Gluconeogenesis

What is a normal physiological circulating range of blood glucose in a non-diabetic?

What is average fasting blood glucose concentration in a non-diabetic?

Below which circulating blood glucose is there a risk of coma/death?

Glucose can cross the blood-brain barrier.

Glucose yields a low amount of ATP per mole compared to fatty acids.

We cannot synthesise glucose from fatty acids.

Gluconeogenesis is the synthesis of glucose from non-carbohydrate sources in the liver. Which of the following are substrates of gluconeogenesis?

Gluconeogenesis involves the bypass of three irreversible reactions of which reaction in glucose metabolism?

How do we bypass the three irreversible reactions to complete reverse glycolysis?

Which of the following are the irreversible reactions of glycolysis that we bypass in gluconeogenesis?

Which enzyme do we need to form oxaloacetate from pyruvate in the first reaction of gluconeogenesis?

Which enzyme do we need to dephosphorylation fructose 1,6-bisphosphate to fructose 6-phosphate in the 6th reaction of gluconeogenesis?

How do we form phosphoenol pyruvate from oxaloacetate in the 2nd reaction of gluconeogenesis?

What enzyme do we need to dephosphorylate glucose 6-phosphate to glucose in the final reaction of gluconeogenesis?

ATP is required to convert pyruvate to oxaloacetate.

What is hydrolysed when oxaloacetate is converted to phosphoenolpyruvate by phosphoenol pyruvate carboxykinase?

Carbon dioxide is released when oxaloacetate is converted to phosphoenoyl pyruvate by phosphoenol pyruvate carboxykinase.

Phosphate is released when both fructose 1,6-bisphopshate and glucose 6-phosphate are dephosphorylated.

Fill in the blanks below to describe the reactions of gluconeogenesis. 1. [blank_start]Pyruvate[blank_end] is converted to [blank_start]oxaloacetate[blank_end] by [blank_start]pyruvate decarboxylase[blank_end]. This requires [blank_start]ATP[blank_end] hydrolysis. 2. [blank_start]Oxaloacetate[blank_end] is converted to [blank_start]phosphoenol pyruvate[blank_end] by [blank_start]phosphoenol pyruvate carboxykinase[blank_end]. This requires [blank_start]GTP[blank_end] hydrolysis and releases [blank_start]CO2[blank_end]. 3. [blank_start]Phosphoenol pyruvate[blank_end] is hydrated to [blank_start]3-phosphoglycerate[blank_end] by [blank_start]enolase[blank_end]. 4. [blank_start]3-phosphoglycerate[blank_end] is phosphorylatied to [blank_start]1,3-bisphospholgycerate[blank_end] by [blank_start]phosphoglycerate kinase[blank_end]. This requires [blank_start]ATP[blank_end] hydrolysis. 5. [blank_start]1,3-bisphosphoglycerate[blank_end] is converted to [blank_start]fructose 1,6-bisphosphate[blank_end]. This causes the production of [blank_start]NAD+[blank_end] from [blank_start]NADH[blank_end]. 6. [blank_start]Fructose 1,6-bisphosphate[blank_end] is dephosphorylated by [blank_start]fructose 1,6-bisphosphatase[blank_end] to form [blank_start]fructose 6-phosphate[blank_end]. This releases an [blank_start]inorganic phosphate[blank_end]. 7. F[blank_start]ructose 6-phosphate[blank_end] is isomerised to [blank_start]glucose 6-phosphate[blank_end] by [blank_start]phosphoglucose isomerase[blank_end]. 8. [blank_start]Glucose 6-phosphate[blank_end] is dephosphorylated to [blank_start]glucose[blank_end] by [blank_start]glucose 6-phosphatase[blank_end]. THis releases [blank_start]inorganic phosphate[blank_end].

Where do we receive glycerol for gluconeogensis from?

Where do we receive glucogenic amino acids for gluconeogenesis?

Which enzymes does glucagon activate?

What molecule activates pyruvate carboxylase?

How does insulin affect the liver?

What is true of GLUT2 transporters on the liver?

How does insulin affect the adipose tissue?

How does insulin affect skeletal muscle?

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