Carb Met Flashcards
GLUT 1
Ubiquitous but high expression in RBCs and brain
High affinity
GLUT 2
Main transporter in liver
Low affinity
GLUT 3
Main transporter in neurons
- High affinity
GLUT 4
Present in skeletal muscle, heart, adipose tissue
- Insulin dependent
3 Phases of Glycolysis
Investment, Splitting,, Recoup/Payoff
Step 1 of Glycolysis
Glucose to Glucose6Ph
Reg Step
Hexokinase vs Glucokinase
Hexokinase: found in all cells, high affinity for glucose, inhibited by Gluc 6 Phosphate
Glucokinase: found in hepatocytes and pancreatic B cells, low affinity for glucose and affinity increases based on “fed” state, not that negatively impacted by Gluc 6 Phosphate
Rate Limiting Step of Glycolysis
F6P to F1,6BP
via PFK1
Regulation of PFK1
+: AMP, Insulin, F2,6BP
-: Citrate, Glucagon, ATP
PFK2/FBPase Regulation
PFK2 is active in dephosph form (impacted by insulin signaling)
FBPase is active in phosph form (impacted by Glucagon signaling = phosphorylation cascade)
Which enzyme cleaves F1,6BP
Aldolase A
What reaction in Glycolysis produces 2NADH
G3P to 1,3BPG
which also is a phosphorylation but not with ATP hydrolysis
it is done by glyceraldehyde 3P dehydrogenase (GAPDH)
Which reactions do substrate level phosphorylation in Glycolysis
1,3BPG to 3PG
via phosphoglycerate kinase
PEP to Pyruvate via Pyruvate
Kinase
Which enzyme creates pyruvate
PEP to Pyruvate via Pyruvate Kinase
Tauri Disease
Def in PFK 1
Exercise-induced muscle cramps and weakness bc lactate buildup
Hemolytic anemia
High bilirubin and jaundice
Symptoms can be mild; true incidence may be higher due to lack of recognition and diagnosis
Regulation of Pyruvate Kinase
Activated by F1,6BP and insulin
Inhibited by ATP, alanine, and glucagon
High insulin: stimulates protein phosphatase, dephosphorylation of PK, activated form
High glucagon: cAMP activates PKA, phosphorylation of PK, inhibited form
Which glycolysis product is a hub for other carb metabolisms?
Gluc 6 Phos
What is a common etiology associated with ineffective glycolysis?
hemolytic anemias
mainly PK problems
Type 1 Diabetes
severe insulin deficiency due to loss of pancreatic β cells (likely due to immune destruction).
Type 2 Diabetes
insulin resistance that progresses to loss of β cell function
clinical markers of hemolytic anemia
elevated lactate dehydrogenase, unconjugated bilirubin
Fanconi-Bickel syndrome
Autosomal recessive disorder.
Caused by mutation in GLUT 2 transporter (located in liver, pancreatic β cell, enterocytes and renal tubular cells).
Unable to take up glucose, fructose and galactose
where does gluconeogenesis occur
liver kidney small intestine
what does gluconeogenesis convert
pyruvate into glucose
precursors for gluconeogenesis
lactate, amino acids, glycerol
is gluconeogenesis a reversal of glycolysis?
NO
it just bypasses the energy barriers of the 3 glycolysis reactions
pyruvate carboxylase
converts pyruvate to oxaloacetate in gluconeogenesis CO2 and ATP dependent activated by acetyl CoA and cortisol Biotin cofactor MITOCHONDRIAL ENZYME
phosphoenolpyruvate carboxykinase
OAA to PEP in gluconeogenesis
release of CO2 and GDP produced
Fructose 1,6 Bisphosphatase
counterpart for PFK1 in gluconeogenesis
when glucagon stimulates cell, it phosphorylates the enzyme complex and activates the phosphatase and inactivates the PFK1 = no F26BP made
Glucose 6 Phosphatase
gluconeogenesis counterpart of glucokinase and hexokinase
Positive Regulators of Glycolysis
Insulin AMP Glucose F2,6BP F1,6BP
Negative Regulators of Glycolysis
Glucagon, ATP, Citrate, Gluc 6 Ph, Fruc 6 Ph, alanine
Positive Regulators of Gluconeogensis
Glucagon, citrate, cortisol, thyroxine, acetyl CoA
Negative Regulators of Gluconeogenesis
ADP, AMP, Fru 2-6BP
how does pyruvate come out of the mitochondria in gluconeogenesis
pyruvate converted to OAA
OAA is not permeable through Mit Mem
OAA is reduced into malate via mito malate dehydrog
malate is transported to cyto via malate shuttle
malate reoxidized to OAA = NADH made in the process
via cytosolic malate dehydrog
PEPCK
Concurrent decarboxylation and phosphorylation of oxaloacetate to PEP (GTP used)
Transcription activated by cortisol, glucagon, thyroxine
in Gluconeogenesis