What hormone indirectly affects glucose blood levels, causing hyperglycemia and increasing insulin resistance in tissues?

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Cortisol is the Hormone that Indirectly Affects Glucose Blood Level, Causing Hyperglycemia and Increasing Insulin Resistance

The correct answer is A. Cortisol (Cortisone) is the hormone that indirectly affects glucose blood levels, causing hyperglycemia and increasing insulin resistance in tissues.

Mechanism of Cortisol Action on Glucose Metabolism

  • Cortisol acts directly on the liver to stimulate endogenous glucose production through gluconeogenesis, contributing to elevated blood glucose levels 1
  • During stress, cortisol release leads to peripheral insulin resistance and increased hepatic glucose production, creating a state of "stress hyperglycemia" 2, 1
  • Cortisol specifically increases hepatic glycogen supply and stimulates neoglucogenesis in the liver, with a direct impact on blood glucose levels 1

Cortisol's Role in Insulin Resistance

  • Cortisol antagonizes insulin action in peripheral tissues, primarily in muscle and adipose tissue, leading to decreased glucose uptake and utilization 3
  • Higher serum cortisol levels are significantly associated with decreased insulin secretion, further contributing to hyperglycemia 4
  • Cortisol-induced insulin resistance occurs even when serum insulin levels are high, demonstrating its potent anti-insulin effect 5

Pathophysiological Effects of Cortisol on Glucose Homeostasis

  • Excess cortisol exposure (as in Cushing's syndrome) causes hyperglycemia and insulin resistance that can lead to diabetes 2
  • Cortisol works synergistically with other hormones (epinephrine, glucagon) to produce a greater than additive hyperglycemic response 6
  • Prolonged cortisol elevation leads to persistent insulin resistance and hyperglycemia, affecting patient outcomes 1

Comparison with Other Options

  • Thyroxine (Option B): While thyroid hormones can affect glucose metabolism, they do not primarily cause insulin resistance in tissues 2
  • Glucagon (Option C): Glucagon primarily increases blood glucose through glycogenolysis and gluconeogenesis but doesn't significantly increase insulin resistance 2
  • Growth hormone (Option D): Growth hormone can antagonize insulin action, but its effect on insulin resistance is less pronounced than cortisol 2, 7

Clinical Implications

  • Medications containing cortisol or synthetic glucocorticoids (like prednisone) commonly cause hyperglycemia as a side effect 8
  • Excess glucocorticoids can precipitate diabetes in individuals with preexisting insulin resistance 2
  • Understanding cortisol's effect on glucose metabolism is crucial for managing stress-induced hyperglycemia in clinical settings 1

Common Pitfalls in Understanding Hormone Effects on Glucose

  • Normal blood glucose values don't always indicate normal metabolism, as counter-regulatory hormones like cortisol can be actively working to maintain euglycemia despite underlying metabolic disturbances 2
  • The same euglycemic state can disguise very different counter-regulatory hormonal activities and significantly different biochemical states of cellular metabolism 2
  • Prolonged hyperglycemia itself can induce insulin resistance, creating a vicious cycle that further worsens glucose control 2

References

Guideline

Cortisol's Role in Gluconeogenesis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Regulation of Glucose Homeostasis by Glucocorticoids.

Advances in experimental medicine and biology, 2015

Research

Effect of dexamethasone and cortisone on insulin receptors in normal human male.

The Journal of clinical endocrinology and metabolism, 1980

Guideline

Metabolic Syndrome in Older Adults

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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