Metabolism

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Carbomoyl phosphate synthase
Hormone sensitive lipase
Adipose triglyceride lipase
CPT1
Fatty acid oxidase
Acetyl coA carboxylase
HMG CoA synthase
CPT- 2
Glycogen synthase
Protein kinase A (PKA)
Phosphorylase kinase
Glycogen phosphorylase
Glucokinase regulatory protein (GKRP)
Phosphofructokinase 1
PFK-2
AMP kinase
Alcohol dehygrogenase
Glucose 6 phosphatase
Fructose 1 6 phosphatase
Pyruvate carboxylase
Malate dehydrogenase
Phosphoenolpyruvate carboxykinase
Lactate dehydrogenase enzyme
Pyruvate dehydrogenase complex
ETC complex I
ETC complex II
ETC complex III
ETC complex IV
ATP synthase
HIF1 ( hypoxia- inducible factor 1)

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Control step for the entry of the urea cycle. Coverts ammonia and CO2
This enzyme converts oxaloacetate to phosphoenolpyruvate in order to continue gluconeogenesis.
Converts NADH to UQ- does pump protos
The alpha subunit is normally degraded in norrmoxia but stabilises in hypoxia. This enzyme downregulates mitochondrial biogeesis and proliferation via the PGC-1 transcription factor and encourages autophagy of existing mitochondria. Up regulates glycolysis genes.
The enzyme that is vital for fatty acid breakdown. Converts fatty acid to acetyl CoA and reduced cofactors.
Creates ATP using the energy form the release of H+ down an electrochemical gradient from the space between the mitochondrial membranes.
The enzyme that phosphorylates and activates glycogen phosphorylase.
This enzyme converts oxaloacetate to malate so that it can exit the mitochondrial membrane. This is the key enzyme in the malate shuttle.
Reverses the reaction that is catalysed by Glucokinase. Converts glucose -6-p to glucose
Prominent phosphorylation enzyme, responds to cAMP and as such is prominent in glucagons metabolic control.
The enzyme that controls the location of hepatic glucokinase. Releases GK i response to high sugar conc.
Converts FADH to UQ - does not pump protons
Converts triacyglycerides to diacylglycerdes.
This enzyme is present in the heart tissue and is activated by AMPK. It produces fructose-26- P2. Which allosterically activatess PK1
This enzyme is vital for the synthesis of fatty acids. it converts citrate derived acetyl CoA into malonyl coA
Unidirectional 3 stage enzyme that converts pyruvate to acetyl CoA. Active when not phosphorylated. Requires Vit B1 as a cofactor.
Cytochrome C to O2 - does pump protons
Responsible for the breakdown of glycogen within cells. Activated by phosphorlyation cascade.
Converts pyruvate to lactate in the muscle and the reverse in the liver.
Heterotrimer that can sense energy levels using its gamma subunit. Increase GLUT presence in the cell membrane in order to increase glucose uptake. This enzyme will also deactivate ACC in order to maximize the Beta oxidation in the cell.
Converts the carnitine phosphate back into fatty acyl CoA once it is back in the mitochondria.
This enzyme breaks down ethanol into Acetylaldehyde. This creates lots of NADH and ends up producing high levels of acetyl CoA
Control stage for the synthesis of glycogen.
The first enzyme involved in gluconeogensis. Converts pyruvate to oxaloacetate.
The enzyme that converts fructose-6-p to fructose-1,6-P2 The rate limiting step in glycolysis.
Converts fructose-1,6- P2 to F1P. Reverses the reaction of PFK
Coverts UQ to cytochrome C - does pump protons
The control step for ketone body synthesis, creates HMG CoA from acetyl coA and acetoacetyl CoA
Control step for triglyceride breakdown. Converts TAG to glycerol and 3 FA's
This enzyme is vital to the carnitine shuttle that allows the movement of fatty acids across the mitochondrial membrane. Converts acylated fatty acids to carnatine phosphate and pass them over the membrane

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McArdle's - Type V
Von Gierke's disease- Type I
Her's disease- type VI
Galactosemia Type I
Fructose intolerance
Pyruvate dehydrogenase deficiency
Phenylketoneuria
Maple syrup urine
MCAD
Familial hypercholesterolaemia

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Fructose aldolase deficiency. Fructose 1 phosphate build up in the liver and kidneys. Inhibits glycogenolysis and gluconeogensis. Can lead to renal and hepatic failure.
Deficiency in branched chain alpha ketoacid dehydrogenase. Can't breakdown branched amino acids so they build up and are excreted in the urine. Carefully controlled amounts.
Rare. Results in a lactate build up.
Due to deficiency in galactose-1- phosphate uridyl transferase. Inability to digest galactose. Results in high blood levels and hypoglycemia and acidosis develop in affected infants. The main component of breast milk is galactose. If untreated the infant well get cataracts and mental retardation.Treatment is a galactose free diet.
Deficiency in glycogen phosphorylase, liver specific. prevents access to the stored hepatic glycogen. Fasting Hypoglycemia and enlarged liver.
Medium chain acyl CoA dehydrogenase deficiency. Ketoacidosis, low blood sugar and presence of fats. regular food is the treatment.
Reduced LDL receptors in the liver. Less removal of LDL from circulation. High blood cholesterol, tendon xanthomas and premature coronary heart disease. Diet modification, statins and bile acid binding resins.
The lack of muscle glycogen phosphorylase prevents the breakdown of glycogen. This leads to rapid muscle fatigue during exersize followed by a second wind when gluconeogensis has time to act.
Impaired conversion of phenylalanine into tyrosine. This leads to a build up of it and it's derivatives in the blood. Ths is due to a lack of phenylalanine hydroxylase or more rarely a problem with teh recycling of the cofactor dihydrobiopterin - dihydrobiopterin reductase. develops at 3-6 months of age. Developmental delay, hypersensitivity and exczema and mental retardation. Phenylalanine restricted diet and tyrosine supplements.
This condition is a deficiency in glucose-6-phosphatase which is needed for gluconeogenesis. Prevents availability of hepatic glycogen and the synthesis from glucogenic amino acids and lactate. Hypoglycemia in fasting, enlarged liver and lactic acidosis.

Metabolism

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Match the enzymes to their function

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Carbomoyl phosphate synthase

Hormone sensitive lipase

Adipose triglyceride lipase

CPT1

Fatty acid oxidase

Acetyl coA carboxylase

HMG CoA synthase

CPT- 2

Glycogen synthase

Protein kinase A (PKA)

Phosphorylase kinase

Glycogen phosphorylase

Glucokinase regulatory protein (GKRP)

Phosphofructokinase 1

PFK-2

AMP kinase

Alcohol dehygrogenase

Glucose 6 phosphatase

Fructose 1 6 phosphatase

Pyruvate carboxylase

Malate dehydrogenase

Phosphoenolpyruvate carboxykinase

Lactate dehydrogenase enzyme

Pyruvate dehydrogenase complex

ETC complex I

ETC complex II

ETC complex III

ETC complex IV

ATP synthase

HIF1 ( hypoxia- inducible factor 1)

Control step for the entry of the urea cycle. Coverts ammonia and CO2

This enzyme converts oxaloacetate to phosphoenolpyruvate in order to continue gluconeogenesis.

Converts NADH to UQ- does pump protos

The alpha subunit is normally degraded in norrmoxia but stabilises in hypoxia. This enzyme downregulates mitochondrial biogeesis and proliferation via the PGC-1 transcription factor and encourages autophagy of existing mitochondria. Up regulates glycolysis genes.

The enzyme that is vital for fatty acid breakdown. Converts fatty acid to acetyl CoA and reduced cofactors.

Creates ATP using the energy form the release of H+ down an electrochemical gradient from the space between the mitochondrial membranes.

The enzyme that phosphorylates and activates glycogen phosphorylase.

This enzyme converts oxaloacetate to malate so that it can exit the mitochondrial membrane. This is the key enzyme in the malate shuttle.

Reverses the reaction that is catalysed by Glucokinase. Converts glucose -6-p to glucose

Prominent phosphorylation enzyme, responds to cAMP and as such is prominent in glucagons metabolic control.

The enzyme that controls the location of hepatic glucokinase. Releases GK i response to high sugar conc.

Converts FADH to UQ - does not pump protons

Converts triacyglycerides to diacylglycerdes.

This enzyme is present in the heart tissue and is activated by AMPK. It produces fructose-26- P2. Which allosterically activatess PK1

This enzyme is vital for the synthesis of fatty acids. it converts citrate derived acetyl CoA into malonyl coA

Unidirectional 3 stage enzyme that converts pyruvate to acetyl CoA. Active when not phosphorylated. Requires Vit B1 as a cofactor.

Cytochrome C to O2 - does pump protons

Responsible for the breakdown of glycogen within cells. Activated by phosphorlyation cascade.

Converts pyruvate to lactate in the muscle and the reverse in the liver.

Heterotrimer that can sense energy levels using its gamma subunit. Increase GLUT presence in the cell membrane in order to increase glucose uptake. This enzyme will also deactivate ACC in order to maximize the Beta oxidation in the cell.

Converts the carnitine phosphate back into fatty acyl CoA once it is back in the mitochondria.

This enzyme breaks down ethanol into Acetylaldehyde. This creates lots of NADH and ends up producing high levels of acetyl CoA

Control stage for the synthesis of glycogen.

The first enzyme involved in gluconeogensis. Converts pyruvate to oxaloacetate.

The enzyme that converts fructose-6-p to fructose-1,6-P2 The rate limiting step in glycolysis.

Converts fructose-1,6- P2 to F1P. Reverses the reaction of PFK

Coverts UQ to cytochrome C - does pump protons

The control step for ketone body synthesis, creates HMG CoA from acetyl coA and acetoacetyl CoA

Control step for triglyceride breakdown. Converts TAG to glycerol and 3 FA's

This enzyme is vital to the carnitine shuttle that allows the movement of fatty acids across the mitochondrial membrane. Converts acylated fatty acids to carnatine phosphate and pass them over the membrane

Match the genetic condition to it's description

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McArdle's - Type V

Von Gierke's disease- Type I

Her's disease- type VI

Galactosemia Type I

Fructose intolerance

Pyruvate dehydrogenase deficiency

Phenylketoneuria

Maple syrup urine

MCAD

Familial hypercholesterolaemia

Fructose aldolase deficiency. Fructose 1 phosphate build up in the liver and kidneys. Inhibits glycogenolysis and gluconeogensis. Can lead to renal and hepatic failure.