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174 Cards in this Set
- Front
- Back
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AA with a H side-chain
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Glycine
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Only AA with a Nitrogen ring side-group
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Proline
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Hydrophobic AA
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LIV PTT
leucie, isoleucine, valine phenylalanine, tyrosine, tryptophan |
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AA with Hydroxyl side-chains
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serine, threonine
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AA with Sulfur
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cysteine, methionine
-Ox of 2 cysteine sulfhydryl groups produces cystine |
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AA that are amides
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asparagine, glutamine
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2 parts of a glycolipid
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-glycerol backbone
-esterified fatty acid |
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phosphoglyceride
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glycerol with FA at positions 1 & 2, and a phosphoryl group at postion 3 (phosphocholine)
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3 classes of sphingolipids
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sphingomyelin-contains phosphocholine
cerebrosides-contain sugar residue gangliosides- contain >1 sugar residue |
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precursor of prostaglandins and leukotrienes
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aracidonic acid
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4 functions of proteins in cell membranes
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1 .transport
2. enzymes 3. receptors 4. mediators of signal transduction/2nd messengers |
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2 rings of a nucleotide
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purine and pyrimidine
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nucleoside structure
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nucleotide w/ sugars linked to a nitrogenous base
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nucleotide structure
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nucleoside w/ phosphoryl groups
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nucleotide functions (5)
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1. energy stores (ATP)
2. conenzymes (NAD+) 3. signaling intermediates (cAMP) 4. allosteric modifier of enzymes 5. Genetic information (DNA/RNA) |
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Where is fructose metabolized?
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Liver-
-fed-->pyruvate -fasting-->gluconeogenesis |
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What is the pathway of fructose metabolism
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1. phosphorylated by ATP to F-1-P by frutokinase
2. F-1-P to DHAP & glyceraldehyde by aldolase B 3. glyceraldehyde converted to G-3-P and along with DHAP goes into glycolysis. |
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Deficiency of aldolase B causes
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hereditary fructose intolerance-->fructose cannot be metabolized and can lead to life-threatening buildup in liver
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deficiency of fructokinase causes
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benign fructosuria-fructose accumulates in urine & excreted
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higher affinity for glucose-
hexokinase or glucokinase |
glucokinase
hexokinase Km is ~5% that of glucokinase |
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aldose reductase
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glucose to sorbitol
pathway to produce fructose from glucose |
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how do you generate fructose fro glucose
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glucose-->sorbitol (aldose reductase)-->fructose (sorbitol dehydrogenase)
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metabolism of galactose
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1. galactose-->galactose-1-P (galactokinase)
2.G-1-P+ UDP-glucose=glucose-1-P + UDP-galactose (galactose-1-P uridylytransferase 3. UDP-galactose-->UDP-glucose (epimerase) 4. cycle |
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galactosemia
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deficiency of galactose 1-P uridylyltransferase
hepatomegaly, jaundice, hypoglycemia, convulsions, lethargy |
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glycolysis steps
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glucose-->G-6-P (glucokinase)-burns an ATP
G-6-P-->F-6-P F-6-P-->F-1,6-bisP (PFK-1)-burns an ATP F-1,6-bisP-->DHAP & Glyceraldehyde-3-P DHAP & Glyceraldehyde-3-P-->1,3-bisphosphoglycerate (G-3-P DH)-Creates an NADH+H+ -->generates ATP-->-->PEP PEP-->pyruvate (pyruvate kinase)- generates an ATP nets 2 ATP, 1 NADH |
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PPP- oxidative pathway
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G-6-P-->ribulose-5-P (2 NADPH+CO2)
ribulose-5-P-->xylulose-5-P X-5-P-->ribose-5-P-->nucleotide synth OR X-5-P-->F-6-P (reenter glycolysis) |
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PPP- nonoxidative pathway
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glycolysis-->F-6-P
F-6-P-->ribose-5-P-->nucleotide synth *reversible* |
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glucose-6-P dehydrogenase
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G-6-P--> -->--> ribulose-5-P in PPP
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Uses for NADPH
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FA synth
Glutathione reduction Other |
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transketolase
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Non-ox PPP
requires TPP (thiamine pyrophosphate) |
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glutathione uses
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-prevent oxidative damage by reducing H2O2
-transport of AA across membranes of some cells |
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How is ribose-5-P generated?
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Through the PPP:
If NADPH is high-->non-ox path If NADPH is low-->oxidative path product inhibition |
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What is ribose-5-P used for?
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nucleotide synthesis
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Polyol pathway
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glucose-->sorbitol-->fructose
for sperm fuel reduction (glucose-->sorbitol) NADP oxydation (sorbitol-->fructose) NADH |
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Why might a diabetic develop cataracts
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High blood sugar (esp. fructose, galactose, & sorbitol) increase osmotic pressure in eye, lead to glycosylation of lens proteins
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benign fructosuria
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fructokinase deficiency
-high blood fructose (excreted in urine) -hexokinase can still metabolize at a reduced rate |
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hereditary fructose intolerance
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-aldolase b deficient
-F-1-P buildup-no metabolic fate -Locks up cellular Pi -Inhibits glycogenolysis and gluconeogenesis -AMP metabolized b/c no Pi to regenerate ATP (fatigue) -develop aversion to fructose |
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lactose deficiency
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-reduced lactase activity
-Primary-->activity declines over years -Secondary-->brush border damage -congenital-->rare, no lactase at all |
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classical galactosemia
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Galactose-1-P uridyltransferase deficiency
-serious -hepatomegaly, jaundice, hypoglycemia, convulsions, lethargy, cataracts, sepsis (E.Coli infections) |
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galactokinase deficiency
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-high galactose in blood
-converted to galactictol -can lead to liver & brain damage, cataracts |
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key regulatory steps of glycolysis and regulation mechanism
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1. hexokinase (PI)
2. PFK-1 (AI-->ATP, AA-->AMP, F-2,6-bP) 3. Pyruvate kinase (PEP-->pyruvate, inhibited by phosphorylation |
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key regulatory steps of gluconeogenesis and regulation mechanism
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1. pyruvate-->PEP
PEP carboxykinase (transcrition) 2. F-1,6-bP-->F-6-P F-1,6-bPase (transcriptionally activated by fasting, inhibited by AMP, F-2,6-bP) 3. G-6-P-->glucose G-6-Pase (PI) |
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Steps in glycolysis
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glucose
G-6-P F-6-P F-1,6-P DHAP glyceraldehyde-3-P 1,3-bisphosphoglycerate 3-phosphoglycerate 2-phosphoglycerate phosphoenolpyruvate (PEP) pyruvate |
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Steps in gluconeogenesis
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pyruvate
phosphoenolpyruvate (PEP) 2-phosphoglycerate 3-phosphoglycerate 1,3-bisphosphoglycerate glyceraldehyde-3-P DHAP F-1,6-bP F-6-P G-6-P glucose |
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What cells require glucose as fuel
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brain, RBC
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3 sources of carbon for gluconeogenesis
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anaerobic glycolysis-->lactate (lactate dehydrogenase)
deg. of muscle protein-->AA, mostly alanine (transamination w/ a-ketogluterate<-->glutamate) TG lipolysis-->glycerol |
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Source of energy for gluconeogenesis
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oxidation of beta-FA-->ATP
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where is pyruvate-->PEP
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cytosol
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where does most of gluconeogenesis occur
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mito matrix
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what is the first step of gluconeogenesis
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pyruvate-->OOA (pyruvate carboxylase w/biotin cofactor and ATP-->ADP)
OOA directly converted to PEP |
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what is the second step of gluconeogenesis
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OOA--> either aspartate or malate
OOA cannot cross the mito membrane, must be converted and transported via malate-aspartate shuttle reconverted to OOA in cytosol |
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how does cortisol effect blood glucose levels
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cortisol-->binds SRE
glucagon-->cAMP-->PKA-->phosphorylates CRE -PEP-CK gene activated -PEP-CK protein expressed -gluconeogenesis Cortisol stimulates gluconeogenesis and increases blood glucose |
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How is futile cycling prevented in gluconeogenesis
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In the fasted state:
1. pyruvate kinase is inhibited by PKA 2.PDH inhibited by acetyl CoA (from FA ox) 3. pyruvate carboxylase rx favored (pyruvate-->OOA) b/c of high acetyl CoA (PI) 4. PEP-CK trascription activated by PKA Prevents synthesized PEP from being converted back to pyruvate |
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what pathway is PFK-1 involved it and how is PFK-1 regulated
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Glycolysis:
Activated by AMP & F-2,6-bP Inhibited by ATP & citrate |
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What pathway is F-1,6bPase involved in and how is it inhibited
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Gluconeogenesis:
Inhibited by AMP & F-2,6-bP |
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How do F-2,6-bP and AMP function to regulate gluconeogenesis
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Activate-->glycolysis (PFK-1)
Inhbit-->gluconeogenesis (F-1,6-bPase) |
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F-2,6-bP activates and inhibits which pathways
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Activates glycolysis (PFK-1)
Inhibits gluconeogenesis (F-1,6-bPase) |
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What does pyruvate carboxylase do and how is it activated
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pyruvate-->OOA
activated by acetyl CoA |
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What does PDH (pyruvate dehydrogenase) do and how is it inactivated
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pyruvate-->acetyl CoA
NADH, acetyl CoA, & ATP from FA-->Acetyl CoA rx |
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What does (PK) pyruvate kinase do and how is it inactivated
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Glycolysis:
PEP-->pyruvate + ATP Inhibited by glucagon (via cAMP and PKA, phosphorylates PK to inactivate) Inhibits reformation of pyruvate from new PEP |
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What does PFK-1 do and how is it regulated?
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F-6-P-->F-1,6-bP
Activated by F-2,6-bP, AMP Inhibited by ATP, citrate |
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What does F-1,6-bPase do and how is it regulated?
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F-1,6-bP-->F-6-P
Inhibited by F-2,6-bP |
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What does glucokinase do and does it have a high or low Km for glucose
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glucose<-->G-6-P
High Km -Inactive in low glucose situations (fasting/gluconeogenesis) -Active in high glucose situations (fed/glycolysis) |
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What is the major AA that feeds gluconeogenesis
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Alanine
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What happens to the nitrogen in AA metabolism
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converted to urea and excreted
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where is glycerol derived from and what is it used for
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derived from TG breakdown, used for ketone body synthesis and can-->glycerol-3-P-->DHAP-->glucose via gluconeogenesis
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What role do even-chain FA function in gluconeogenesis
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-no net synth of glucose
-provide ATP for gluconeogenesis |
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What does pyruvate dehydrogenase do?
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Pyruvate-->acetyl CoA
-not reversible -high [acetyl CoA] inhibits, as in FA oxidation during gluconegenesis |
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What role do odd-chain FA function in gluconeogenesis
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3 carbons at omega-end converted to propionate, which enters TCA cycle as succinyl CoA
Succinyl CoA-->malate (intermediate for glucose formation) |
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Where does energy for gluconeogenesis come from
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Beta-ox of even-chain FA
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How much glucose will 1 mol pyruvate make?
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1/2 mol (2 pyruvate/1 glucose)
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How many net phosphate bonds does it require for 1 mol glucose (from pyruvate)
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6 mol phosphate
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How many net phosphate bonds does it require for 1 mol glucose (from glycerol)
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2 mol
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What effect will a high carbo meal have on blood glucagon levels
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glucagon will decrease
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what effect will a high protein meal have on glucagon levels
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glucagon will increase
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What effect will a balanced meal have on glucagon levels
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glucagon will remain relatively constant, insulin will increase
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how does glucose enter the liver
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insulin-dependent GLUT-2 transporters
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excess glucose becomes:
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glycogen & TG in VLDLs
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how does insulin stimulate glycogen synthesis
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insulin stimulates glycogen phosphatase-->dephosphorylates (activates) glycogen synthase
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what is the fate of dietary glucose in:
liver? muscles? adipose tissue? |
liver-->glycogen & TG's
muscles-->glycogen adiopcytes-->glycerol |
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How long does it take for glucose levels to return to fasting levels after a meal
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~2 hours (80-100mg/DL)
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How long after a meal does it take for glucagon levels to begin to rise?
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~2 hours
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How long after a meal does it take for the liver to supply glucose from gluconeogenesis and glycogenolysis?
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~4 hours
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What stimulates cAMP production in the liver
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glucagon
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what effects does glucagon secretion by the liver have on fasting glucose production
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glucagon activates cAMP in the liver, causing 2 effects:
1. activates glycogenolysis (need more energy) 2. inhibits PEP-->pyruvate cycling (futile cycling, forces PEP into glyceraldehyde-3-P & DHAP products for gluconeogenesis) |
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TG's produce what products in lipolysis
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Glycerol-->gluconeogenesis carbon
FA-->ketone bodies &ATP for gluconeogenesis via beta-ox |
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how long does glycogenolysis supply fuel for the body?
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~8-12 hours
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how long does gluconeogenesis supply fuel for the body?
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starts at ~4 hours, increasing role as glycogen is consumed
equal to glycogenolysis at ~16 hours only source after ~30 hours |
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how does metformin work and what is it used for
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management of type 2 diabetes
inhibits hepatic gluconeogenesis |
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what happens in starvation?
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after 5-6 weeks, gluconeogenesis slows, ketone body synthesis increases
b/c gluconeogenesis slows, urea production decreases muscle protein is spared |
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how does muscle tissue maintain glucose levels during exercise
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1. ATP is consumed
2. creatine phosphate, then glycogen oxidation regenerates ATP 3. High AMP levels activate phosphorylase b, Ca2+/calmodulin activates phosphorylase kinase, epinephrine causes cAMP to be produced, all of which stimulate glycogenolysis 4. |
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What molecule is synthesized when calorie consumption exceeds expenditure
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Acetyl CoA is directed to Fatty Acid synthesis (rather than the TCA Cycle)
High NADH from the isocitrate-->alpha-ketogluterate rx inhibits isocitrate dehydrogenase |
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what is the pyruvate/malate cycle?
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mitochondrial pyruvate-->OOA & acetyl CoA-->citrate-->cytosol citrate-->OOA & acetyl CoA
acetyl CoA-->FA synth OOA-->malate +NAD+-->pyruvate+NADPH (malic enzyme) |
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what is the purpose of the pyruvate/malate cycle
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1. transports acetyl CoA from mitochondria to cytosol
2. produces NADPH for FA synthesis |
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malonyl CoA regulates what
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FA oxidation. It is an allosteric inhibitor of carnitine palmitoyl transferase-1
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what is the rate-limiting step in FA synthesis
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Acetyl CoA-->malonyl CoA (acetyl CoA carboxylase)
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What is the rx sequence of beta-oxidation of FA's
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1. Oxidation
2. Hydration 3. Oxidation 4. Bond Cleavage |
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What is the rx sequence of FA synthesis and what enzyme performs each step
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1. Oxidation
2. Reduciton 3. Dehydration 4. Reduction Fatty acid synthase |
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What cofactor is incorporated in FA Synthase
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phosphopantetheinyl
-reactions of FA synth take place bonded to it -when 4 steps are complete, the 2-carbon complex is transferred to the growing chain at a cysteine residue |
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how long does FA Synthase make the FA chain
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16 carbons long
palimitate |
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3 uses for FA's
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1. energy storage
2. signaling 3. cell membrane constituents |
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Can FA chains exceed 16 carbons? How?
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palimitate is transferred to a CoA (plamitoyl CoA)
-elongation can continue in the ER by the same process as by FA Synthase |
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What are the two most important dietary FA's? Why?
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Linoleic and linolenic.
Aracadonic acid (and thus, eicosinoid) producion |
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Can humans produce omega-3 and omega-6 fatty acids?
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No. Primary source is fish oil. Essential for eicosinoid synthesis
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How many carbons long does a FA need to be to make an unsaturation.
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At least 9
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What are the 4 main types of FA's
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1. Triacylglycerols (storage)
2. Glycerophospholipids 3. Phospholipids 4. Sphingolipids 2-4-->structure and signaling |
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What are the precursors for TG synthesis
|
Glycerol-3-P and palmitoyl CoA
Diacylglycerol is an intermediate, important for signaling |
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What is the function of LPL?
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Facilitates transfer of TG's from VLDL's to adipocytes.
*TG's must be broken down into FA+glycerol to leave the VLDL and enter the adipocyte |
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4 Functions of glycerophospholipids
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1. Cell membranes
2. Lung surfactant 3. Bile 4. Lipoproteins |
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What is the prefix of many glycerophospholipids?
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phosphatidyl...
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What enzyme modifies phosphatidylinositol?
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Can be phosphorylated to form phosphatidylinositol phosphate (PIP...or PIP2, or PIP3)
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What is the basic structure of a glycerophospholipid?
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Glycerol backbone, 2 FA chains,
a phosphate (position 3) attached to a head group (variable) |
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What are ether glycerolipids (plasmalogens)?
|
Glycerol backbone
Pos. 1-->ether Pos. 2-->FA Pos. 3-->Phosphate-Headgroup |
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What are plasmalogens used for?
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Myelin sheath of neurons (ethanolamine)
Platelet activating factor (choline head group) |
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What is a sphingolipid?
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Ceramide backbone (serine & palimtoyl CoA).
Serine can be phosphorylated posttranslationally to act as a switch for the protein Very important for signaling |
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Sphingomyelin purpose?
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Sphingolipid in the myelin sheath.
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What two major peptide hormones are secreted from adipocytes?
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Adiponectin and leptin
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What cell does adiponectin come from?
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Adipose tissue
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What tissue does leptin come from?
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Adipose tissue
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What does adiponectin do?
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1. Senses rise in TG levels (like the TG insulin)
2. Insulin sensitizer 3. Decreases FA synth and Increases FA oxidation 4. As size of adipocyte increases, adiponectin secretion decreases |
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What does leptin do?
|
Satiety hormone.
Released in response to high TG levels. |
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What is the mechanism of leptin activation?
|
1. Leptin binds to receptor, dimerizes
2.JAK protein phosphorylates receptor to create a docking site 3. STAT protein attracted to docking site, docks and is phosphorylated 4 STAT enters nucleus to trigger transcription of anorexigenic factors |
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pH in a lysosome?
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4.5-5, maintained by ATP-driven proton pumps
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how are lysosomal proteins directed to the lysosome?
|
mannose-6-phosphate tag
|
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How can fetal lung function be assessed?
|
Ratio of phosphatidylcholine to sphingomyelin
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Phospholipid backbone?
|
Glycerol
Phosphatidyl... |
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Cerebrosides and gangliosides use what for a backbone/
|
Serine
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Cerebrosides are made of?
|
Ceramide base plus a glucose or galactose
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What are globosides?
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Cerebroside (ceramide+glucose or galactose) with two or more sugars
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What is a ganglioside?
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A cerebroside/globoside with oligosaccarides, plus NANA
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Defects in enzymes that cause glycolipid breakdown are called?
|
Lysosomal storage diseases.
|
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Examples of lysosomal storage diseases?
|
1. Niemann-Pick
2. Fabry 3. Krabbe 4. Gaucher 5. Tay-Sachs 6. Meatchromatic leukodystrophy |
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What causes Tay-Sachs?
|
Lysosomal storage disease
Inability to break down gangliosides Enzyme hexosamidinase A (1 alpha/2 beta chains) alpha-chain defective. In Standoff's, beta-chain is defective and both hexosamidinase a & b affected (beta-chain defective) |
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What causes Gaucher's?
|
inability to metabolize cerebrosides
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What causes Fabry disease?
|
inability to metabolize glucose-galactose-galactose globosides
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What are proteoglycans?
|
Highly glycosylated proteins
-long, unbranched disaccaride chains -extracellular -"shock absorbers" -bottle brush -negative charge, readily absorb water |
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Where might you find proteoglycans?
|
-synovial fluid
-cartilage -vitreous humor of eye |
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What is the difference between type A, B, and O blood?
|
A & B have a single sugar difference in a carbohydrate chain on the cell surface.
O is missing both of these sugars |
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What causes jaundice?
|
heme breakdown produces biliverdin, reduced to bilirubin, which is glycosylated by 2 glucuronates to make it more soluble for excretion. Exceeding the system's capacity results in bilirubin buildup.
|
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What are 4 types of jaundice?
|
1. Neonatal--glucuornate conjugating system is immature
2. Hemolytic--excessive RBC destruction 3. Hepatocellular--low-functioning liver, as in alcoholics 4. Obstructive--bile drainage blocked (stones, tumor, etc.) |
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How many ATP are netted per NADH, FADH2, and total for the ETC?
|
NADH-->10 ATP/NADH*3=30
FADH2-->6 ATP/FADH2*1=6 36 total ATP, plus 2 from glycolysis=38 |
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|
What happens if you don't get enough O2?
|
ETC slows, causes fatigue.
|
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|
What is the major vitamin in the cofactor FADH2?
|
Riboflavin
|
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What molecules provide the electrons used to produce ATP in the ETC?
|
NADH & FADH2
|
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|
Where is the pH higher, in the IMS or the mito matrix?
|
Matrix
|
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Where is the pH lower, in the IMS or in the mito matrix?
|
IMS (Intermembrane space)
|
|
|
How do protons cross the inner mito membrane
|
1. Through ATP synthase
2. Proton leakage 3. Uncoupling agents |
|
|
What are some ETC uncoupling molecules and where do they act?
|
1. Rotenone-->complex I/coenzyme Q
2.Antimycin A-->cytochrome C (complex III) 3. CN-, CO-->complex IV O2 delivery/reduction |
|
|
How many protons are pumped for each NADH each complex in the ETC?
|
I-->4
II-->0 III-->2 IV-->4 10 total 12 H+ fill 3 rx spots (3 ATP)=4 H+/ATP=2.5 ATP/NADH |
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How many protons are pumped for each FADH2 in each complex of the ETC?
|
I-->0
II-->0 III-->2 IV-->4 6 total 4 H+/ATP= 1.5 ATP/FADH2 |
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What chemical inhibits ATP Synthase?
|
Oligomycin (binds to stalk)
|
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|
How does an iron deficiency effect the ETC?
|
Most of the ETC enzyme complexes have FeS centers on them.
|
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What matrix ETC enzyme is also a part of the TCA cycle?
|
Succinate dehydrogenase (succinate-->fumerate)
The rx contributes FADH2 to the ETC |
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Which ETC complex doesn't pump any e- into the IMS?
|
Complex II
|
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Which part of the ETC can generate free radicals?
|
Quinone in Coenzyme Q
|
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What is unique about quinone?
|
Can accept either one or two e-, possibly generating free radicals.
|
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What happens to the ETC if there is no ADP in the matrix?
|
It slows. The cell has enough energy.
-[H+] rises in the IMS -NAD+ + H+ is inhibited, so [NADH] rises -(-) on TCA cycle, shunts products to other, biosynthetic pathways |
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What byproduct is produced when e- are passed through the ETC?
|
Heat
|
|
|
What does thermogenin do?
|
Uncouples ATP synthesis to generate heat in infants.
|
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|
What is dinitrophenol and what does it do?
|
ATP synthase uncoupler. Generates heat, sold as a weightloss drug in the 1930's.
Dangerous b/c it can cause hyperthermia |
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What is the role of xyulose-5-P?
|
Signals to the liver that there is energy to process.
|
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What does PFK-2Pase do and how is it regulated?
|
Converts F-6-P to F-2,6-bP.
Activated by PP2A-(protein phosphatase 2A) (increases F-2,6bP) Inhibited by PKA phosphorylation (glucagon).(decreases F-2,6-bP) |
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How is X-5-P a key regulator of energy regulation in the body?
|
X-5-P activates PP2A which:
1. Activates PFK-2Pase which increases [F-2,6-P] and thus, glycolysis. 2. Activates ChREBP in the nucleus to activate transcription, activating the following: A. LPK (liver pyruvate kinase) B. 5 different areas of TG synthesis |
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|
What is a major function of the PPP in RBC's?
|
PPP produces NADPH (energy) to maintain a reduced form of glutathione (protection from H2O2)
|
|
|
What is the rate-limiting step of the TCA cycle?
|
malate<--> OOA
|
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How do pancreatic beta-cells detect glucose (for insulin release)?
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Increasing [NADPH] from the TCA cycle.
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What are NEFA's?
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Non-esterified fatty acids. Free-floating FA's in the blood.
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What is a leading theory behind insulin resistance?
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NEFA's are absorbed by beta-cells and metabolized to create NADPH in the cytosol (beta-ox).
TCA is reversed in cytosol, from citrate to malate Malate-->pyruvate+NADPH (malic enzyme) Also, isocitrate-->a-ketogluterate+NADPH Artificially increases [NADPH], so when glucose is introduced, cell doesn't detect a significant increase in [NADPH] and doesn't secrete insulin |
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What behavior would rats exhibit if leptin transcription was knocked out?
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Hyperphagia...never full.
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What adipokine is responsible for clearing FA's?
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Adiponectin
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How are adiponectin levels influenced by obesity?
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Secretion decreases, leading to decreased clearance of FA's.
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How does obesity affect GLUT4 expression
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GLUT4 expression is decreased.
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What effect do high plasma SRBP levels have on the body?
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SRBP's impair muscle insulin response and activate liver gluconeogenesis.
This is the last thing you want, b/c you are already hyperglycemic! |
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What can cause SRBP levels to increase?
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Obesity.
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