Endocrine Disorders and Growth Hormone Regulation

Summary

The endocrine system orchestrates physiological growth, metabolism and tissue repair through hormone secretion by specialised glands. Growth hormone (GH), produced by the anterior pituitary, acts both directly and via insulin-like growth factor 1 (IGF-1) to regulate somatic growth, carbohydrate and lipid metabolism, bone density and organ function. Dysregulation of GH signalling underlies a spectrum of disorders: GH deficiency causes impaired growth and metabolic disturbances, whereas GH excess—most often due to pituitary somatotroph adenomas—leads to acromegaly, characterised by disfiguring tissue overgrowth, cardiovascular complications and reduced life expectancy if untreated. Management strategies encompass surgical resection of pituitary tumours, medical therapy with somatostatin analogues or GH receptor antagonists, and radiotherapy when necessary. Advances in molecular endocrinology have refined our understanding of GH receptor activation, downstream JAK-STAT and Src kinase pathways, and negative feedback regulators, opening avenues for targeted diagnostics and personalised treatments. Effective control of GH and IGF-1 levels not only ameliorates clinical symptoms but also reduces comorbidity and improves long-term quality of life. Ongoing research seeks to integrate novel imaging and data-driven tools for early diagnosis and optimise therapeutic sequencing to achieve biochemical remission and minimise adverse effects.

Research from Nature Portfolio

Recent structural and pharmacological analysis of somatostatin receptor 2 (SSTR2) has elucidated how first-generation peptide analogues such as octreotide and newer small-molecule agents achieve subtype selectivity and signal bias. High-resolution cryo-electron microscopy of drug–receptor–Gi complexes reveals distinct ligand recognition motifs and conformational states, offering a blueprint for the design of next-generation therapeutics with improved efficacy in neuroendocrine tumours and acromegaly.

An international consensus statement has redefined therapeutic outcome measures for acromegaly, integrating advances in receptor ligand pharmacology, growth hormone receptor antagonists and dopamine agonists. By establishing unified biochemical, clinical and imaging endpoints, this guidance streamlines treatment algorithms and sets benchmarks for remission, tumour control and patient-centred quality-of-life outcomes.

Endocrine Disorders and Growth Hormone Regulation publication trend

The graph below shows the total number of articles in endocrine disorders and growth hormone regulation across all publications each year (not limited to Nature Index journals).

Technical terms

Growth hormone (GH): A peptide hormone secreted by the anterior pituitary that stimulates growth and metabolism.

Insulin-like growth factor 1 (IGF-1): A peripheral mediator of GH action, produced mainly by the liver, which promotes cell proliferation and survival.

Somatostatin analogue: A synthetic molecule that mimics somatostatin to inhibit GH secretion via somatostatin receptors.

Somatotroph adenoma: A benign pituitary tumour that secretes excess GH, leading to acromegaly.

JAK-STAT pathway: A principal intracellular signalling cascade activated by GH receptor engagement to regulate gene expression.

References

  1. Current and Future Advances in Surgical Therapy for Pituitary Adenoma. Endocrine Reviews (2023).
  2. Prospect of acromegaly therapy: molecular mechanism of clinical drugs octreotide and paltusotine. Nature Communications (2023).
  3. A Consensus Statement on acromegaly therapeutic outcomes. Nature Reviews Endocrinology (2018).
  4. A Pituitary Society update to acromegaly management guidelines. Pituitary (2020).
  5. The Growth Hormone Receptor: Mechanism of Receptor Activation, Cell Signaling, and Physiological Aspects. Frontiers in Endocrinology (2018).
  6. Preoperative prediction of cavernous sinus invasion by pituitary adenomas using a radiomics method based on magnetic resonance images. European Radiology (2018).

About these summaries

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