The intriguing connections of leptin to hyperparathyroidism

Endocrine. 2017 Sep;57(3):376-387. doi: 10.1007/s12020-017-1374-6. Epub 2017 Jul 20.

Abstract

Purpose: Leptin has been implicated in bone metabolism, but the association with parathyroid gland function has not been fully clarified. This review aimed to summarize evidence of the association between leptin and hyperparathyroidism, both primary and secondary, elucidating the potential pathophysiologic and therapeutic consequences between leptin and parathyroid hormone, hopefully prompting the design of new studies.

Results: Experimental studies indicate a positive loop between leptin and parathyroid hormone in primary hyperparathyroidism. Dissimilar, parathyroid hormone seems to inhibit leptin expression in severe secondary hyperparathyroidism. Data from clinical studies indicate higher leptin levels in patients with primary hyperparathyroidism than controls, but no association between parathyroid hormone and leptin levels, as well as a minimal or neutral effect of parathyroidectomy on leptin levels in patients with primary hyperparathyroidism. Clinical data on secondary hyperparathyroidism, mainly derived from patients with chronic kidney disease, indicate a potential inverse association between leptin and parathyroid hormone in some, but not all studies. This relationship may be affected by the diversity of morbidity among these patients.

Conclusions: Data from experimental studies suggest a different association between leptin and parathyroid hormone in primary and secondary hyperparathyroidism. Data from clinical studies are conflicting and potentially affected by confounders. More focused, well-designed studies are warranted to elucidate a potential association between leptin and parathyroid hormone, which may have specific clinical implications, i.e., targeting obesity and hyperleptinemia in patients with hyperparathyroidism.

Keywords: Leptin; Obesity; Parathyroid glands; Parathyroid hormone; Primary hyperparathyroidism; Secondary hyperparathyroidism.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Adipose Tissue, White / drug effects
  • Adipose Tissue, White / metabolism
  • Animals
  • Anti-Obesity Agents / therapeutic use
  • Chief Cells, Gastric / drug effects
  • Chief Cells, Gastric / metabolism
  • Hormone Replacement Therapy
  • Humans
  • Hyperparathyroidism, Primary / complications
  • Hyperparathyroidism, Primary / drug therapy
  • Hyperparathyroidism, Primary / metabolism*
  • Hyperparathyroidism, Primary / physiopathology
  • Hyperparathyroidism, Secondary / complications
  • Hyperparathyroidism, Secondary / drug therapy
  • Hyperparathyroidism, Secondary / metabolism*
  • Hyperparathyroidism, Secondary / physiopathology
  • Insulin Resistance
  • Leptin / blood*
  • Leptin / genetics
  • Leptin / metabolism
  • Leptin / therapeutic use
  • Models, Biological*
  • Obesity / blood
  • Obesity / complications
  • Obesity / drug therapy
  • Obesity / metabolism
  • Parathyroid Glands / drug effects
  • Parathyroid Glands / physiopathology
  • Parathyroid Hormone / blood*
  • Parathyroid Hormone / genetics
  • Parathyroid Hormone / metabolism
  • Parathyroid Hormone / therapeutic use
  • Recombinant Proteins / therapeutic use
  • Reproducibility of Results
  • Severity of Illness Index

Substances

  • Anti-Obesity Agents
  • Leptin
  • PTH protein, human
  • Parathyroid Hormone
  • Recombinant Proteins