Glucose and Fat Metabolism in Acromegaly: From Mice Models to Patient Care

Jakob Dal1, Edward O List, Jens Otto L Jørgensen

  • 1Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark.

Neuroendocrinology
|May 1, 2015
PubMed

Insights

Active acromegaly causes insulin resistance and type 2 diabetes risk, often with a lean phenotype. Treatment reverses these metabolic changes, highlighting growth hormone

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Diabetes Pathophysiology

Background:

  • Active acromegaly is linked to insulin resistance, glucose intolerance, and increased type 2 diabetes risk.
  • Acromegaly patients often exhibit a lean phenotype with enhanced free fatty acid mobilization and oxidation.
  • Surgical removal of growth hormone (GH)-producing adenomas can reverse these metabolic disturbances.

Purpose of the Study:

  • To investigate the metabolic actions of growth hormone (GH) in acromegaly.
  • To compare metabolic characteristics and GH-induced insulin resistance mechanisms between humans and mouse models.
  • To evaluate the impact of different acromegaly treatment modalities on insulin sensitivity and glucose tolerance.

Main Methods:

  • Analysis of clinical data from patients with active acromegaly.
  • Utilizing mouse models of acromegaly to study metabolic phenotypes.
  • Comparison of metabolic effects across various treatment strategies, including surgery, somatostatin analogs, and GH antagonists.

Main Results:

  • Acromegaly is associated with insulin resistance, glucose intolerance, and a lean phenotype.
  • Mouse models mimic key metabolic features of human acromegaly but show species-specific differences in substrate oxidation and GH action.
  • Treatment outcomes vary: GH antagonists restore insulin sensitivity, while somatostatin analogs can suppress insulin secretion.

Conclusions:

  • Growth hormone significantly impacts glucose and fat metabolism, contributing to insulin resistance in acromegaly.
  • Understanding species-specific mechanisms is crucial for translating findings from animal models to clinical practice.
  • Tailoring acromegaly treatments based on their distinct effects on insulin sensitivity and secretion is essential for managing metabolic complications.

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