Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
|
where does beta oxidation take place? what cofactors are required?
|
takes place in mito, uses NAD+ --> NADH, FAD --> FADH2
|
|
|
where does fatty acid synthesis occur? what cofactors are required?
|
in the cytosol, uses NADPH --> NADP
|
|
|
northern blot
|
mRNA levels
|
|
|
nuclear run-on
|
gene-activation of enzyme (transcription)
|
|
|
cyclohexamide
|
protein synthesis inhibitor
|
|
|
pulse-chase experiment
|
half-life of enzyme
|
|
|
Action of Insulin + mechanism
|
-promote uptake of blood glucose
-via RTK insulin receptor -promotes phosphorylation of many enzymes for glycolysis -ultimately works through PHOSPHATASES |
|
|
Delta G of ATP hydrolysis? of 1,3 BPG? phosphoenolpyruvate?
|
7-8 Kcal/mol for ATP, 12-14Kcal/mol for 1,3BPG, PEP
|
|
|
What is the basic reaction of glycolysis? How do different factors affect the reaction?
|
glucose --> 2CH3COCOOH + 2NADH + 2ATP
activated by insulin (high blood glucose) suppressed by glucagon, epi (low blood glucose, stress) |
|
|
What can fatty acids form?
|
Fatty Acids are precursors for cholesterol, steroid hormones, amino acids, ribose
|
|
|
Where are glucagon and epi receptors?
|
glucagon receptors only on fat and liver cells
epi receptors on ALL tissues |
|
|
What are the general intracellular effects of Insulin, glucagon, epinephrine?
|
Insulin promotes the dephosphorylation (activate/inactivate) of Rate Limiting Enzymes
Glucagon promotes the phosphorylation (inactivate/activate) Rate Limiting Enzymes Epinephrine like Glucagon for the most part |
|
|
metabolic consequences of diabetes
|
1. impaired glucose metabolism
2. fat metabolism increased: much of the fat oxidized to ketone bodies --> ketoacidosis 3. glycosylation 4. glucose reduced by aldol reductase --> sorbitol, increasingosmotic pressure (i.e. in the lens) |
|
|
action of GC
|
promotes gluconeogenesis, glycogenolysis, TG breakdown --> FFA's,
|
|
|
action of Insulin
|
promotes glycolysis, glucose uptake (in muscle, adipose), FA synthesis, glycogen formation, protein synthesis, increasing critical enzyme activity/synthesis of these enzymes
|
|
|
mechanism of Insulin Receptor pathway
|
1. Insulin binds α-subunit, causing autophosphorylation.
2. β-subunit phosphorylates IRS 1 and 2 (Insulin Receptor Substrate) 3. IRS1,2 phosphorylates PI3K 4. PI3K activates AKT 5. pAKT activates phosphatases (like protein phosphatase 2A), PKC, mTOR, which carry out the effects |
|
|
mechanism of Glucagon (Epi) Receptor pathway
|
1. GC binds in liver, adipose whereas epi binds everywhere to serpentine GPCRs, activating via GDP->GTP switch
2. the βγ receptor subunits activate Adenylate Cyclase (AC), increasing cAMP levels 3. cAMP activates PKA via subunit dissociation 4. PKA phosphorylates substrates, causing effects until cAMP lowered by phosphodiesterase |
|
|
How does Glucose get into various cells?
|
1) Passive carriers in Liver, Brain, RBC, Pancreas, and most cells via GLUT1 and GLUT3 - Low Km
2) Liver and Pancreas also hae GLUT2 - high Km > [serum blood glucose] 3) Muscle and Fat contain GLUT4 - insulin releases golgi-sequestered GLUT4 receptors 4) GLUT 5 actively transports glucose in GI tract and kidney |
|
|
Purposes of glycolysis
|
1. Energy (2 ATP, 2NADH, 2 pyruvate)
2. α-GP for TG, phospholip. synthesis 3. 2,3-BPG in RBC for Hb O2 binding 4. Acetyl CoA from pyruvate --> fats, ketone bodies, steroids, amino acids |
|
|
Hexokinase reaction properties
|
Glucose + ATP --> G6P
Needs initial energy input Low Km Inhibited by G6P, ADP |
|
|
Glucokinase
|
Glucose + ATP --> G6P
High Km Not inhibited by G6P, ADP |
|
|
phosphoglucoisomerase (PGI)
|
G6P -> F6P
|
|
|
phosphofructokinase (PFK)
|
F6P + ATP --> F-1,6-BP + ADP
Rate limiting step in glycolysis Inhibited by ATP, citrate Stimulated by ADP, Pi, NH4, and its product F-1,6-BP Thus, 2 substrate BS, 2 allosteric inhib. sites, 4 allost. activ. sites Also regulated by Insulin, Glucagon via PBFK (phospho2,6bisfructokinase: F-6-P --> F-2,6-BP) and FBPP (phosphofructophosphatase: PFP --> F-6-P + Pi) |
|
|
F2,6 bis phosphokinase
|
F6P + ATP -->ADP + F2, 6 bis P
F2, 6 bis P is a powerful activator of PFK enzyme active when dephosphorylated activated by insulin pathway inactivated by GC/Epi pathway |
|
|
F2, 6 bis phosphofructophosphatase
|
F2, 6 bis P --> F6P + Pi
enzyme active when phosphorylated |
|
|
Aldolase products and fates
|
F-1,6-BP --> DHAP + G3P + 2 ADP
DHAP can be reduced to α-GP for TG and phospholip. synthesis DHAP can be converted to G3P by triose phosphate isomerase. |
|
|
G3PDH
|
G3P + NAD + Pi -> 1,3BPG + NADH
1,3BPG produces ATP in the next rxn heavy metals such as lead, mercury, cadmium are toxic because they inhibit glycolysis at this step b/c interfere with reactive Thiol Groups |
|
|
phosphoglycerokinase reaction, products, and fates
|
1,3bis PGA + ADP -->3 PGA + ATP
RBCs have a mutase to make 1,3BPG into 2,3 BPG to regulate Hb O2 interaction 3PGA can make serine! Arsenic competes for G3P and decomposes to heat |
|
|
phosphoglyceromutase
|
3 PGA --> 2 PGA
|
|
|
Enolase
|
dehydrates 2PGA to make PEP
|
|
|
Pyruvic kinase
|
PEP + ADP --> pyruvate + ATP
Strongly regulated Inhibited by ATP, NADH, acetyl CoA Stimulated by F-1,6-BP regulated by glucagon via cAMP-PKA (inactivated via phosphorylation) regulated by isulin via phosphatase dephosphorylating/activating PK Requires high [K+] Pyruvate can form alanine |
|
|
Irreversible steps of glycolysis
|
hexokinase, PFK, PK reactions
these are bypassed in gluconeogenesis |
|
|
Fructose metabolism
|
fructose --> F6P via hexokinase
in the liver: fructokinase, aldolase, triosephosphate kinase fructose --> F1P via fructokinase F1P --> DHAP + Glyceraldehyde via aldolase Glyceraldehyde --> G3P via triosephosphokinase |
|
|
Galactose metabolism
|
galactokinase, gal.1p-uridyl transferase, phosphoglucomutase
galactose --> gal-1-P via galactokinase gal-1-p --> G-1-P via galactose 1-P uridyl transferase G-1-P --> G-6-P via phosphoglucomutase |
