What effect does high insulin and low glucagon have on PFK-1?

What effect does high insulin and low glucagon have on PFK-1?

• A. Activation through ATP
• B. Inhibition via citrate
• C. Activation through Fructose 2,6-bisphosphate
• D. Stimulation via glucose

Answer: (C)

High insulin and low glucagon levels lead to a metabolic state characterized by increased glycolysis and fatty acid synthesis. One key regulatory enzyme in glycolysis is phosphofructokinase-1 (PFK-1), which is crucial for controlling the flow of glucose into the glycolytic pathway. In the context of elevated insulin, there is an increase in the concentration of fructose 2,6-bisphosphate, a potent allosteric activator of PFK-1. Insulin stimulates the enzyme phosphofructokinase-2 (PFK-2), which converts fructose 6-phosphate into fructose 2,6-bisphosphate. This increase in fructose 2,6-bisphosphate enhances PFK-1 activity, leading to an accelerated conversion of fructose 6-phosphate to fructose 1,6-bisphosphate. This mechanism effectively promotes glycolysis when energy needs are high, such as after carbohydrate-rich meals. Consequently, insulin's role in stimulating this specific pathway explains why high levels of insulin in conjunction with low levels of glucagon favor the activation of PFK-1 through fructose 2,6-bisphosphate.

High insulin and low glucagon levels lead to a metabolic state characterized by increased glycolysis and fatty acid synthesis. One key regulatory enzyme in glycolysis is phosphofructokinase-1 (PFK-1), which is crucial for controlling the flow of glucose into the glycolytic pathway.

In the context of elevated insulin, there is an increase in the concentration of fructose 2,6-bisphosphate, a potent allosteric activator of PFK-1. Insulin stimulates the enzyme phosphofructokinase-2 (PFK-2), which converts fructose 6-phosphate into fructose 2,6-bisphosphate. This increase in fructose 2,6-bisphosphate enhances PFK-1 activity, leading to an accelerated conversion of fructose 6-phosphate to fructose 1,6-bisphosphate.

This mechanism effectively promotes glycolysis when energy needs are high, such as after carbohydrate-rich meals. Consequently, insulin's role in stimulating this specific pathway explains why high levels of insulin in conjunction with low levels of glucagon favor the activation of PFK-1 through fructose 2,6-bisphosphate.