Exam 3 Flashcards
length of short, medium, and long chain FA
6
6-10
>=12
majority of dietary FA are this length
long chain
Delta system of FA naming count carbons from this end
carboxyl end
omega system of FA naming count carbons from this end
methyl end
properties of SFA (2)
solid a room temp
single bonds
found in animal fats, palm oil, palm kernal oil, coconut oil
SFA
properties of MUFAs (2)
generally plant based
one double bond
examples of this FA are olive oil, peanut oil, canola oil
MUFA
Properties of PUFAs (2)
more than one double bond
generally plant based, but also found in fish
examples of this FA are corn oil, sunflower oil, fish oils, nuts and seeds
PUFAs
Properties of Trans fatty acids (5)
Trans configuration double bond form naturally, or thorugh hydrogenation of PUFA extend shelf life increase baking properties solid at room temp
T/F: hydrogenated oils, or partialy hydrogenated vegetable oil on a label is the same as SFA
F, Trans fats
T?F: TFA are found in fried food, commercial baked goods, processed foods, and margerine
T
Linoleic acid (omega-6) and alpha-linolenic acid (omega 3) are examples of this
essential fatty acids
Reason why there are essential FA
your body cannot from CC double bonds before the 9th carbon, it does not have the correct enzymes
This is the enzyme in plants that can make the essential FA that animals are lacking
desaturase
This essential fatty acid deficiency disease causes growth retardation, skin disorders, infection susceptibility, and poor wound healing
cystic fibrosis
acid and alcohol coming together from this type of bond
ester bond
triglycerides are made of these compounds
glycerol and 3 FA bound by ester bonds
linoleic, y-linolenic, arachidonic acid are all examples of
omega 6 FA
a-linolenic, stearidonic, eicosapentaenoic, docosahexaenoic acids are all forms of
omega 3 FA
these make up 95% of dietary fat
TAG
enhanced taste and texture, energy, supply essential fatty acids, carriers of fat-soluble compounds, storage from of energy, and cell signaling/gene expression are all functions of this structure
TAG
Easiest way to remove cholesterol from the body is through this mech
GI tract
T/F: a cholesterol molecule is a steroid molecule with an extra OH, CH3, and FA group attached to it
t
What makes a cholesteryl ester different that a cholesterol molecule
cholesteryl ester have a FA bound to the OH group through an ester bond
Sex hormones, bile acids, vitamin D, and corticosteroids are made from these
sterols and steroids
What is helpful about ingestion of phytosterols
they help eliminate cholesterol through the diet (compete for absorption)
These function as emulsifiers, cell membrane and lipoprotein components
phospholipids
T/F: phospholipids can interact with polar and non polar compounds
T
In most cases the two FA tails on a phospholipid are this type of FA
SFA
The hydrophilic portion of a phospholipid is called this
polar head group
Phospholipids act as signaling molecules which lead to the activation of this, or the release of this
activation of protein kinase C leading to enzyme activation
release of Ca2+ leading to enzyme activation, or other hormonal responses
This is the main phospholipid
lecithin
these have a SFA in position 1 and a UFA in position two
glycerophosphatides
examples of a glycerophosphatide
lecithin, cardiolipin
a type of phospholipid that is abundant in nerve tissue
sphingolipids
This are structural lipids in nerves and brain tissue that have a saccaride component
glycolipids
Estimated intake of TAG, PL, Chol/phytosterols
100-150 g/d
~5 g/d
200-400 mg/d
Fat spoils due to this
oxidation
these accelerate oxidation of fat
double bonds
these factors limit fat oxidation (4)
limit exposure to air
cold temp
antioxidants
partial hydrogenation
This enzyme is used to convert eholesterol esters into cholesterol and FFA
Cholesterol esterase (cholesterol ester hydrolase)
How does bile aid in lipid digestion
increases surface area of the lipids, so enzymes can interact
How does lingual lipase aid in lipid digestion
it is good at cleaving short chain FA
Turns TAGs into DAGs and FFA
This enzyme accounts for 10-30% TAG digestion
gastric lipase
Gastric lipase aids lipid digestion by
it is good at cleaving short chain FA
Turns TAGs into DAGs and FFA
How does pancreatic lipase aid in lipid digestion
breaks down the ester bonds on the ends of the TAG to from MAGs and 2FFA
The majority of lipid digestion occurs here
upper jejunum
How does phospholipase A2 aid in lipid digestion
removes the middle FA from a phospholipid forming a FFA and a lysophospholipid
a lysophospholipid is this
a digested phospholipid
Cholesterol esterase is produced here, and acts on this
pancreatic acinar cells
sterol esters
These four compounds are produced by pancreatic acinar cells
cholesterol esterase
phospholipase A2
Procolipase
pancreatic lipase
gastric lipase is produced by this
chief cells of the stomach
how does colipase aid in lipid digestion
activates pancreatic lipase
Examples of pancreatic lipase inhibitors
orlistat
xenical
alli
why should people take a pancreatic lipase inhibitor
trouble with lipid digestion
weight loss
The 5 final products of lipid digestion
lysophospholipids nonesterified (free) cholesterol nonesterified (free) FA Nonesterified (free) Plant Sterols 2-Monoglycerides
This is a way to deliver FA and fat soluble vitamins in an aqueous enviornment
mixed micelles
This percent of FA are absorbed in the diet, and this percent of cholesterol
> 95%
~50%
This percent of FA in the diet are LCFA
92-96%
This carries medium chain fatty acids in the blood
albumin
How are SCFA and MCFA absorbed
directly into the capillaries
T/F: use medium chain FA if you have a hard time absorbing lipids such as in cystic fibrosis
T
This FA length increases energy expenditure after a meal
MCFA
The mixed micelle interacts with this
untirred water layer of the brush boarder
FFA go here, while the Chylomicron formed from the golgi app. go here
portal vein
lymphatic system
most important protein on a chylomicron
apo B-48
Chylomicrons from here
distal duodenum and jejunum
the majority of the chylomicron is made up of this
triglycerides
T/F: LCFA first go to the liver, while SCFA and MCFA first go to systemic circulation
F
Chylomicron activity peaks this long after a meal
30 min
the lymp system goes to tissues in this order
muscles
adipose
liver
this enzyme is in the adipose, muscle, mammary gland, brain, macrophages, and kupffer cells
lipoprotein lipase (LPL)
this enzyme facilitates deposition of FAs in tissues for storage or energy production
lipoprotein lipase (LPL)
In this state, activity is high in adipose and low in skeletal and heart muscle for LPL
fed state
In this state, activity is low in adipose and high in skeletal and heart muscle for LPL
fasted
These carry absorbed dietary lipids, carry lipids from liver to cells, and carry lipids to liver for excretion
lipoproteins
examples of lipoproteins (4)
chylomicron
VLDL
LDL
HDL
characteristic apoprotein for VLDL
apo B-100
characteristic apoprotein for LDL
apo B-100
characteristic apoprotein for HDL
apo A-I
These act as identification, stablizie, specificity, and aid in recognition of lipoproteins
apoproteins
chylomicrons originate here
golgi app of intestinal cells
chylomicrons are composed of
mostly TAG with little phospholipid, cholesterol and protein
VLDL originate here
liver (golgi app)
VLDL are composed of
mostly TAG with a little more phospholipids, cholesterol, and protein than chylomicrons
carry lipids from liver to cells, deliver TG to cells then shrink to become IDL
VLDL
LDL originate from this
IDL
LDL are taken up by this
B-100 receptors fround in the liver and hon-hepatic tissue
These are generated from the VLDL during circulation, carry lipids to cells, mainly carry cholesterol (large proportion), uptaken by LDL receptor
LDL
Chylomicrons follow this pathway, while VLDL and IDL follow this pathway
exogenous
endogenous
T/F: the more cholesterol in the cell, the less LDL receptors are formed
T
This occurs when LDL is absorbed in the cell
lysosome digests
free cholesterol is packaged by the golgi app, and esterified with ACAT and stored in the cell
exogenous lipids (gut to liver)
chylomicron
endogenous lipids (liver to periphery)
VLDL
LDL
reverse transport (periphery to liver)
HDL
synthesized from liver and intestine in a lipid free nascent form
HDL
Mostly protein composes its structure
HDL
This LP returns lipids (cholesterol) to liver for re-use or excretion
HDL
T/F: there are smaller fluctuations in LDL and HDL concentrations in the blood than in CM, VLDL, IDL
T
This tissue synthesizes bile salts, VLDL, HDL, and new lipids from non-lipid precursors
Liver
this tissue absorbs TAG and cholesterol from chylomicrons through lipoprotein lipase, and stores TAG
adipose tissue
What is lipoprotein lipase
found on adipose and muscle tissue, removes FA from TAGS in chylomicrons and VLDL and brings them into the cell
this helps to transfer cholesterol to the liver and eventually excrete it
cholesterol ester transfer protein
This percent of adipose tissue is lipid material
85%
HDL acts inconjuction with these two enzymes to move cholesterol from the peripheral tissues to the liver via the plasma
cholesterol esterifying enzyme
lecithin: cholesterol acyltransferase (LCAT)
these are cholesterol delivery trucks, and increase risk of CVD
LDL
these are cholesterol garbage trucks and perform reverse cholesterol transport, decrease risk of CVD
HDL
Chylomicrons are made here
enterocytes
secretion of chylomirons
exogenous, intestinal cell to lymph, to blood
chylomicrons change to this during dirculation
chylomicron remnant
physiological role of chylomicrons
deliver FA to the peripheral cells (adipocytes)
Key enzyme in cholesterol synthesis
HMG-CoA reductase
What is the rate-limiting step of cholesterol synthesis
HMG-CoA reductase
where are VLDL and LDL synthesized
hepatocytes
where is HDL synthesized
hepatocytes (80%) enterocytes (20%)
earliest stage of HDL
nascent HDL
First step of FA metabolism
extract lipids from LP via LPL (lipoprotein lipase)
the cleavage of a staturated CC bond during FAox yields this many ATP
5
Glycerol cannot be utilized by the cell, so it is sent here
liver
Phase 1 of FA oxidation
activation of FA by CoA (acyl-CoA synthetase) forms Acyl-CoA
Phase 2 of FA oxidation
Transfer of fatty acyl-coa into the cell via carnitine acyltransferase 1,2
What is the rate limiting step of FA oxidation
Carnitine acyltransferase 1,2 (1 on outer membrane, 2 on inner mitochondrial membrane)
what is produced from the B-ox of FA
FADH2, NADH, actyl-CoA
these FA will generate C3 coA to conversion to C4 CoA (succinyl-coa)
odd-numbered FA
What causes ketogenesis
low glucose in the body
when there is not enough of this compound acetyl-coa is oxidized into ketoacids
oxaloacetate
T/F: ketone bodies can’t cross the blood brain barrior, FA can
F
Ketogenesis is common in these two conditions
type 1 diabetics, starvation
T/F: ketone bodies are acidic
T
Ketone bodies make up this percent of fuel during starvation
75%
T/F: Ketogenesis reaction goes one way in extra hepatic tissues, but is reversable in the liver
F
This rises during accelerated FAox + low CHo intake or impaired CHO use
ketone concentration
What role does does ketogenesis p[lay in energy metabolism
provides energy that can be used by tissues such as the brain during periods of low blood CHO
From what substrate are FA synthesized from
acetyl-CoA
T/F: pyruvate to acetyl coa is a reversable reaction
F
What triggers FA synthesis
alot of acetyl-coa in the mitochondria
this enzyme activates acetyl-coa for FA synthesis
acetyl-coa carboxylase
this is the basic building block for FA synth
malonyl-coa
During FA synthesis this energy source is used to get rid of double bonds
NADPH
This is generally the final product of FA synthesis
Palmatic acid
How do eicosanoids synthesized from n-6 FA differ from those synthesized from N-3 FA
N-6 are pro-arrythmic, platlet activators, vasoconstrictors, pro-inflammatory compounds
n-3 are the opposite
There are more of this type of FA in the western diet that make eicosanoids than this
n-6 than n-3
improved vision, neuroprotection, successful aging, memory protection, cardioprotection, and use as a signaling molecule are all benefits of this type of FA
n-3 (DHA)
How does CHO balance affect the processes of lipid metabolism
more CHO in the system leads to lower catabolism, and greater anabolism of FA
T/F: insulin lowers lipolysis activity
T (see page 53 of lipid notes)
how does brown fat differ from white (normal) fat tissue
it is highly vascularized
abundant mitochondria
mitochondria have H+ pores (uncoupling protein) which promote thermogenesis
uncoupling protein is inhibited by these
free purine nucleotides
t/f: lean subjects have higher amounts of brown adipose tissue
T
Two systems used to metabolize alcohol
alcohol dehydrogenase pathway
microsomal ethanol oxidizing system
alcohol resembles this compound, but is metabolized like this compound
CHO
FA
T/F: mass production of Acetyl-coa during ADH alcohol metabolism lowers TCA cycle activity and lends to production of FA
T
ADH is found here
gastric mucosal cells
How does alcohol effec energy metabolism in the body
alters NADH processes in the body
This is tghe cause of the flushing associated with alcohol consumption
acetaldehyde
Alcohol tolerance is due to this pathway
MEOS
The benefits of alcohol have the strongest correlation of this and not this
amount of alcohol consumed, not the type
T/F: alcohol lowers oxidative stress
T
T/F: alcohol improves insulin sensitivity
T
T/F: Diabetes is improved from alcohol
T
T/F: inflammation is increased with alcohol
F
T/F: alcohol decreases HDL
F
T/F: dementia is improved with alcohol
T
T/F: consumption of alcohol may suppress proliferation of smooth muscle cells underlying the endothelium of arterial walls
T
Outline the progression of atherosclerosis
LDL enters intima followed by monocyte
monocyte turns into macrophag and begins to take up LDL
Macrophage dies and froms foam cell
smooth muscle begins to enter intima
outline the progression of an athrosclortic lesion
fatty streak forms
fibrous cap froms over fatty streak
the fiborous cap thins
eventually the plaque (fiberous cap) bursts froming a thrombus
Sites of greatest predilection for atherosclerosis development
branching points
These two things increase LDL cholesterol
SF
TF
these three things decrease LDL
soluble fiber
plant sterols
saponins
This decreases HDL
Trans fat
smoking
This increases HDL
moderate alcohol (1 to 2 drinks/d depending on sex) exercise
4 parts of the basic amino acid strcuture
central carbon
amino group
carbaxy group
side chain
What are essential amino acids
amino acids needed in the diet because your body cannot make them
which amino acids are essential
PVT TIM HaLL Phenylalanine Valine Threonine Tryptophan Isoleucine Methionine Histidine Leucine Lysine
Conditionally essential amino acids
Tyrosine cysteine proline arginine glutamine
This AA becomes essential with phenylketonuria
tyrosine, unable to produce tyrosine from phenylanine
4 levels of protein structure
primary
secondary
tertiary
quaternary
What protein sources are complete
animal
soy
quinua
which protein sources are incomplete
plant
changes 3/d structure of protein, destroys function
protein denaturation
heat, acid, mechanical force, salt
mechanisms of protein denaturation
Protein digestion location: pepsin
stomach
PProtein digestion location: trypsin
intestine
Protein digestion location: chymotrypsin
intestine
Protein digestion location: carboxypeptiase A and B
intestine
Protein digestion location: aminopeptidases
intestine
products of protein digestion
free AA
dipeptides
tripeptides
absorption of AA occurs here
duodenum
jejunum
These AA are absorped most quickly
essential AA
these AA are absorbed slowly
Neg charge
This is a cotransporter of AA
Na
This is how a majority of AA are absorbed, and are faster than AA transporters
Peptide transporter
T/F: not all di/tri peptidases are all the way broke down before passing into circulation
T
AA enter this circulation
portal
The amino acid pool is utilized in these three ways
energy production
syntesis of glucose and FA
synthesis of nonprotein molecules that contain nitrogen
T/F: the main way to use AA in the body is in the formation of body proteins
T
Where are amino acids primarily catbolized
liver
what are the features of sickle cell anemia
glu is switched out for valine
this structure of hemoglobin is distorted in sickle cell anemia
3d (tertiary)
What is transamination
transfer of amino group from one AA to AA carbon skeleton or a-keto acid
what is deamination
removal of amino group, no transfer
The enzyme responsable for deamination is called this rather than this because the reaction process by loss of elements of water
dehydratase
deaminase
These are required by dehydratase
B6
PLP
What is the role of the urea cycle
formation of urea (nitrogen containing compound) as a waste product
What is the role of the glucose-alanine cycle
regeneration of intermediates from AA and transport of N to live
how is nitrogen disposed of in the muslce
pyruvate is converted to alanine which can leave the muscle and enter circulation, eventually ending up in the liver
Functional categories of proteins
catalysts messengers structural elements buffers fluid balancers immunoprotectors transporters acute phse responders
what are the three BCAA
valine
leucine
isoleucine
in ability to process BCAA and metabolites causing the uring to look and smell like maple syrup
maple syrup urine disease
T/F: BCAA’s help with muslce building and recovory
T
AA that is major source of energy for intestinal cells
glutamine
What are recommended intakes of protein for adults
0.8g/kg or 10-35%kcal
how does lean muscle mass change throughout the lifetime
lean mass increases throughout childhood and adolescence (to age 25) after age 50 there is a 1-2% lose per year
How is ammonia handled in the body
converted to urea in the liver, and excreated trhough the kidney
review starvation v stress in protein, last page of protein notes
okay
