Resistin is co-secreted with adiponectin in white mouse adipocytes.

Biochem Biophys Res Commun

Department of Physiology/Metabolic Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Medicinaregatan 11, SE-405 30, Göteborg, Sweden. Electronic address:

Published: January 2021

AI Article Synopsis

  • The study examines how resistin, an adipose hormone linked to metabolic diseases, is regulated in mouse fat cells.
  • Resistin is secreted from white adipocytes in rodents but produced by different cell types in humans.
  • The research finds that increased cAMP and calcium levels stimulate resistin release, which is significantly reduced in fat cells from obese and diabetic mice, suggesting a connection with adiponectin in their secretion process.

Article Abstract

In the current work we have investigated the cellular and molecular regulation of resistin secretion in cultured and primary mouse adipocytes. Resistin is an adipose tissue hormone proposed to contribute to metabolic disease. In rodents, resistin is secreted from white adipocytes whereas it is in humans synthesised and released from other cell types within white adipose tissue. The metabolic importance of resistin has been studied in both mouse and man, but the regulation of its release remains poorly investigated. Here we define that, in mouse adipocytes, resistin secretion is triggered by an intracellular elevation of cAMP and/or Ca. Resistin release is stimulated via activation of beta 3 adrenergic receptors (βARs) and the downstream signalling protein exchange protein activated by cAMP (Epac). The secretion of resistin is markedly abrogated in adipocytes isolated from obese and diabetic mice. Immunocytochemical staining demonstrates a significant overlap between signals for resistin and the adipocyte hormone adiponectin. Our data propose that resistin and adiponectin are contained within the same vesicles in mouse adipocytes and that the two hormones are co-secreted in response to the same exocytosis-triggering signals.

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Source
http://dx.doi.org/10.1016/j.bbrc.2020.11.013DOI Listing

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