Biochem

Question 1

GLUT 2 vs GLUT 4 compare and contrast

which tissues?
purpose?
Km and kinetics?

Answer 1

glucose uptake receptors- independant on Na+

Which tissues?

• GLUT 2= hepatocytes and pancreatic B (beta) islet cells
• GLUT 4= adipose tissue, muscle cells

Purpose:
-GLUT 2- picks up glucose after meal (high conc.) from hepatic portal vein so excess can be stored in liver. glucose [] below Km= enters peripheral circulation. Serves as glucose sensor for beta cells in pancreas- high glucose=insulin release

-GLUT 4- responsive to insulin. Stimulates movement of additional GLUT 4 to membrane via exocytosis so glucose from peripheral blood can be taken in. Muscle cells- glycogen. Adipose- glucose forms DHAP to form glycerol phosphate to store fatty acids as triacylglycerol

Kinetics/Km:

• GLUT 2= high Km= first order kinetics= glucose transport rate increases proportional to []. If glucose below Km- enters peripheral circulation
• GLUT 4= low Km close to normal glucose levels- gets saturated at slightly higher blood glucose levels= zero order kinetics- constant rate. Increase uptake of glucose with insulin- trigger more GLUT 4 to go to membrane

Question 2

Hexokinase vs glucokinase

Answer 2

1st step of glycolysis- convert glucose to G6P to prevent it from leaving cell through transporter (specific). Requires ATP and Mg+2 as a cofactor!!!!! Kinases!

hexokinase- most tissues, low Km (saturated quickly, zero order), inhibited by G6P
glucokinase- only in liver and pancreatic B- islet cells, high Km (first order), induced by insulin in hepatocytes. Also acts as glucose sensor in B-cells along with GLUT 2

Question 3

Rate limiting enzymes for:
glycolysis
fermentation
glycogenesis
glycogenolysis
gluconeogenesis
Pentose-Phosphate Pathway

Answer 3

glycolysis= phosphofructokinase 1 (PFK-1)
fermentation= lactate dehydrogenase
glycogenesis= glycogen synthase
glycogenolysis=glycogen phosphorylase
gluconeogenesis= fructose 1,6 bisphosphotase
Pentose-Phosphate= 6GP (glucose-6-phosphate) dehydrogenase

Question 4

PFK 1 and PFK 2 aka Phosphofructokinases and what happens to fructose 1,6 biphosphate

please also describe regulation!!!!!

Answer 4

PFK 1:
F6P- fructose 6- phosphate is phosphorylated to fructose 1,6 biphosphate— requires ATP
F6P made from isomerase acting on G6P
Rate limiting step of glycolysis:
- inhibited by ATP, citrate
-activated by AMP, fructose 2, 6 biphoshpate (in liver)

fructose 1,6 biphosphate split by aldose in next step into two 3 carbon compounds- DHAP and glyceraldehyde 3-P

PFK 2:

• activated by insulin= converts F6P to fructose 2,6 biphosphate= activates PFK 1 in hepatocytes
• inhibited by glucagon—- leads to inhibition of PFK 1
• allows liver do glycolysis even when lots of ATP around for other processes

Question 5

Glyceraldehyde 3-P dehydrogenase

Answer 5

adds phosphate to glyceraldehyde 3P and oxidizes it to become 1,3 bisphosphoglycerate (high energy). NADH made.

Question 6

3-phosphoglycerate kinase

Answer 6

1,3 bisphoshoglycerate loses phospate, forming ATP and 3-phosphoglycerate—–substrate level phosphorylation

Question 7

Pyruvate kinase+ feed forward activation

Answer 7

PEP- phosphoenolpyruvate (high energy) loses phosphate and becomes pyruvate= ADP to ATP!!!

activated by fructose 1,6 bisphosphate (product of PFK-1) —- feed forward activation

Question 8

Fermentation process

Answer 8

Enzyme- lactate dehydrogenase
NADH to NAD+
pyruvate to lactate (3C)
poor oxygenation- anaerobic conditions

yeast- make ethanol (2C) and CO2 (1 C)

Question 9

DHAP (two fates)

Answer 9

formed by aldose splitting fructose 1,6 bisphosphate.

• can be isomerized to glyceraldehyde 3P to continue glycolysis
• glycerol 3P dehydrogenase can be to convert DHAP to glycerol 3-P in liver and adipose tissue to form glycerol= triacylglycerols!

Question 10

Irreversible enzymes of glycolysis

Answer 10

PFK-1, hexokinase/glucokinase, pyruvate kinase (all the kinases push forward the process)

Question 11

High energy intermediates of glycolysis- make ATP

Answer 11

1,3 BPG (3-phosphoglycerate kinase), PEP (pyruvate kinase)

Question 12

Red blood cells- glycolysis what is produced and what is its effect

Answer 12

1,3 BPG is converted to 2,3 BPG by bisphosphoglycerate mutase.

Allosteric effect on hemoglobin HbA- decreases affinity for O2= hemoglobin releases O2= delivered to tissues.

Curve shifts right- for same amount in blood (PO2) less bound to hemoglobin (less saturation)

doesn’t bind to fetal hemoglobin

Question 13

hemoglobin abbreviation

Answer 13

HbA

Question 14

Galactose metabolism

Answer 14

lactose splits into galactose and glucose (lactase brush enzyme)

• galactokinase converts it to galactose 1-P, using ATP (traps in cell)
• Gal-1-P-uridyltransferase and an epimerase converts galactose 1-P to glucose 1-P which can be used to make G6P or glycogen

excess galactose= galactitol in lens= cataracts in eye

Question 15

Fructose metabolism

Answer 15

sucrose disaccharide splits into glucose and fructose by sucrase (brush enzyme)
fructose from honey, fruits, etc.

fructokinase converts to fructose 1- phopshate (traps in cell)
aldolase converts fructose 1P to DHAP and glyceraldehyde— becomes glyceraldehyde 3P

Question 16

Pyruvate dehydrogenase complex (PDH)

• describe reversibility
• products of reaction
• regulation( inhibition and activation)

Answer 16

pyruvate (3C) to acetyl CoA (2C)

irreversible

NADH made and CoA added
CO2 released

inhibited by acetyl CoA, if enough acetyl CoA, pyruvate used to make oxaloacetate or fatty acids

insulin activates it in liver, whereas brain no hormones effect

Question 17

Glycogen storage and purpose in its two locations

Answer 17

Stored in cytoplasm of liver and skeletal muscle cells as granules

protein cores
polyglucose chains coming off of the core
- linear= highest density near core
-branched= highest density near periphery for rapid release of glucose

purpose;
liver=maintain constant blood glucose levels
muscle= energy reserve

Question 18

Glycogenesis- steps and all enzymes involved + describe RDS and control on enzymes

Answer 18

G6P converted to G1P.
G1P coupled with UDP= UDP-glucose (made by UTP and loss of two phosphate)

glycogen synthetase removed UDP and integrates the glucose into the glycogen chain by forming alpha 1-4 glycosidic bonds

branching enzyme- hydrolyzes 1,4 bond, transfers oligoglucose chain, and attaches it via alpha 1,6 linkage to make branch

glycogen synthetase= rate limiting step.
stimulated by insulin and G6P= insulin=more glucose storage
inhibited by epinephrine and glucagon= less glucose storage

Question 19

Glycogenolysis

Answer 19

Rate limiting enzyme= glycogen phosphorylase

• —breaks alpha 1-4 glycosidic links, releasing G1P, which is converted to G6P
• –activated by glucagon in liver and activated by AMP and epinephrine in muscle
• –inhibited by ATP
• –can’t work on 1,6– need debranching enzyme

debranching enzyme:
-made up of two enzymes. One enzyme breaks 1-4 bond closest to branch and transfers sugar to end of open chain. Other enzyme releases one monomer of glucose by breaking 1-6 bond.

Question 20

Glycogen storage diseases

Answer 20

accumulation of lack of glycogen in one or more tisses

enzymes can be affected- activity and isoform (diff. form of same protein)

Question 21

Gluconeogenesis

location, purpose, control

Answer 21

Done in the liver (and kidneys)
Promoted by glucagon and epinephrine- raise blood sugar levels— especially during fasting when glycogen drops and no glucose source external!!!!!
only source of glucose after 24 hours (glycogen all gone)
inhibited by insulin

Question 22

Pentose Phosphate pathway (PPP)/ Hexose Monophosphate shunt (HMP)

-location, purpose, control

Answer 22

Occurs in cytoplasm of all cells

1. production of NADPH (2)
2. source of ribose-5-phosphate for nucleotide synthesis

G6P oxidized to 6-phosphogluconate by G6P dehydrogenase, making NADPH. 6-phosphogluconate oxidized and decarboxylated to ribulose 5P. (NADPH made)

fructose 6P, glyceraldehyde and ribose 5P interconverted via intermediates—– done by TPP and transaldolase

rate limiting enzyme is glucose-6-phosphate dehydrogenase
activated by NADP+ and insulin!- anabolic
inhibited by NADPH

Question 23

NADPH

Answer 23

not same as NADH

• acts as electron donor, reducing agent
• biosynthesis- fatty acids and cholestrol
• cellular bleach production in leukocytes- bactericidal
• protects cells from free radical oxidative damage caused by peroxides like H2O2 made during respiration—- glutathione is reducing agent that reverses radical formation and NADPH is used to maintain its supply

Question 24

Steps of citric acid cycle- remember mnemonic, def. of flavoprotein.

Describe intermediates, enzymes, and what produced in each step please

Answer 24

Mnemonic for citric acid substrates: Please, Can I Keep Selling Seashells For Money, Officer?

P- pyruvate. Step 0= pyruvate to acetyl CoA- pyruvate dehydrogenase- NADH made. CO2 released

C- citrate (6C). Step 1= oxaloacetate (4C) and acetyl (2 C) CoA combine= citrate (6 C) and CoA- citrate synthetase

I-isocitrate (6C) Step 2= citrate isomerized to isocitrate via aconitase, requires Fe+2.
Remove water= cis-aconitate, and add water= isocitrate

K- alpha-ketoglutarate (5C). Step 3= isocitrate oxidized to oxalosuccinate by isocitrate dehydrogenase, forming NADH. Oxalosuccinate becomes alpha-ketoglutarate via a loss of CO2.
CO2 made, NADH made

S-succinyl CoA (4C). Step 4= alpha ketoglutarate dehydrogenase complex adds CoA, removes CO2, and oxidizes= NADH production.
CO2 made, NADH made

S- succinate (4C). Step 5= succinyl CoA- lose CoA and make succinate. GTP formation= direct ATP. Succinyl CoA synthetase (not synthase- require energy input to create bonds)

F- fumarate (4C). Step 6= oxidation of succinate by succinate dehydrogenase to make fumarate and FADH2 from FAD. Occurs on inner mitochondrial membrane.
Succinate dehydrogenase= flavoprotein= bonded to FAD
FADH2 passes electrons to ETC to make 1.5 ATP. Enzyme is part of complex 2 of ETC.

M- malate (4C). Step 7= fumarate to malate (alkene to alkane), requires water. — fumarase

O- oxaloacetate (4C) Step 8=malate dehydrogenase oxidizes malate to oxaloacetate. NADH formed.

Question 25

Net results of citric acid cycle and glycolysis

Answer 25

pyruvate dehydrogenase complex= 1 NADH, 1 CO2 citric acid cycle= 3 NADH, 1 FADH2, 1 GTP, 2 CO2 4 NADH= 10 ATP (2.5 ATP each) 1 FADH2=1.5 ATP 1 GTP=1 ATP 12.5 ATP per pyruvate= 25 per glucose dehydrogenase- formation of NADH/FADH2 glycolysis: 2 net ATP per glucose, 2 NADH made. 2.5*2=5+2=7 30-32 ATP?

Question 26

Location and regulation/control of citric acid cycle

Answer 26

citrate synthetase- inhibited by ATP, NADH, succinyl CoA, citrate (allosteric) isocitrate dehydrogenase- inhibited by ATP, NADH so stimulated by ADP, NAD+ alpha-ketoglutarate dehydrogenase complex- inhibited by ATP, NADH, and succinyl CoA (its product). Stimulated by Ca+2 and ADP. both CO2 losses, and first step

Question 27

Pyruvate dehydrogenase complex regulation

Answer 27

Phosphorylated= inactivated-- done by pyruvate dehydrogenase kinase (high ATP) Dephosphorylated= active-- done by pyruvate dehydrogenase phosphatase (high ADP) also inhibited by ATP, NADH, and acetyl CoA (which can be made from fat)

Question 28

ETC- oxygen role

Answer 28

O2 has high reduction potential- good electron acceptor. Combines with electrons as H- to make H20.

Question 29

Lipid mobilization from adipose tissue | HSL!!!! LPL

Answer 29

Postabsorptive state- falling insulin levels, like at night. Fatty acids are released from adipose tissue for energy Low insulin/high epinephrine and cortisol= activate HSL= hormone sensitive lipase Hydrolyzes triacylglycerol to glycerol (used in glycolysis/gluconeogenesis in liver when glucagon up) and fatty acids (B-oxidation in liver) Need LPL- lipoprotein lipase to metabolize triacylglycerol in VLDL or chylomicrons into fatty acids and glycerol released into adipose/tissues

Question 30

Lipid transport (free fatty acids vs cholesterol vs triacylglycerols)

Answer 30

Free fatty acids- transported in blood via albumin | Cholesterol and triglycerides= need lipoproteins

Question 31

Lipoproteins

Answer 31

aggregates of apolipoproteins and lipids. Named according to protein density (more protein, less fat= high density) HDL>LDL>IDL>VLDL>chylomicrons

Question 32

Chylomicrons

Answer 32

transport dietary triacylglycerols, cholestrol, and cholesteryl esters in blood/lymph from intestines to adipose tissues and liver- assembly in intestines

Question 33

VLDL

Answer 33

produced and assembled in liver- transport triacylglycerols and fatty acids from liver to tissues liver assembles triacylglycerols

Question 34

IDL

Answer 34

Remnants of VLDL from triacylglycerol removed from it. Reasborbed by liver Picks up cholesteryl esters from HDL to become LDL transition between triacylglycerol transport and cholestrol transport

Question 35

LDL

Answer 35

deliver cholesterol to tissues for biosynthesis and cell membranes (and also to make bile and hormones)

Question 36

HDL

Answer 36

synthesized in liver and intestines. - Cholesterol recovery- cleaning excess cholesterol from blood vessels for excretion!!!!!!! - transfer apolipoproteins to other lipoproteins - delivers cholesterol to steroidogenic tissues

Question 37

Apoproteins/Apolipoproteins

Answer 37

receptor molecules- involved in signaling apoA-1- activates LCAT for cholesterol esterification apoB-48- chylomicron secretion apoB-100- uptake of LDL by liver apoC-2- lipoprotein lipase (LPL) activation apoE- uptake of chylomicron remnants and VLDL by liver

Question 38

Cholesterol sources/synthesis

Answer 38

LDL and HDL. De novo synthesis of cholesterol occurs in the liver driven by acetyl CoA and ATP citrate shuttle carries acetyl CoA to cytoplasm. NADPH acts as a reducer. Synthesis of mevalonic acid in SER is rate limiting step catalyzed by HMG CoA reductase

Question 39

Regulation of cholesterol synthesis

Answer 39

high cholesterol= inhibit insulin- promotes cholesterol synthesis regulation of HMG-CoA reductase

Question 40

Enzymes involved in transport of cholesterol

Answer 40

LCAT- activated by HDL apoproteins. Adds fatty acid to cholesterol= cholesteryl esters. HDL can distribute these esters to IDL-- becomes LDL, facilitated by CETP (cholesteryl ester transfer protein)

Question 41

Bioenergetics- thermodynamic considerations for biological systems

Answer 41

open system- biology cellular/subcellular= closed system delta U= Q-W W= zero- deltaV=0 Q mostly considered delta G= deltaGstandard + RTlnQ delta G standard- 25 C, 1 atm, standard concentrations of 1 M. However, 1 M of H+ too acidic for body, so use modified delta G with ph 7 as standard 10-7 M H+ (delta G standard)'

Question 42

ATP as energy carrier

Answer 42

mid level energy carrier- can't get back lost energy 30 kj/mol so if rxn requires only 10 kj/mol, 20 kj wasted- can't get it back. Thats why not too much energy very negative delta g- neg charges and resonance stabilization for loss of phosphate (-30 kj/mol) cAMP, creatinine phosphate- even higher energy G6P, AMP lower energy

Question 43

Electron carriers name

Answer 43

high energy electon carriers NADH, NADPH, FADH2, ubiquinone, cytochromes, gluthathione soluble electron carriers, membrane bound ones FMN- membrane bound, complex 1 of ETC proteins with iron sulfer prosethetic group= good electron carriers

Question 44

Flavoproteins

Answer 44

modified B2= modified riboflavin nucleid acid derivatives----- FAD/FMN mitochondria and chloroplasts as electron carriers other roles: - modify other B vitamins to be active - function as coenzymes of oxidation of fatty acids, deccarboxylation of pyruvate, reduction of glutathione

Question 45

Which steps of glycolysis make ATP

Answer 45

1,3 BPG to 3PG done by 3 phosphoglycerate kinase PEP to pyruvate by pyruvate kinase (irreversible step also)

Question 46

Which steps of glycolysis use ATP

Answer 46

PFK-1 : also irreversible and RDS F6P to F1,6P glucokinase/hexokinase : also irreversible glucose to G6P

Question 47

Metabolism of lactose and sucrose leads to which intermediates of glycolysis

Answer 47

galactose---- glucose 1P to G6P fructose----- DHAP and glyceraldehyde----- G3P

Question 48

Which steps of glycolysis make NADH

Answer 48

3GP to 1,3 BPG | glycerol 3 phosphate dehydrogenase

Question 49

Where does G1P (glucose 1 P) come from?

Answer 49

galactose 1P G6P to G1P during glycogenesis G1P to G6P---glycogenolysis

Question 50

Gluconeogenesis important intermediates

Answer 50

glycerol 3 phosphate (from glycerol of triacylglycerols) --------- converted to DHAP by glycerol 3 dehydrogenase, make NADH ------DHAP can be converted to G3P (glyceraldyhde 3P) lactate (from fermentation) ---lactate dehydrogenase, lactate to pyruvate, make NADH (Cori Cycle) glucogenic amino acids (alanine) -------------alanine to pyruvate via alanine aminotransferase make stuff like pyruvate, oxaloacetate, others

Question 51

glucogenic vs ketogenic amino acids and how proteins catabolized

Answer 51

glucogenic-- all amino acids besides lysine and leucine (can be converted to intermediates feeding into gluconeogenesis)- glucose ketogenic- W, F, Y, I, T, L, K (can be converted to ketone bodies) proteins unlikely since so important for other shit deamination/transamination must happen and then carbon skeleton used for energy amino groups toxic- must be excreted- urea cycle

Question 52

pyruvate carboxylase

Answer 52

gluconeogenesis, mitochondrial enzyme converts pyruvate to oxaloacetate, uses ATP and one carbon dioxide to do so OAA eventually leads to glucose production activated by acetyl CoA acetyl CoA inhibits pyruvate dehydrogenase- no more acetyl CoA needed, satiated cell- no more burning glucose, need to make more glucose so activates pyruvate carboxylase in times of no glucose---- high fats--- acetyl CoA made!!!. acetyl CoA----- pyruvate carboxylase activate--- OAA made--- eventually leads to gluconeogenesiss

Question 53

PEPCK --- phosphoenolpyruvate carboxykinase

Answer 53

cytoplasm enzyme, gluconeogenesis oxaloacetate made by pyruvate carboxylase from pyruvate to enter cytoplasm-----malate aspartate shuttle OAA to malate----cytoplasm--- malate to OAA OAA converted by PEPCK to PEP (requires GTP) PEP can go all the way back to F1,6BP (rest of rxns reversible) requires GTP. Induced by glucagon and cortisol to raise glucose levels PEPCK and pyruvate carboxylase together accomplish the pyruvate to PEP process since that is irreversible

Question 54

Fructose 1,6 Biphosphatase

Answer 54

converts F1,6 BP to F6P rate limiting step of gluceoneogenesis - ---oppose PFK (kinase) - ---activated by ATP (high levels so can make glucose, not burn) - ---inhibited by AMP and F2,6BP F2,6 BP- made by PFK 2- inhibited by glucagon- which promotes gluconeogenesis while insulin stops by increasing F2,6 BP levels

Question 55

Summary of gluconeogenesis

Answer 55

pyruvate made (alanine dehydrogenase, lactate dehydrogenase) OAA made - from pyruvate (pyruvate carboxylase)--- high acetyl CoA levels - glucogenic AA OAA to PEP (PEPCK)--- high glucagon and cortisol levels F 1,6 BP made -----reversible reactions from PEP and DHAP (made from glycerol 3 phosphate from triacylglycerol using glycerol 3 phosphate dehydrogenase) F1,6 BP to F6P------ fructose 1,6 biphosphatase----- rate limiting step of gluconeogenesis - ---oppose PFK (kinase) - ---activated by ATP - ---inhibited by AMP and F2,6 biphosphate ``` G6P made (from FGP) G6P converted to glucose by glucose 6 phosphatase ``` Finally have glucose---- gluconeogenesis done in liver. Now, can give glucose to other tissues if blood glucose levels are really low. Not done as energy source for liver. Requires lots of energy/ATP- provided by B-oxidation of fatty acids to acetyl CoA (done when low blood sugar) adipose tissue to liver with fatty acids during starvation- acetyl CoA- ketone bodies used too acetyl CoA activates pyruvate carboxylase also

Question 56

Glucose 6 phosphatase

Answer 56

lumen of ER of liver cells G6P transported to ER, acted upon by enzyme, and glucose transported to cytoplasm and can leave cell to raise blood sugar enzyme not used in muscles- can't convert G6P to glucose to raise blood sugar, only liver can. G6P in muscles---- used only for muscle energy oppose glucokinase/hexokinase

Question 57

Ketone bodies - purpose - names

Answer 57

during starvation! fasting state fatty acids to acetyl CoA in liver mitochondrial matrix (B-oxidation) -excess acetyl CoA converted to ketone bodies via ketogenesis Ketone bodies= acetoacetate and 3-hydroxybutyrate Ketone bodies are transported to mitochondrial matrix various tissues- cardiac and skeletal muscle, brain, and renal cortex where they can be metabolized to acetyl CoA and put in citric acid cycle to make energy ---- via ketolysis brain---- prolonged fasting only. 2/3 of energy from ketone bodies. glucose uptake decreases and so does glycolysis

Question 58

Ketogenesis

Answer 58

-HMG-CoA synthase converts acetyl CoA to HMG-CoA. -HMG lyase breaks HMG-CoA to acetoacetate (byproduct of it is acetone) -acetoacetate reduced to 3-hydroxybutyrate with NADH

Question 59

Ketolysis

Answer 59

Thiophorase activates acetoacetate, becomes acetoacetyl CoA to 2 acetyl CoA to be used in citric acid cycle to make ATP enzyme only present in tissues outside liver so it can't use its own ketone bodies

Question 60

Ways to make acetyl CoA Summary

Answer 60

pyruvate dehydrogenase complex fatty acid (beta) oxidation ketogenic AA catabolism ketone body (reverse rxn of making them)] alcohol ------alcohol dehydrogenase and acetaldehyde dejhydrogenase used to make acetyl CoA from alcohol -----accompanied by NADH buildup so block citric acid cycle -----acetyl CoA made by this only used for fatty acid synthesis

Question 61

Problems with using alcohol to make acetyl CoA

Answer 61

- -----alcohol dehydrogenase and acetaldehyde dejhydrogenase used to make acetyl CoA from alcohol - ----accompanied by NADH buildup so block citric acid cycle - ----acetyl CoA made by this only used for fatty acid synthesis

Question 62

Pyruvate dehydrogenase mechanism

Answer 62

complicated shit, not feeling it bro | look at damn pic and pg 342/341 in kaplan BC

Question 63

What all is acetyl CoA used for

Answer 63

- citric acid cycle (muscle and adipose) - fatty acid synthesis - ketone bodies - activates pyruvate carboxylase (gluconeogenesis) - inhibits pyruvate dehydrogenase - cholesterol synthesis muscle and adipose- actyl CoA from fatty acids) enters citric acid cycle liver- fasting state: acetyl CoA stimulates gluconeogenesis and in fasting state more present than used in citric acid cycle so excess converted to ketone bodies nonfasting state: fatty acid synthesis

Question 64

Fatty acid synthesis - location - purpose

Answer 64

occurs in liver-- then transported to other tissues excess carbs and protein converted to adipose for storage stimulated by insulin end product is palmitate

Question 65

acetyl-CoA shutting- fatty acid synthesis major enzyme

Answer 65

acetyl CoA accumulates post meal in mitochondria, citrate thus accumulates as acetyl CoA+ oxaloacetate combine-slowing of citric acid cycle once satisfied energtically. citrate diffuses into cytosol and citrate lyase splits into acetyl CoA (cytoplasm) and oxaloacetate (goes back to mitochondria)----- OAA in cytoplasm to pyruvate can happen- gluconeogenesis (but this happens when starving)- high acetyl CoA levels! OAA to PEP though needs high glucagon!- won't happen

Question 66

acetyl CoA carboxylase | -importance to fatty acid biosynthesis

Answer 66

RDS for fatty acid biosynthesis enzyme- requires biotin and ATP activated by insulin and citrate acetyl CoA + CO2= malonyl CoA

Question 67

fatty acid synthase/palmitate synthase

Answer 67

multienzyme complex high insulin levels stimulate requires B5 NADPH required NADPH made from pentose phosphate pathway and also from malate to pyruvate! malonyl CoA , remove CO2= palmitate! 8 acetyl CoA for palmitate (16C)

Question 68

beta oxidation | location, regulation

Answer 68

mostly in mitochondria, some in perioxisomes insulin=inhibits glucagon= stimulates

Question 69

Beta oxidation process name enzyme involved/overall job activation entry into mitochondria beta oxidation

Answer 69

activation- fatty acyl CoA synthetase (attach acetyl CoA) short and medium chains diffuse to enter mitochondria long chain fatty acids require transport by carnitine shuttle, important enzyme= CPT1 RDS- carnitine palmitoyltransferase 1 beta oxidation- make acetyl CoA and lots of NADH and FADH2- produce ATP via ETC

Question 70

beta oxidation process

Answer 70

1. oxidation of fatty acetyl CoA to form double bond between alpha and beta carbons 2. hydration of double bond to form hydroxyl on beta carbon 3. oxidation of hydroxyl on beta carbon to form carbonyl 4. Splitting of fatty acid into acyl CoA (fatty acyl CoA) + acetyl CoA with addition of CoA-SH - -- beta carbon sticks with acyl CoA and alpha and carbonyl carbons + S-CoA= acetyl CoA

Question 71

even number fatty acids vs odd number fatty acids

Answer 71

at end: even #= two acetyl CoA odd #= one acetyl CoA + one propionyl CoA proponiyl CoA to methylmalonyl CoA (propionyl CoA carboxylase- biotin) methylmalonyl CoA to succinyl CoA (methylmalonyl CoA mutase- B12) succinyl CoA to citric acid cycle/gluconeogenesis also

Question 72

enoyl CoA isomerase 2,4 dienoyl CoA

Answer 72

B oxidation with unsaturated fatty acid enoyl CoA Isomerase: moves double bond to 2,3 position - mononsaturated 2,4 dienoyl CoA: -converts conjugated double bond to single one so enoyl CoA isomerase can act- polyunsaturated

Question 73

ETC complex 1

Answer 73

NADH to coenzyme Q (ubiquinone)- 4 protons pumped NADH + FMN (flavoprotein coenzyme)= NAD+ + FMNH2 FMNH2 + 2iron sulfur cluster= FMN + 2reduced Fe-S 2Fe-S reduced + CoQ (ubiquinone)= 2Fe-S + CoQH2

Question 74

ETC complex 2

Answer 74

no proton pumping, succinate to coenzyme Q succinate+ FAD (covalently bound to compelx 2)= fumarate+ FADH2 (succinate dehydrogenase- rxn from citric acid cycle is the enzyme that is complex 2) FADH2+ Fe-S cluster= FAD+ +Fe-S reduced Fe-S reduced +CoQ+ 2 H+= Fe-S + CoQH2

Question 75

ETC Complex 3

Answer 75

cytochrome reductase- other name coenzyme Q to cytochrome C--- Q cycle 4 protons pumped cytochromes involved- have Fe+2 reoxidized to Fe+3 happens twice for 2 CoQH2 molecules CoQH2+ 2 cytochrome c (Fe+3)= CoQ + 2 cytochrome c (Fe+2)+ 2H+

Question 76

ETC Complex 4

Answer 76

cytochrome c to oxygen 2 protons pumped cytochrome oxidase- becomes oxidized, oxygen reduced to make water cyanide= inhibitor of cytochrome a and a3 which does this!!!!! 4 cytochrome c (Fe+2) + 4H+ + O2= 4 cytochrome c (Fe+3) + 2H2O

Question 77

ETC proton motive force

Answer 77

established as protons pumped into intermembrane space energy from transferring electrons to things with higher and higher reduction potentials- used to pump protons against gradient

Question 78

NADH shuttle mechanisms purpose

Answer 78

NADH can't cross into matrix. Electrons from NADH must be transferred to a carrier that can cross membrane-- two mechanisms, each differ in amount of ATP per NADH

Question 79

Glycerol 3-phosphate shuttle

Answer 79

1.5 ATP, FADH2 glycerol 3 phosphate dehydrogenase DHAP to glycerol-3P uses NADH to do so ----done in cytosol glycerol 3P to DHAP- another glycerol 3P dehydrogenase on inner mitochondrial membrane that is FAD dependant FAD to FADH2 then FADH2 to ETC complex 2 1.5 ATP

Question 80

Malate aspartate shuttle

Answer 80

cytosolic oxaloacetate reduced to malate malate dehydrogenase--- NADH to NAD+ when malate crosses membrane into matrix, malate dehydrogenase converts malate to oxaloacetate= NAD+ to NADH NADH in matrix, sent electrons to complex 1---- 2.5 ATP oxaloactate- transamination to form aspartate asparate crosses into cytosol----- converted back to oxaloacetate- cytosolic

Question 81

Chemioosmotic coupling vs conformational coupling

Answer 81

chemioosmotic: protons flow through F0 ion channel of ATP synthase into matrix F1 portion of ATP synthase harnesses energy released to do ADP to ATP conformational: - indirect relationship between gradient and synthesis - F1 is like a turbine- harnesses gradient energy, then ADP to ATP done- conformational change

Question 82

Regulation of oxidative phosphorylation

Answer 82

O2 limited- rate decreases, NADH FADH2 concentration increase= inhibit citric acid cycle respiratory control high ADP- allosterically activates isocitrate dehydrogenase---- increase rate of electron transport

Question 83

Postprandial absorptive state

Answer 83

shortly after eating anabolism and fuel storage> catabolism high blood glucose levels- insulin released by Beta cells of pancreatic iselts of Langerhans insulin secretion directly proportional to plasma glucose -------enter B cells, increases ATP levels, leads to exocytosis of insulin Insulin effects: - glucose uptake in liver and skeletal muscle - -----doesn't affect uptake in nervous tissue, RBCs, beta cells of pancreas, intestinal mucosa, kidney tubules - glycogen synthesis in liver and muscle - after glycogen done, excess sugar converted to fatty acids by liver- lipid biosynthesis - VLDL and chylomicron fatty acid deposit via lipoprotein lipase and triacylglycerol synthesis, and supress fatty acid release - adipose tissue - protein synthesis - muscle tissue

Question 84

postabsorptive (fasting) state

Answer 84

fasting state catabolism--- need energy low blood sugar glucagon, cortisol, epinephrine, norepinephrine, growth hormone, low insulin fastest response (immediate) - glycogenolysis in liver to increase blood sugar- glucagon - release of amino acids from skeletal muscle - release of fatty acids from adipose tissue (hormone sensitive lipase in liver)------ boxidation - AA and fats go to liver---- energy for gluconeogenesis (acetyl CoA needed for pyruvate carboxylase, AA for glucogenic!) later responses (12 hours) - gluconeogenesis- liver - glucagon - ------OAA to PEP up (PEPCK) and also F2,6BP decrease so F1,6BP to F6P - excess acetyl CoA- ketone bodies glucagon- liver actions (alpha cells----acts on liver and secreted with low blood sugar ) cortisol-stress--inceased lipolysis and AA degredation and increases blood glucose through gluconeogenesis and enhaces activity of other above catecholamines- promote glycogenolysis (muscle and liver), lipolysis

Question 85

prolonged fasting (starvation)

Answer 85

- high glucagon levels and epinephrine - gluconeogenesis primary source of glucose - high levels of lipolysis + beta oxidatio - ketone bodies from excess acetyl CoA once fatty acids and ketone bodies heavily prevalent in blood, muscles and brain will use brain shift to ketone (2/3 use)---- reduces need for gluconeogenesis-- preserves necessary proteins

Question 86

thyroid hormones

Answer 86

increase basal metabolic rate T4- long lasting, slow acting T3- fast acting, short lived epinephrine needs them, also help increase rate of intestinal glucose absorption cholesterol clearance

Question 87

liver- fuel source + role

Answer 87

preferred fuels: - glucose and excess amino acids (well fed) - fatty acids (fasting) role: - after meal, takes in extra glucose from hepatic portal vein and makes glycogen - excess glucose= fatty acid synthesis, which are converted to triacylglycerol and released into blood as VLDL - gluconeogenesis and glycogenolysis during fasting - forming ketone bodies!

Question 88

adipose tissue- fuel source and role

Answer 88

preffered fuels well fed= glucose fasting= fatty acids/ketones well fed: - takes in glucose and triggers fatty acid release rom VLDL and chylomicrons - ----------lipoprotein lipase induced by insulin - reesterified fatty acids for storage and glycerol 3P from DHAP from glycolysis with glucose helps make triacylglycerols - prevents fatty acid release from tissue fasting - hormone senstivie lipase- releases fatty acids into circulation - epinephrine

Question 89

skeletal resting muscle- fuel source and role

Answer 89

well fed: use glucose + excess AA for energy --build up protein and glycogen fasting: use free fatty acids in blood for energy + ketone bodies

Question 90

skeletal active muscle- fuel source and role

Answer 90

short fast energy- creatinine phosphate short bursts- anaerobic respiation from stored glycogen moderate intensity, continous-- oxidation of glucose and fatty acids ------if glycogen stores deplete, then fatty acids!

Question 91

cardiac muscle- fuel source

Answer 91

well fed state+ fasting: prefer fatty acids as fuel and also ketones if present

Question 92

brain- fuel source

Answer 92

well fed= glucose between meals- glucose from hepatic glycogenolysis or gluconeogenesis prolonged fasting= ketone bodies insulin useless fatty acids can't cross blood brain barrier

Question 93

red blood cells

Answer 93

all states- glucose- anaerobic | insulin useless

Question 94

BMI

Answer 94

>30 is obese mass/height^2 25-30= overweight

Question 95

Ph

Answer 95

protonated

Question 96

Ph>pka

Answer 96

deprotonated