In stress hyperglycemia, how does gluconeogenesis contribute to hyperglycemia?

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Multiple Choice

In stress hyperglycemia, how does gluconeogenesis contribute to hyperglycemia?

Explanation:
Under stress, counterregulatory hormones rise and signal the liver to produce more glucose. Gluconeogenesis increases hepatic glucose output by converting substrates like lactate, alanine, and glycerol into glucose. Hormones such as cortisol, glucagon, and epinephrine boost the activity and expression of gluconeogenic enzymes (for example, PEPCK and glucose-6-phosphatase) through signaling pathways that raise cAMP and drive transcription. This provides a steady stream of new glucose to the bloodstream, contributing to stress-related hyperglycemia. While glycogenolysis also increases and insulin levels may be reduced or insufficient, the key factor driving the rise in glucose is the upregulated gluconeogenesis.

Under stress, counterregulatory hormones rise and signal the liver to produce more glucose. Gluconeogenesis increases hepatic glucose output by converting substrates like lactate, alanine, and glycerol into glucose. Hormones such as cortisol, glucagon, and epinephrine boost the activity and expression of gluconeogenic enzymes (for example, PEPCK and glucose-6-phosphatase) through signaling pathways that raise cAMP and drive transcription. This provides a steady stream of new glucose to the bloodstream, contributing to stress-related hyperglycemia. While glycogenolysis also increases and insulin levels may be reduced or insufficient, the key factor driving the rise in glucose is the upregulated gluconeogenesis.

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