biochem Flashcards
glycolysis production phase
G3P is ox by G3P dehydrogenase to 1,3 BPG
then PEP to pyruvate using #pyruvate kinase
** fructose 1,6 bisphosphate upregulates this, downregulated by ATP
- this one is irreversible
- made 2 ATP and NADH per pyruvate
G6P fates
- glycolysis (glucagon), PPP or glycogenesis (insulin)
- can only be undone to glucose by liver and kidneys
fates of pyruvate
- converted into acetyl coa by #pyruvate dehydrogenase
- oxaloacetate by pyruvate carboxylase
- lactate using lactate dehydrogenase
PPP irreversible ox phase (RLS?)
- makes 2 NADH ribulose 5 P
- G6P is turned into 6 phosphogluconolactone using glucose 6 P dehydrogenase RLS!!
- then 6 phosphogluconate makes ribulose 5 p using 6 phosphogluconate dehydrogenase
PPP non ox phase
- ribose 5 P makes fructose 6 p and G3P
- isomerase makes ribulose 5 p to ribose ( makes DNA)
- epimerase makes xyulose from ribulose
- transketolase transfers 2C from xyulose to ribose making sedahepulose and G3P
- transaldolase removes 3 C from sedaheptulose to make erythrose 4 P adding the last carbons to G3P making fructose 6 P
- if xs xyulose then transketolase transfers 3c from xyulose to erythrose making G3P and fructose 6 phosphate
– uses 3 ribulose!!!
gluconeogenesis
- *pyruvate in mito by pyruvate carboxylase turns to oxalo
- *then #phophoenol pyruvate carboxykinase makes PEP
- G3P made then turned to fructose 1,6 bisphosphate
- turns to fructose 6 P using fructose 1,6 bisphosphatase RLS!!!!
- limited by inuslin and on by glucagon
- then make gluc 6 phosphate to be turned to gluc in liver ER by phosphatase
**oxalo is diverted to form energy!
malate shuttle
transports oxalo across mito to cytosol using malate dehydrogenase in gluconeo
krebs
- # pyruvate dehydrogenase turns pyruvate to acetyl coa in mito
- *citrate synthetase adds it to oxalo (- reg by atp)
- RLS: isocitrate made then turns to a keto glu using isocitrate dehydrogenase (- by ATP, NADH, + by ca)
- *a keto glu turns to succinyl coa by a keto glu dehydrogenase (- by nadh, succinyl coa and atp)
- succinyl coa to succinate = GTP using succinate thiokinase
- succinate makes fumerate using succinate dehydrogenase (FADH!!!)
- malate to oxalo by malate dehydrogenase
**energy made is through substrate level phos
atp synthase structure
- f1 faces the matrix (all the a,b units)
- f0 faces intermem space with all the c1s
- upreg by adp leading to more ox consumption leading to more stim of TCA to make NADH!
anaerobic conditions
- make 2 atp and 2 lactic acid
chylomicrons
- only transport dietary fat
- not associate with fasting state
- structure is monophopholipid layer, cholesterol and TG core
- have apo b48 made in INTESTINE and allows secretion from SI!!!!!
- made in enterocyte ER, then nascent is TG rich. mature when its picked up APOc2 and ApoE from HDL
- apoc2 activates LIPOPROTEIN lipase in capillary then hydrolyze tag to FA
- remenant chylo is taken up by liver after losing apoc2 (but still apo E present E= exit thru liver)
- release TAG in enterocyte and lip sol vitamins
fa nomenclature
- first c is anomeric, last is omega
- shorthand: # of carbons: # of double bonds
- form micelles
- adding coa to fa activates it to stay in cell since hydrophilic
albumin
carries free fa that are less than 12c long
TAG, Bile things too
- usually the 2 c spot is where essential fa are! (unsat usually while the others are sat
- can’t cross enterocyte mem so must be broken down (esp if 12c+) by bile micelles
- bile recruits panc lipase to cleave at 3 and 1 pos (preserving essential FA!!). makes di glycerol then monoglycerol.
- but immediately after crossing SI mem, FA are esterified to glycerol to make TAG then make chylomicrons
omega FA
- essential fa are linoleate and linolenate since make C12 and 15 (we can’t do past 10)
- omega 3 and 6 are counted from the back end carbon!
- omega 6 is linoleic, 3 is linolenate
- high ratio of omega 3 to 6 is best
- 3 is anti inflam, 6 is pro
trans fat
- behave like saturated FA since can stack well
- worst fats mostly in margarine, dessert, creamer etc
- labels say 0 trans fat if less than 0.5!!! so serving add up
- 2 g per day increases cardio disease by 20%
olestra
- man made where fats are linked to sucrose backbone!! CAN’T BE DIGESTED so pooped out
- stop abs of fat sol vitamins
fat sol vitamins
- vit a, d, e, K
- stored in fat so can be toxic
- A can be made from diet
- vit D made from sterol. xs leads to kidney stones and weak muscles
- vit E diet is antiox and decreases cardio and cancer
- vit K diet and made is made for clotting
FA digestion
lingual lipase would digest fa less than 12 c. gives energy to mouth cells
gastric lipase does some TAG digestion in stomach
CCK made by small intestine to stim release of bile to emulsify fat also release panc enzymes like lipase, colipse, cholesterol esterase and phospholipase A2mi
- CCK also stim release of secretin that release bicarb to raise pH for optimum Digest in SI
Km and lipase
muscle: has high affinity low km so can take up free FA even when chylomicron is low. esp cardiac
adipocytes have high Km low affinity so only chylomicron take up for storage (in insulin)
* liver has high afffinity, low km
cholesterol esterase and phopholipase A2
- ester digests partially cholesterol in animal products
- A2 is for both animal and plant. cleavage at cc2 from phospholipid!!
how are fa moved from fat to blood
GPCR CAMP and PKA turn on hormone sensitive lipase and phosophorylates perilipin. perilipin breaks adipose shell so lipase can cleave tag to FFA and glycerol
- only RBC don’t have FA transporter (into cell)
FA oxidation
- activation by adding acyl coa using acyl coa synthetase. uses 2 ATP (diff for peroxisome and mito)
- enter into inner mito mem using carnitine by carnitine acyl transferase. (then removed using carnitine palmitoyl transferase) - by malonyl coa from FA synth
- palmitoyl coa gets dehydro using acyl coa dehydrogenase to make FADH2
- isomer by ADDING WATER HYDRATION
- dehydrogenation: make an NADH
- acyl coa acetyltransferase (THIOLASE) makes acetyl coa (2c) and acyl coa (that is 2C shorter) – by ATP, NADH, FADH, acetyl coa
** to use these acetyl coa, must have oxalo from pyruvate, this we need carbs!!!
of C and cycles of b ox
- if 14 c, then 6 cycles leads to 7 acetyl coas
- each cycle makes 1 NADH (2.5 ATP) and 1 FADH2 (1.5 ATP)
if 16 C then what is b ox yield
- 8 acetyl coa, 7 nadh, 7 fadh
AMPK
- activated by high AMP to upregulate catabolic process like fa ox, less gluconeo and downreg anabolic like fa, choles, and protein synth
- inhibit hmg coa reductase and decrease choles synth
- this is in the cytosol!!! whereas the NADH sensor are in mito
peroxisome
- 20c+ fa ox here
1. gives H2o2, not FADH like mito ox broken by catalase
5. dehydrogenation: make an NADH
4. acyl coa acetyltransferase (THIOLASE) makes acetyl coa (2c) and acyl coa (that is 2C shorter) – by ATP, NADH, FADH, acetyl coa
2. stops when reach 4-6 C then go to mito then do b ox using carnitine etc
FA ox disorders
- bad mito: means less energy so muscle breakdown, heart grows in size, less capacity to exercise. INCREASED acylcarnitines in blood
- primary/secondary carnitine def: can’t bring FA inside so same symptoms. secondary is caused by dialysis, AIDS
lipogenesis
- FA are made in liver CYTOSOL in fed state, but acetyls are made in mito. get NADPH from PPP and malic enzyme process
1. ***turn acetyl coa into malonyl using acetyl coa carboxylase and biotin (ATP) - by AMP, acetyl coa (to let fa enter mito) + by insulin, citrate - malonyl also inhibits carnitine palmitoyl transfase so no FA enter mito for ox!!
2. FAS: - condensation by adding acetyl to malonyl on ACP, then reduction by using NADPH, dehydration making double bond then reduction with NADPH to make it fully unsaturated
- grows 2 c at a time
3. palmitate is cleaved by thioesterase (16 C reached)
– needs 14 NADPH and 7 ATP
4. can be stored in adipose, made into phospholip, or packaged into VLDL
VLDL
- carries de novo synth FA!!
- has Apob100 from liver. its a ligand for LDL receptor and picks up apoc2 (activate LPL on capillary) and apo E from HDL
lipogenesis regulation using glucose pathways
more acetyl coa inhibits #pyruvate dehydrogenase (makes acetyl coa) and activates pyruvate carboxylase (makes oxalo)
- OAA condensing with acetyl to make citrate increases PDH activity and decrease PC
- when high flux of TCA leads to NADH, citrate is transported to cytosol!!
malic enzyme pathway
- when citrate booted to cytosol, we make NADH by turning it into OAA using citrate lyase (ATP) then malate using malate dehydrogenase and NADPH using malic enzyme
- back to pyruvate for TCA
FAS complex
- makes reaction faster, stops dilution of reactants, protect surface from competing rxns
- homodimer aligned antiparallel and 7 catalytic sites
- has ACP and CE, thioesterase, transferase
- malonyl always on ACP!!
where is biotin
in all carboxylases, even pyruvate carboxylase!
regulation of b ox
- AMPPK inhibits malonly coa (from fa synthesis) so it can make carnitine
- acetyl coa stops thiolase
regulation of acetyl coa carboxylase
- fa synth and makes malonyl coa
– by palmitoyl (0 feed) and AMPK
+ by citrate and insulin
also acyl coa stops it, allows fa to enter mito for ox
cholesterol
- can’t be broken down!! either made into esters, excreted, used to form bile, steroid hormones or vit d
- 4 rings
- low choles leads to alzhiemers, depression, memory loss, suicide and violent behavior
- made in liver (makes HIGH BMR!)
- 25% in brain
high cholesterol clinical
- xanthoma is where fats build up
- white eye patch
- hyperlipidemia in plasma and white ring around iris
choles uptake from diet
- enter enterocyte using neimann pick NPc1L1 protein using micelle
- esterified by ACAT then into chylomidron to lymph
OR comes back out of cell using ATP binding cassette ABCG5 and 8 (form sterolin complex) that couples ATP hydrolysis to transport choles back to lumen
cholesterol synthesis
- all cells do it, but mostly liver cytosol and ER
1. ***3 acetyl coa units via thiolase enzyme to make acetoacetyle coa - HMG coa synthase to make HMG Coa
**cytosol - HMGcoa reductase makes mevalonate and anchor to ER!!
2. polymerization of 6 5C isoprene units dephos and decarb - uses 3 ATP
3. head to tail condensation forms geranyl pyrophos then farnesyl (geranyl geranyl) to make squaline
3. cyclization of squaline to form sterol ring (irreverse) - lanosterol is first closed ring
statins
- block HMG Coa reductase so less choles made
- also block formation of geranyl and farnesyl which are needed to form lipid anchors on membranes
- also no formation of ubiquinone (CoQ) so less energy from ETC. need supplement
- no dolichol (for glycosylation of proteins)
- muscle weakness
- this also makes cells constantly need to pick up choles, so decrease xcell choles!!! good since take up LDL (and less ox time to make plaque)
fate of choles after synthesis
- added to plasma mem, esterified by ACAT to make choles ester (stored), transported in lipoproteins, precursor for other comps
- often contains linoleic!! can use this to store essential FA!!!
HMG coa reductase regulation
+ insulin
- glucagon, choles stim proteolysis of the enzyme!!! (- feed)
- THIS IS upreg BY glucagon STEROLS!! the proteolysis (this is longer term control)
- by AMPK
SREBP regulation
SREBP: sterol regulatory element binding protein increase anabolic process and synth of choles
- enhance HMGCOA transcription binding to reg element
- SREBP is bound to SCAP in ER when choles is high
- when low, SREBP: SCAP is transported into golgi, where proteolysis to release DNA binding domain
- binding domain activates SRE allowing transcription
bile acid formation
- cholesterol using 7 a hydroxylase makes chenodeoxycholic acid and cholic acid
- bile salts are more amphiphilic
- 95% recycled
cholestasis + malformation syndromes
- yellow spots in liver from bile accumulation
- bad secretion by liver cells or obstructed bile flow
- this means xcreted fat so muscle weakness (no fat energy source)
- genetic malformations from cholesterol meta lead to cleft palate
steroid hormone synth
- cholesterol then choles monooxygenase using 3 NADPH make prenenolone
- progesterone then cortisol, aldosterone, testosterone
- MITO!!
- these take up more LDL to synth stuff
IDL
- has apo e and apo b 100
LDL
- apo b 100 and e
- made from VLDL in circulation
HDL
apoA 1,2 and E
- NO APO B 100!!!!!!!!
- most protein and less fat
- exchanges choles ester for TAG of VLDL by CETP (choles ester transfer protein)
- also donates ApoE and c2 to chylomicrons and VLDL
- once c2 turns on LPL on chylo or VLDL, it is returned to HDL
- decreases xcell choles levels
Apo A1
HDL, activates LCAT
apo C2
on CM, VLDL, HDL
- activates LPL!!!!
apo E
on all of them
- allow clearance
pathway of VLDL meta
- glucose starts in blood then FA and pick up by VLDL then goes to blood, c2 and LPL help it release to tissues for energy
- turns into IDL which can either go to liver (60%)
OR go to peripheral cells via LDL mediated endocytosis (40%) after being released by hepatic triacylglycerol lipase!!!! - both make stuff like choles, AA, FA, glycerol
- LDL can also be ox to make foam cells that contribute to plaque formation (when in blood for some time)
reverse cholesterol transport
- HDL
- cells use ABCA1 to move choles to outer cell mem from inner
- HDL picks up from surface and converts to choles ester with LCAT (turned on by apo A1)
- esters go back to liver to make bile or repackaged
- HDL is scavenged by SRB1 RECEPTOR
**garbage pick up guy
LCAT VS ACAT
LCAT
- esterifies choles in core of HDL, and turned on by Apo A1
- uses lecithin
- L = lipoprotein associated
ACAT
- incell ester formation
incell choles regulation
- done by balance of choles synth and LDL uptake
- gene expression can decrease LDL receptor made so less taken up ( BAD)
- LDL receptor has binding domain and glycos region
- when need choles, take up via LDL endocytosis then stored using ACAT. also more LDL expression and choles synth
- increased choles in cell stops HMGcoa reductase and less LDL receptor made
protein digestion
- gastrin hormone from mucosal glands stim parietal cells to make HCl and chief cells to make pepsinogen
- HCL makes pepsin then does protein denaturing
- endopeptidase: then CCK release protease and cleaved in duodenum by cleaving trypsin then chain (chymotrypsin, elastase)
- exopeptidase: now we have small AA units so cleave 1 by 1 (carboxypeptidase)
intestinal cells make aminopeptidase (brush border, cleave 1 at a time) and intracell peptidase (in cytosol of epi cells) that act on small peptides
- abs involves active na AA cotransport
AA derived from glycolysis intermediates
- G3p: transamination makes serine (NH3 from glutamate), then cysteine (add sulfur from MET) and glycine (THF)
- PYRUVATE MAKES ALANINE
AA derived from TCA intermediates
- alpha keto glu: transamination makes glutamate (****REVERSIBLE using glu dehydrogenase. uses NADP and NAD) then glutamine x2 AA group (by adding NH3 via glutamine synthetase) and proline
- oxaloacetate: transamination makes aspartate (using glutamate), then asparagine and threonine
tyrosine
- made using phenyalanine and PA hydroxylase
- OH RXN!!! using BH4 cofactor
- can be oxidized to make fumerate and acetoacetate (ketone body)
gluco and ketogenic AA
- where they feed into post oxidation
- PITTT is BOTH
- lazy L is ketogenic
ketone bodies
- source of energy in states of prolonged starvation, exercise or diabetes/alcoholism
fates of AA
- make protein, make AA derivatives like NT, urea, carbon skeletons can be used to make FA< glucose, ketone bodies, atp and choles
FED state: dietary protein is for synthesis or converted to gluc/ TAG and given to tissues
fasting state AA meta
muscle is digested as either alanine or glutamine
- kidney deaminates so make urine + transaminates glutamine to alanine
- intestine also does glu to ala
- liver uses ala to make urea, ketone bodies or glucose
** even digestive enzymes are digested!
transamination
- transfer of amine groups
- needs b6 cofactor!! and enzyme is aminotransferase/transaminase
- a keto glu becomes glu then alanine becomes pyruvate
where does NH3 on glu go?
oxidative deamination
- GLUTAMATE ONLY
- glu goes to liver mito where glu dehydrogenase adds an ox and makes a keto glu and urea!
how does ammonia reach the liver
- glutamate added ammonia to make glutamine (converted back via (Glutaminase) NEEDS ATP
- glucose alanine cycle in muscles: a keto glu and ammonia mate glutamate then transamine to alanine. goes back to glutamate and pyruvate (with a keto glu)
glutamate in the liver mito
- deaminated to ammonia and a keto glu OR transaminated to asp (can enter urea cycle with ammonia)
- this is done using glu dehydrogenase (ONLY REVERSIBLE STEP)
what happens to pyruvate in all AA processess
- muscles make it into lactate or acetyl coa
urea cycle
- remove amino via transaminase
- take to liver mito (ox deamination)
- ammonia added to co2 using carbamoyl phosphate synthetase RLS!!!! needs atp in mito of liver
- regulated by substrate availability OR allosteric induction using N acetyl glutamate
- moves out to fuse with aspartate (carries second nitro group) to make either fumerate (TCA in CYTOSOL) or arginine (cts urea cycle or make urea)
** all irreversible xcept glu dehydro
** NH comes from AA catabolism, purine catabolism, heme
type 1 dia
- onset after age of 4, peak in puberty
- strong genetic with prone to other immune disease
- 90% autoimmune response to b cells
- can also be more prone to virus in immune mediated
- idiopathic is 10% where no evidence of b cell prob (mostly asian or african)
latent autoimmune dia of adults
- type 1.5 or slow progressing insulin dependent
- more than 30+ age
- to check vs type 2, not treated with insulin within first 6 mos
type 2 dia
- 90% are this
- resistance to insulin
- years to dev, lifestyle factors
obese type: 70%
- defect in insulin or resistance
non obese type is absent or blunted early phase of insulin release. majority are idiopathic and asian
childhood type is 45% new cases in kids!! due to foods, lack of movement. high in hispanic, black and asian
gestational dia
- increased risk with materal obesity
- mom high sugar leads to bb high insulin!!
- normal postpartum
- leads to risk in developing type 2 dia, metabolic syndrome, cardio (mom), obesity (bb)
signs of diabetes
- xs hunger, xs pee, xs thirst, diabetic ketoacidosis (more in type 1 than 2)
^hyperglycemic - also weight loss, decreased muscle mass, parasthesias (tingling peripheral nerves)
- tiredness
- chronic yeast infections (lots of glucose to feed)
signs of diabetes, type 2 specific
- hyperosmolar hyperglycemic non ketotic syndrome
- leads to confusion mental stuff
diagnosing diabetes
-urinanalysis giving glucosuria and ketonuria
- HbA1C test. 5.6% is good. 6.5% is diabetes. 9% is ER!!
- 70-100 mg/dL is normal using glucose oxidase strips** refer to doc if over 400!!
- serum glucose
- oral glucose tolerance test (b4 and after 2hr of drinking soda)
complications of dia
- lots of AGEs leading to cell damage and RAGES (receptors) activate inflam
- can’t be broken down into other things, so bad
- eye problems, brain and stroke risk, wound healing, tingling limbs, gangrene
- xerostomia, caries, infection, statodynia (oral neuropathy), lichen planus bumps, periodontitis
perio and dia
- sugar problems can lead to perio problems like gingivitis, bone loss, lost teeth
- goes both ways where perio can increase risk of nephropathy and vascular disease
qns to ask a diabetic patient
- type, how to monitor levels,
FROM: fasting blood sugar, normal range, oral inrake, medications - HbA1c result, do u have fluctuations in blood sugar, disorientation, mouth sores/dry mouth, ant other medical problems/history of gum disease
dental treatment and diabetes
- check HbA1C, antibiotics for poor control patients, short am appointments 1.5-3 hrs after breakfast
- avoid treatment if 400 mg or higher
- have glucose source available
- limit epi to minimize spikes
- keep sugar available
- afterwards, adjust insulin dose, avoid glucocorticoids
ketogenic diet
- lipid carb ratio is 3:1
- used for ppl with no PDH or GLUT
- high in medium chain fa that make most ketone bodies
- complications inclue acidosis, hypoglycemic, higher tag and choles
- ketosis is when most energy from ketone bodies. not bad as long as maintain glucose levels
- need some carbs to burn fats
- leads to more glucagon and repressed acetyl coa carboxylase and FAS
ketone body formation
- in liver mito
- increased conversion of oxalo to malate
- release carnitine transferase from block by malonly
- decreased acetly coa carboxylase activity
- thiolase, last step of b ox does this when levels are high!
- makes acetoacetate then spontaneous breakdown into b hydroxybuterate and acetone done by hydroxybuterate dehydro)
- HMG coa synthetase is here too
- liver can’t use ketone bodies
ketolysis
- used mostly by brain!! can’t be used by liver or RBC
- happens in mito of tissues
- can be used by fetus
- b hydroxybuterate turns back into acetyl coa
- using hydroxybuterate dehydro
why is fructose bad
- makes DHAP and G3P that convert in liver to pyruvate
- aldolase converts fructose 1 P and fructose 1,6 bp
- bypass PFK1 so unregulated!!
food meal times and what happens
12 hr after meal, glucagon
- only use AA after 12 hours fasting
starved state is 3-5 days and makes more ketone, glucose sparing
- decreased baseline of hormones, and remain constant (insulin and glucagon). muscle wasting BAD
- spare the protein also, ketone only used by RBC and brain
high blood sugar
- PFK2 on, pyruvate kinase, glycogen synthase, pyruvate dehydrogenase, acetyl coa carboxylase
low blood sugar
- PFK2, phosphorylase kinase, glycogen phosphorylase
insulin production and paths
- glucose taken up by GLUT2 then insulin stim
- makes insulin and c peptide
- rapid response: fast uptake of gluc and AA
- intermediate is making proteins, stop degredation, break glyco
**GLUT 2 is on surface of B cells, while GLUT4 is non B cell receptor that MOVES to surface
AGE products
- carbs binding to NH
- have receptor RAge that dfoes inflam
- first becomes schiff base then amadori product (reversible)
- after weeks/months and ox, it becomes AGE
- RBC last 120 days so can change with diet
- for every 1% Hb change, there is 36 mg/dL change in mean glucose
genetics and type 2 dia
- GLUT 2 bad so can’t sense glucose and make insulin on b cells
- bad insulin receptors so can’t send signals
obesity, inflam, and insulin
- chronic inflam in fat cells for obesity since fat cells act full and high FFA
- stop releasing fat too
- leads to fat deposition in wonky places like muscles, increase in immune cells = inflam
- white fat happens in diabetes and obesity
- brown fat happens in exercise
- beige fat is mix of both, ratio = health
- insulin resistance leads to stim of lipolysis, gluconeo so more ketone bodies!!! leads to AGE, ox of LDL, less reverse choles transport etc
ethanol meta with the dehydros
- easy uptake since water sol
- microsomal oxidizing system (MEOS) is minor route of digestion in liver with cyto P450 in ER that uses NADPH to make acetaldehyde
- alcohol dehydro (cytosol) makes NADH
- liver dehydro (ADH1) is low km, high affinity. majority of OH meta in liver
- ADH4 and ADH7 present in oral cavity NOT LIVER. ADH4 is most active!!!
- ALDH acetaldehyde dehydro in mito. low km high affinity. takes acetaldehyde and makes acetate making NADH
alcohol problems
- glossitis, gingivitis, cheilitis
- perio problems
- nutrient def and liver problems
- can have acetaldehyde dehydro varients where some are less active, resulting in max vomiting!!!
- hepatic steatosis, alcoholic hepatitis (reversible)
- cirrhosis is worst with nodules and fibrosis (2+ years)
- meta leads to higher NADH so stop gluconeo, b ox and flux of tca, ketoacidosis, hypoglycemia, FA storage, less uric acid out so gout since more lactate
high acetaldehyde
** high acetaldehyde leads to nausea!
- acetate turns into acetyl coa (cytosol in liver, mito in muscle)
- alcoholics are treated with ALDH inhibitors!!!!
- leads to DNA prob, chromosome rearrangement, DNA clumping
lipoprotein problems
- dyslipidemia is high choles, tag or both or low HDL = arthosclerosis
- same signs as cholesterol
- no symptoms!! but leads to vascular disease including stroke
- can be genetic, resulting in higher HDL too!!! best thing (familial hyperalphalipoproteinemia)
- hypercholesterolemia is LDL receptor prob so high choles
oxidized LDL
- make foam cells that can’t be removed!!
- worsened by smoking, h2020, cigarette, bacteria etc
- vit ECA protect!!
fatty streak and plaque
- LDL ox then uptake by intima by scavenger cells making Foam cells. collection = fatty streak
2. fibrous cap grows on top from smooth muscle growth = plaque in artery
metabolic syndrome
- 5 conditions that lead to heart disease, dia, stroke etc
1. high BP, high glucose, low HDL, high TAG and fat waist
lab result numbers
- choles less than 200 ok
HDL 40+ is good
LDL less than 120 is good
hypoglycemic vs hyper indications
hypo: shakiness, nervous, sweaty
hyper: xs hunger, xs pee, xs thirst,
NADH ox coupling
- makes atp, reduction og o2 to h20 and makes proton gradient
acetyl coa can’t turn into
glucose via gluconeo since only 2c! which is why its stored as ketone body
urea cycle regulation
- feed forward, only when energy available, flux controlled by protein synthesis, allosteric
urea cycle regulation
- feed forward, only when energy available, flux controlled by protein synthesis, allosteric
vitamins needed for krebs
- vit A, thiamine (vit B)
niacin
NEEDED to make nadh
riboflavin
needed to make fadh
vit e
decrease LDL ox
vit c
needed to make carnitine
