-
Fatty acids are broke down to
Acetyl CoA
-
The primary source of energy (ATP) under conditions of oxygen limitation in tissues is
Glycolysis
-
The most important allosteric regulator of glycolysis is
Fructose 2, 6-bisphosphate
-
Gluconeogenensis
The "reverse of glycolysis", making glucose
-
What organs are in need of a constant supply of glucose
- Brain
- Testes
- RBC's
- Kidney medulla
- Eye
- Exercising muscles
-
What are the metabolic starting points for Gluconeogenesis
- Lactic acid
- Amino Acids
- Glycerol
- "If you don't have them you LAG"
-
What stimulates gluconeogenesis
- Glucogon
- Epinephrine
- Glucocorticoids
-
What is the main inhibitor of gluconeogenesis
Insulin
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What are the steps of the Gluconeogenesis system
- Lactate and Alanine
- Pyruvate
- Oxaloacetate
- Malate
- Oxaloacetate
- Phosphoenolpyruvate
- Fructose 1,6- Bisphosphate
- Fructose 6-phosphate
- Glucose 6-phosphate
- Glucose
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What steps in gluconeogenesis require ATP
- Pyruvate to Oxaloacetate
- Oxaloacetate to Phosphoenolpyruvate
- Phosphoenolpyruvate to Fructose 1,6-Bisphosphate
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Why is oxaloacetate in the gluconeogenesis process twice
In the mitochondria it has to be converted to malate because it can't exit as oxalacetate
-
When is gluconeogenesis most important
After a prolonged fast
-
Cori cycle
Lactate in the liver is turned into glucose via gluconeogenesis (6ATP used), then transferred to the RBC's and broken down to lactate again via glycolysis (2ATP made)
-
Alanine cycle
- Alanine is converted to glucose in the liver via gluconeogenesis (uses 6ATP) transfered to the muscles where it under goes glycolysis (makes 2 ATP)
- ATP is also used to eliminate NH3
-
When lots of ADP is found what does this indicate
ATP is low
-
Enzymes of beta oxidation in the mitochondria break down
Fatty-acyl-CoA
-
Phosphoenolpyruvate Carboxykinase is regulated by
- Insulin inhibits
- Glucagon activates
- Cortisol activates
-
Pyruvate carboxylase is regulated by
- Acetyl CoA activates
- ADP inhibits
-
Fructose 1,6-bisphosphatase is hormonally regulated by what
- Glucogon activates
- Insulin inhibits
- Epinephrine and NorEpi activate
-
Fructose 1,6-bisphosphatase is allosterically regulated how
- Fructose 2, 6-bisphosphate inhibits
- ATP activates
- Citrate activates
-
Glucose 6-phosphatase is regulated how
- Glucagon stimulates
- Insulin inhibits
- Glucose inhibits
-
Glucose 6-phosphatase has what function in gluconeogenesis
Converts Glucose 6-phosphate to glucose (last step)
-
Fructose 1,6-bisphosphatase has what function in gluconeogenesis
Converts fructose 1,6-bisphosphate to fructose 6-phosphate
-
What is the role of Phosphoenolpyruvate Carboxylation (PEP-carboxykinase) in Gluconeogenesis
- Converts Oxalacetate to phosphoenolpyruvate
- Uses ATP
-
Fat breakdown in adipose tissue stimulates
Gluconeogenesis
-
Fatty Acyl-CoA when acted on by Beta oxidation enzymes makes what, having what eventual effect
Acetyl CoA which drives ATP production for Gluconeogenesis
-
The release of fatty acids into the blood stream is under the control of
Glucagon
-
What are the enzymes of fructose metabolism
- Fructokinase
- Aldolase B
- Triokinase
- Fructose makes you "FAT"
-
Why is high fructose a problem
- Low energy occurs because Fructose 1-phosphate accumulates, due to Aldolase B being slow breaking it down
- Excess lactate and triglycerides accumulate in the blood because fructose bypasses PFK-1 controls in glycolysis
-
Essential Fructosuria
This is a defect in Fructokinase with fructose being secreted in the urine
-
Heredity fructose intolerance (Similar to fructose 1,6-bisphosphatase deficiency)
- Defects in Aldolase B
- Poor feeding
- Failure to thrive
- Hepatic and renal insufficiency
- Death
-
What are the enzymes of galactose metabolism
- Galactokinase
- Galactose 1-phosphate uridyl-transferase
- UDP-galactose 4-epimerase
-
Galactosemia has what symptoms
- Patients can't convert galactose to glucose
- AST and ALT are elevated in newborns
- Mental deficiency and cirrhosis of liver results
- Cataracts
-
What is the treatment for Galactosemia
Reduce dietary galactose
-
What is the major role of the Pentose phosphate pathway
Reduce NADPH and ribose
-
What is the function of the Polyol pathway
Provide Fructose
-
Amino sugar synthesis makes what
- Glycolipids
- Glycoproteins
- GAG's
-
Uronic acid pathway makes
GAG's
-
Glucose 6-phosphate DH is inhibited by
NADPH/NADP+
-
What is one of the only ways to get rid of peroxide
Glutathione reductase
-
Uronic Acid pathway makes what, with what function
Acidic sugar (GAG's) used as a buffer
-
Hexoseamine pathway makes what
Amino sugar
-
What inhibits the break down of Glycogen
- ATP
- Glucose
- Glucose 6-P
- Protein Phosphatase
-
Glycogen phosphorylase has what function and is turned on and off by what
- In its active state it converts Glycogen to Glucose
- It is turned on by Glucagon and off by insulin
-
What is Glycogen Synthase turned on and off by
Turned on by Insulin, off by Glucagon
-
What are the chain of events that follow a meal in relation to Glucogen
- Glucose in ingested
- Insulin rises
- Decrease in Glucagon release
- Increase in Protein phosphatase activity
- Glycogen synthase begins
- Glycogen phosphorylase is shut off
-
What are the chain of events that follow a fasting state in relation to Glycogen
- Decreased blood sugar
- Decrease release of Insulin
- Increase release in Glucagon
- Increase Protein Kinase A activity
- Decrease Glycogen synthase
- Increase Glycogen phosphorylase
- Conversion of Glucogen to Glucose
-
Glycogen phosphorylase is inhibited and activated by
- Inhibited by
- ATP
- Glucose 6-P
- Glucose
Activated by AMP and Ca++
-
Glycogen synthase is activated by
-
Protein Kinase B (PKB) has what effect on the formation of Glycogen
- Inhibits Glycogen Synthase Kinase-3 (which inactivates Glycogen Synthase)
- Therefore promoting Glycogen formation
-
Von Gierkes Disease
- Glucose 6-P or Glucose transport deficiency in ER
- These individuals need food every five min of so
-
McCardles Disease
- Muscle Phosphorylase deficiency
- Painful muscle cramps on exercise
- Myoglobin and CK found in blood
-
Pompes disease
- Lysosomal acid alpha-glucosidase deficiency
- Affects heart and muscles
- Heart failure causes infancy deaths
-
The most severe fasting hypoglycemia is caused by deficiencies in
Glucose 6-Phosphatase (because it is the last step of Glucose synthesis, therefore stopping it would back everything else up)
-
Glucose is required for the synthesis of ribose and
NADPH
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