Metabolism

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Match the enzymes to their function

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Padankan teks itu
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
Converts fructose-1,6- P2 to F1P. Reverses the reaction of PFK
Converts the carnitine phosphate back into fatty acyl CoA once it is back in the mitochondria.
Converts pyruvate to lactate in the muscle and the reverse in the liver.
The enzyme that controls the location of hepatic glucokinase. Releases GK i response to high sugar conc.
Converts triacyglycerides to diacylglycerdes.
This enzyme is vital for the synthesis of fatty acids. it converts citrate derived acetyl CoA into malonyl coA
Responsible for the breakdown of glycogen within cells. Activated by phosphorlyation cascade.
Unidirectional 3 stage enzyme that converts pyruvate to acetyl CoA. Active when not phosphorylated. Requires Vit B1 as a cofactor.
The enzyme that converts fructose-6-p to fructose-1,6-P2 The rate limiting step in glycolysis.
This enzyme converts oxaloacetate to malate so that it can exit the mitochondrial membrane. This is the key enzyme in the malate shuttle.
This enzyme converts oxaloacetate to phosphoenolpyruvate in order to continue gluconeogenesis.
The enzyme that is vital for fatty acid breakdown. Converts fatty acid to acetyl CoA and reduced cofactors.
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
Prominent phosphorylation enzyme, responds to cAMP and as such is prominent in glucagons metabolic control.
The first enzyme involved in gluconeogensis. Converts pyruvate to oxaloacetate.
Creates ATP using the energy form the release of H+ down an electrochemical gradient from the space between the mitochondrial membranes.
Control stage for the synthesis of glycogen.
The enzyme that phosphorylates and activates glycogen phosphorylase.
Coverts UQ to cytochrome C - does pump protons
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.
Reverses the reaction that is catalysed by Glucokinase. Converts glucose -6-p to glucose
Cytochrome C to O2 - does pump protons
This enzyme is present in the heart tissue and is activated by AMPK. It produces fructose-26- P2. Which allosterically activatess PK1
Converts FADH to UQ - does not pump protons
The control step for ketone body synthesis, creates HMG CoA from acetyl coA and acetoacetyl CoA
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.
This enzyme breaks down ethanol into Acetylaldehyde. This creates lots of NADH and ends up producing high levels of acetyl CoA

Padankan teks itu
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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Deficiency in glycogen phosphorylase, liver specific. prevents access to the stored hepatic glycogen. Fasting Hypoglycemia and enlarged liver.
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.
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.
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.
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.
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.
Fructose aldolase deficiency. Fructose 1 phosphate build up in the liver and kidneys. Inhibits glycogenolysis and gluconeogensis. Can lead to renal and hepatic failure.
Medium chain acyl CoA dehydrogenase deficiency. Ketoacidosis, low blood sugar and presence of fats. regular food is the treatment.
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.
Rare. Results in a lactate build up.

Metabolism

Soalan 1 of 1

Waktu Kiri

Match the enzymes to their function

Padankan teks (klik dan seret)

(0/0)

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

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

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

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

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

Converts triacyglycerides to diacylglycerdes.

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

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

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

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

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

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

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

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

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

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

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

Control stage for the synthesis of glycogen.

The enzyme that phosphorylates and activates glycogen phosphorylase.

Coverts UQ to cytochrome C - does pump protons

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.

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

Cytochrome C to O2 - does pump protons

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

Converts FADH to UQ - does not pump protons

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

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.

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

Match the genetic condition to it's description

Padankan teks (klik dan seret)

(0/0)

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

Deficiency in glycogen phosphorylase, liver specific. prevents access to the stored hepatic glycogen. Fasting Hypoglycemia and enlarged liver.