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Review
. 2023 Jun;46(6):1065-1077.
doi: 10.1007/s40618-023-02018-2. Epub 2023 Feb 11.

Parathyroid diseases and metabolic syndrome

R Modica  1 , A Liccardi  2 , R Minotta  2 , E Benevento  2 , G Cannavale  2 , A Colao  2   3
Affiliations
Review

Parathyroid diseases and metabolic syndrome

R Modica et al. J Endocrinol Invest. 2023 Jun.

Abstract

Purpose: Parathyroid diseases are related to parathyroid hormone (PTH) dysregulation by parathyroid cells or alteration of PTH function. They include hyperparathyroidism (PTH excess), hypoparathyroidism (PTH deficiency) and pseudohypoparathyroidism (PTH resistance). Little is known about correlation between parathyroid diseases and metabolic syndrome (MetS).

Methods: An electronic-based search using PubMed was performed until October 2022 and articles were selected based on relevance of title, abstract, English language and publication in peer-reviewed journals.

Results: Possible association between PTH alterations and the diverse manifestation of MetS have been proposed and it could be supposed that MetS may negatively influence parathyroid diseases. Available data show significant association for hyperparathyroidism and pseudohypoparathyroidism.

Conclusions: This review highlights the possible implications between MetS and parathyroid diseases. Given the increasing MetS global prevalence and the higher parathyroid diseases awareness and diagnosis, it may be interesting to further explore the possible role of alterations in parathyroid homeostasis in the development of MetS components with dedicated prospective studies.

Keywords: Hyperparathyroidism; Hypoparathyroidism; Metabolic syndrome; Obesity; Parathyroid disease; Pseudohypoparathyroidism.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
A possible mechanism that correlates hyperparathyroidism and obesity. Hypercalcemia PTH-induced may inhibit the lipolysis leading to an increase in body weight
Fig. 2
Fig. 2
A possible mechanism that correlates PseudoPTH and obesity: Ghrelin (orexigen hormone) and Peptide YY-PYY/glucagon-like peptide 1-GLP-1 (anorexigenic hormones) act at the hypothalamic arcuate nucleus to regulate hunger/satiety signaling. Gsa and cAMP production are necessary to allow this mechanism, so their defects could bring to a satiety and energy expenditure alteration causing adipose tissue accumulation
See this image and copyright information in PMC

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