Parathyroid hormone receptor stimulation induces human adipocyte lipolysis and browning

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Peter Breining
  • Steen B. Pedersen
  • Mads Kjolby
  • Hansen, Jacob B.
  • Niels Jessen
  • Bjørn Richelsen

Objective: Activation of brown adipose tissue is a promising strategy to t reat and prevent obesity and obesity-related disorders. Activation of uncoupling protein 1 (UCP1) leads to u ncoupled respiration and dissipation of stored energy as heat. Induction of UCP1-rich adipocytes in white adipose tis sue, a process known as 'browning', serves as an alternative strategy to increase whole body uncoupling capacity . Here, we aim to assess the association between parathyroid hormone (PTH) receptor expression and UCP1 expression in human adipose tissues and to study PTH effects on human white and brown adipocyte lipolysis and UCP1 expression. Design: A descriptive study of human neck adipose tissue biopsies subst antiated by an interventional study on human neck-derived adipose tissue cell models. Methods: Thermogenic markers and PTH receptor gene expression are assessed in human neck adipose tissue biopsies and are related to individual health records. PTH-init iated lipolysis and thermogenic gene induction are assessed in cultured human white and brown adipocyte cell model s. PTH receptor involvement is investigated by PTH receptor silencing. Results: PTH receptor gene expression correlates with UCP1 gene expression in the deep-neck adipose tissue in humans. In cell models, PTH receptor stimulation increases lipo lysis and stimulates gene transcription of multiple thermogenic markers. Silencing of the PTH receptor attenuates t he effects of PTH indicating a direct PTH effect via this receptor. Conclusion: PTH 1 receptor stimulation by PTH may play a role in human adip ose tissue metabolism by affecting lipolysis and thermogenic capacity.

OriginalsprogEngelsk
TidsskriftEuropean Journal of Endocrinology
Vol/bind184
Udgave nummer5
Sider (fra-til)687-697
Antal sider11
ISSN0804-4643
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
This work was supported by The Novo Nordisk Foundation and The Department of Clinical Medicine, Aarhus University.

Publisher Copyright:
© 2021 European Society of Endocrinology.

ID: 272018532