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J Am Coll Surg. 2014 Jun;218(6):1239-1250.e4. doi: 10.1016/j.jamcollsurg.2013.11.013. Epub 2013 Nov 27.

Leptin signaling and hyperparathyroidism: clinical and genetic associations.

Author information

1
Section of Plastic and Reconstructive Surgery, Department of Surgery, Yale University School of Medicine, New Haven, CT.
2
Section of Endocrine Surgery, Department of Surgery, Duke University School of Medicine, Durham, NC.
3
Yale Center of Analytical Science, Yale University School of Public Health, New Haven, CT.
4
Department of Chronic Disease Epidemiology, Yale University School of Public Health, New Haven, CT.
5
Mind and Brain Theme, South Australian Health and Medical Research Institute and Department of Psychiatry, School of Medicine, Flinders University, Adelaide, South Australia.
6
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT.
7
Section of Plastic and Reconstructive Surgery, Department of Surgery, Yale University School of Medicine, New Haven, CT. Electronic address: deepak.narayan@yale.edu.

Abstract

BACKGROUND:

The role of leptin in mediating calcium-related metabolic processes is not well understood.

STUDY DESIGN:

We enrolled patients with hyperparathyroidism undergoing parathyroidectomy in a prospective study to assess postoperative changes to serum leptin and parathyroid hormone levels and to determine the presence of LEPR (leptin receptor) polymorphisms. Patients undergoing hemithyroidectomy under identical surgical conditions were enrolled as controls. Wilcoxon signed-rank test was used to analyze changes in leptin. Pearson correlations and Bland-Altman methods were used to examine the between-subject and within-subject correlations in changes in leptin and parathyroid hormone levels. Five single-nucleotide polymorphisms in the LEPR gene were genotyped, and linear regression analysis was performed for each polymorphism.

RESULTS:

Among the 71 patients included in the clinical study, after-surgery leptin levels decreased significantly in the parathyroid adenoma (p < 0.001) and parathyroid hyperplasia subgroups (p = 0.002) and increased in the control group (p = 0.007). On multivariate analysis, parathyroid disease subtype, baseline leptin levels, age, body mass index, and calcium at diagnosis was associated with changes in leptin. Among the 132 patients included in the genotyping analysis, under a recessive model of inheritance, single-nucleotide polymorphism rs1137101 had a significant association with the largest parathyroid gland and total mass of parathyroid tissue removed (p = 0.045 and p = 0.040, respectively). When analyzing obese patients only, rs1137100 and rs1137101 were significantly associated with total parathyroid size (p = 0.0343 and p = 0.0259, respectively).

CONCLUSIONS:

Our results suggest a role for the parathyroid gland in regulating leptin production. Genetic contributions from the leptin pathway might predispose to hyperparathyroidism.

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