10 carbon saturated fatty acid would yield a total of 66 ATPs
excessive consumption of alcohol can lead to an increase in the ration of NADH to NAD in the cells
under low consumption, ethanol metabolism occurs primarily via cytochrome p450 2E1.
under low consumption, ethanol metabolism occurs primarily via alcohol dehydrogenase