Stress induced hyperglycemia is mediated through which hormone:
Now, the correct answer is probably glucagon because it's a key hormone in increasing blood glucose. Glucagon stimulates glycogenolysis and gluconeogenesis in the liver. But wait, cortisol from the adrenal cortex also plays a role by promoting gluconeogenesis and reducing glucose uptake. Epinephrine, from the adrenal medulla, increases glycogenolysis in the liver and muscles. Growth hormone can also contribute by reducing glucose uptake in peripheral tissues. So which one is the primary mediator here?
The question is about the hormone that mediates stress-induced hyperglycemia. The options might include glucagon, cortisol, epinephrine, and growth hormone. The correct answer is glucagon because it's the primary hormone that directly stimulates the liver to release glucose through glycogenolysis. Cortisol has a slower effect over days, while epinephrine acts more acutely but mainly during acute stress. Growth hormone has a more indirect role.
Wait, but in some contexts, cortisol is considered a major player in stress hyperglycemia, especially in chronic stress. However, the question is about the mediator. Glucagon is more immediate. Let me confirm: during stress, the body releases glucagon to break down glycogen stores, which is a quick response. Cortisol increases gluconeogenesis, which is a longer process. So the primary mediator in stress-induced hyperglycemia is glucagon. Therefore, the correct answer should be glucagon. The other options are incorrect because cortisol acts more slowly, epinephrine is part of the acute response but not the main mediator, and growth hormone has a minor role.
**Core Concept**
Stress-induced hyperglycemia results from counter-regulatory hormones that increase hepatic glucose production. **Glucagon** is the primary mediator, stimulating glycogenolysis and gluconeogenesis in the liver during acute stress.
**Why the Correct Answer is Right**
**Glucagon** (correct answer) activates hepatic glycogenolysis and gluconeogenesis via cAMP-dependent pathways. During stress, glucagon release from the pancreas opposes insulin, ensuring glucose availability for energy-demanding tissues like the brain and muscles. This is critical in conditions like trauma, sepsis, or surgery.
**Why Each Wrong Option is Incorrect**
**Option A: Cortisol** β Cortisol promotes gluconeogenesis but acts over hours/days, not acutely. It is a secondary contributor to stress hyperglycemia.
**Option B: Epinephrine** β Epinephrine increases glycogenolysis in the liver and muscles but is a transient response to acute stress (e.g., "fight-or-flight"), not the primary driver.
**Option C: Growth Hormone** β Growth hormone has mild anti-insulin effects but is not a major mediator of immediate hyperglycemia.
**Clinical Pearl / High-Yield Fact**
Remember the **"glucagon-first"**