Metabolism Pro Comps Spr. 2013 Meredith

Front 1

Protein quality

Back 1

ability of a given pro or mixture of proteins to meet bodys AA needs

Front 2

dietary protein quality depends on

Back 2

digestibility
composition / pattern of Essential AA's

Front 3

Digestibility of protein

Back 3

efficiency w/ which dietary pro is absorbed into body
only digestible part can contribute to AA's
animal = 90-95% digestible
plant = 70-90% digestible

Front 4

2 categories of protein

Back 4

high quality / complete - contain all AA's - Animal
low quality / incomplete - not contain EAAs from single pro in amts needed for growth/maintenance

Front 5

Protein quality score

Back 5

amt of each EAA in food
____________________________
amt of same AA in reference protein

> 80 good quality protein
< 80 poor quality protein
have vs. need
egg = 100 score
Limiting AA is pro w/ lowest % score in relation to egg

Front 6

protein digestibility score

Back 6

chemical score x digestibility of protein

wheat: .47 x .90 = .40
max value is 1.0 for eggs

Front 7

CHD

Back 7

inflammation key factor in development and acute effects of CHD
development of atherosclerosis or build-up of plaque in arteries

Front 8

endothelium

Back 8

single cell layer lining the inside of blood vessels

Front 9

lumen

Back 9

space w/in the tubular blood vessel

Front 10

monocyte

Back 10

cell of immune system; turns into macrophage

Front 11

macrophages

Back 11

cells of immune system found in intima of blood vessels - eat LDL

Front 12

cytokines

Back 12

chemical mediators/ messengers in the inflammation process

Front 13

CRP

Back 13

marker of inflammation in body - risk factor of CHD risk

Front 14

Proteolysis

Back 14

enzymatic breakdown of protein compounds

Front 15

foam cell

Back 15

enlarged macrophage containing LDL

Front 16

thrombus

Back 16

blood clot

Front 17

ischemia

Back 17

loss of blood flow and O2 to tissues

Front 18

Nutrient Factors influencing dev. CVD

Back 18

Folate - suppresses homocysteine formation & decr. CRP
Vit E - decr proinflammatory cytokine release; decr monocyte recruitment to endothelium (reduce inflammation); decr release of CRP
Fe: incr ox stress - incr = incr CRP
Cu: too much incr oxidative stress
Cartenoids: potent antioxidants
Polyphenols: decr proinflammatory cytokines, decr. platelet stickiness
SFA: decr LDL receptor molecule transcription

Front 19

macrophages mechanism

Back 19

release proinflamm cytokines - incr local inflamm, stimulate plaque growth - local inflam leads to proteolysis - plaque rupture - thrombus - ischemia

Front 20

artery

Back 20

lumen in center w/ blood
endothelial layer
intima
smooth muscle

Front 21

blood clot mechanism

Back 21

damage to endothelial lining
LDL gets in
oxidized by Free Radicals
receptors attach endothelial lining signaling monocytes to come
monocytes gather oxidized LDL and collect into Foam Cell
Foam Cells collect w/ tough fibrous cap but can be scraped/lesion = blod clot forms, blocks blood flow - stroke/heart attach

Front 22

Lipid Digestion and absorption

Back 22

enters stomach - SMI
95% absorbed
emulsified by bile acids, phospholipids, cholesterol

Front 23

pancreatic lipase

Back 23

hydrolyzes 1, 3 bonds of TAG
acts as oil/water interface
helps MAG (TAG w/o 1,3) to exit fat droplet

Front 24

Phospholipase

Back 24

hydrolyzes phospholipids to remove 1 FA

Front 25

cholesterol esterase

Back 25

hydrolyzes FA off cholesterol ester

Front 26

mucosal phase

Back 26

fat breaks apart to get thru GI brush border
then put back together
absorbed fats packaged in chylomicron and delivered to lymphatic system to drain into circulatory system

Front 27

secretory phase

Back 27

too big for capillary but move through lymph system
chylomicrons contain absorbed dietary fats - lymph - circulatory
drain into circulatory via large artery
MCT - bypass FA process and skip carnetine shuttle, oxidized quickly, straight to blood

Front 28

HDL
BIG PICTURE

Back 28

remove unesterified cholesterol from cells and return to liver
created in liver #1 source
key property of HDL mediated through Apo A-1 which stimulates LCAT activity to remove chol ester
CE hydrolyzed and free chol excreted in bile as bile salt - major route of chol excretion in body
called referse cholesterol transport - reduces amt of chol deposited in arteries

Front 29

Lipoproteins

Back 29

cargo trucks for different fats
1. chylomicrons - lymph to blood to cells
2. IN BLOOD: VLDL, IDL, LDL, HDL
sphere
dissolves in water

Front 30

Apoproteins

Back 30

provide ID tag for ea to be recognized by specific receptors on cell surfaces
stimulate specific enzymatic reactions w/ associated lipids
provide stability in aqueous blood environment

Front 31

VLDL

Back 31

carries fat that has been recycled
synthesized in liver
contains TG & CE
apoprotein B100, E, C
released into circulation from liver
TG b/c LDL
All LDL in blood comes from VLDL - IDL
circulation time 2hrs life span

Front 32

LDL

Back 32

comes from VLDL - IDL
carries chol
lives long time (2 days)
more LDL in blood than VLDL
MAJOR CARRIER OF CHOLESTEROL
fxn: liver main storage site
LDL receptors on surface of cells - LDL enters & removed from blood - degraded/recycled
?diets high in sat fat and chol tell liver to make less receptors?

Front 33

Adipose Cell Metabolism

Back 33

lipolysis continually & reesterification/TG formation
pool of FFA
FED STATE: insulin dominant hormone; reesterification; lipid storage
FASTING: no glucose in for storage/conversion to TG; FFA out to blood
caffeine decr blood FFA levels!

Front 34

gluconeogenesis

Back 34

glucose synthesis from non-cho sources / compounds
when dietary cho intake low or blood glu levels low
made from AA, lactate, pyruvate, glycerol
made in liver
pathway: reversal of glycolysis

Front 35

Cori CYcle

Back 35

lactate/lactic acid formed from pyruvate under anaerobic conditions
lactate leave muscle - travel to liver - converted to glu

Front 36

options for pyruvate

Back 36

1. oxaloacetate - gluconeogenesis - starvation
2. Acetyl CoA - Krebs Cycle - lots insulin

Front 37

aeromatic AA's

Back 37

phenylalanine
Tyrosine
Tryptophan

Front 38

PKU

Back 38

phenylketonuria - phenylalanine hydroxylase enzyme not working to convert phenylalanine to tyrosine
limit protein intake

Front 39

From tyrosine

Back 39

make acetyl CoA or acetate

Make L-Dopa, Dopamine, norephinephrine, epinephrine via SAM/SAH
neurotransmitters

Front 40

Methionine

Back 40

precursor to homocysteine (CHD) via SAM/SAH
control by converting back to methionine

Front 41

Methyl Folate Trap

Back 41

folic acid/B12 metabolism only works when 1st methyl group taken off

B12 deficiency there is nothing to take methyl off folic acid - shows up as folic acid deficiency

Front 42

LPL

Back 42

Lipoprotein Lipase
needed to put fat in fat cell
controlled by:
insulin - increase; release in fed state; lots of fat in blood for storage
glucagon - decrease; fasting/starving, break down fat & dump in blood

Front 43

endopeptidase

Back 43

pro digestive enzymes that split/break peptide bonds throughout

pepsinogen + hcl = pepsin (can make more of itself)

Front 44

exopeptidase

Back 44

work on very ends of polypeptide chains

Front 45

gastric phase of protein digestion/absorption

Back 45

HCL into lumen
stimulated by gastrin and gastrin releasing peptide
denatures protein (uncoils)

Front 46

pancreatic phase of protein digestion/absorption

Back 46

protein digestive enzymes produced in pancreas and stored as inactive forms, converted in GI track

mucosal cells release enteropeptidase which activates trypsinogen to trypsin - activates other digestive enzymes

active in lumen and SMI

Front 47

Mucosal phase of protein digestion/absorption

Back 47

enzymes located in brush border of SMI
jejunum 1/3 absorbed FAA; 2/3 short peptides

Front 48

protein structure

Back 48

primary (string)
secondary (slight coil)
tertiary (coils into itself some)
quaternary (tight complex coil)
shape = function

Front 49

type of bond for protein peptides

Back 49

covalent

Front 50

AA Metabolism
BIG PICTURE

Back 50

exchange and movement of Amino groups NH2 and carbon skeleton - ketoacid
NH2 -C -Carboxyl
l
side group

Front 51

transamination

Back 51

amino grop moved from one AA and placedo n another ketoacid
catalyzed by aminotransferases
require coenzyme PLP (B6)

Front 52

deamination

Back 52

removal of amino group and subsequent formation of ketoacid
use as fuel requires deamination

Front 53

major reaction in body which amino groups are released is catalyzed by

Back 53

glutamate dehydrogenase
highly active in liver, kidney and brain
in liver, amino group mainly converted to urea
in brain, to glutamine

Front 54

glucose-alanine cycle

Back 54

purpose: transport amino groups (N) from muscle during muscle catabolism/breakdown to the liver for disposal as urea
glutamine - glutamate + NH3 ammonia - pee

Front 55

essential AA

Back 55

Valine
Leucine
Isoleucine
Threonine
Methionine
Lysine
Histidine
Phenylalanine
Tryptophan
PVT TIM HILL

Front 56

indispensable AA's

Back 56

lysine
threonine
histidine

Front 57

synthesis non-essential of AA

Back 57

from glutamate

Front 58

Role of Liver in AA metabolism

Back 58

AAs travel to liver via portal vein
liver monitors absorbed AAs and adjusts rate of metabolism
large portion degrated and converted to urea
liver primary site for catabolism of aa
BRAA metabolised in muscle and kidney
unmetabolized protein problem for kidney

Front 59

AA metabolism & blood levels

Back 59

eating cho, [ ] AA decrease b/c deposit in muscle via insulin-mediated transport

insulin is anabolic - store things... make things

Front 60

2 cycles of protein metabolism

Back 60

protein turnover:
no AA excess storage
systhesis & catabolism
body takes/degrades 300g pro/day
nitrogen balance

Front 61

Nitrogen Balance

Back 61

majority of N in body present as AA/Protein
N balance = N intake - N losses
N(g) x 6.25 = protein g
Output: urea, AA, other N cmpd, feces, skin
+ N bal: preg, infant, wt. lifting
- N bal: starvation, decr pro intake, illness, trauma, disease

Front 62

hormonal control of protein metabolism

Back 62

anabolic hormones: insulin, growth hormone, testosterone: promote synthesis & + N bal

Catabolic hormones: glucagon, cortisol, thyroxine: promote catabolism & - N balance, stimulate gluconeogenesis in liver, stimulate growth

Front 63

gluconeogenesis

Back 63

*can't make glucose from fat
Pyruvate - out of mitochondria as oxaloacetate
PEP - up to glucose
reverse glycolysis

Front 64

tryptophan makes

Back 64

melatonin (sleep)
Niacin
60mg tryptophan = 1 mg niacin

Front 65

VLDL fat transporter to

Back 65

adipose
muscle
any cell that wants fat