Effects and Molecular Mechanism of GST-Irisin on Lipolysis and Autocrine Function in 3T3-L1 Adipocytes

Irisin, which was recently identified as a myokine and an adipokine, transforms white adipose tissue to brown adipose tissue and has increasingly caught the attention of the medical and scientific community. However, the signaling pathway of irisin and the molecular mechanisms responsible for the lipolysis effect remain unclear. In this study, we established an efficient system for the expression and purification of GST-irisin in Escherichia coli. The biological activity of GST-irisin was verified using the cell counting kit-8 assay and by detecting the mRNA expression of uncoupling protein 1. Our data showed that GST-irisin regulates mRNA levels of lipolysis-related genes such as adipose triglyceride lipase and hormone-sensitive lipase and proteins such as the fatty acid-binding protein 4, leading to increased secretion of glycerol and decreased lipid accumulation in 3T3-L1 adipocytes. In addition, exogenous GST-irisin can increase its autocrine function in vitro by regulating the expression of fibronectin type III domain-containing protein 5. GST-irisin could regulate glucose uptake in 3T3-L1 adipocytes. Hence, we believe that recombinant GST-irisin could promote lipolysis and its secretion in vitro and can potentially prevent obesity and related metabolic diseases.

Medienart:

E-Artikel

Erscheinungsjahr:

2016

Erschienen:

2016

Enthalten in:

Zur Gesamtaufnahme - volume:11

Enthalten in:

PloS one - 11(2016), 1 vom: 17., Seite e0147480

Sprache:

Englisch

Beteiligte Personen:

Gao, Shanshan [VerfasserIn]
Li, Fangmin [VerfasserIn]
Li, Huimin [VerfasserIn]
Huang, Yibing [VerfasserIn]
Liu, Yu [VerfasserIn]
Chen, Yuxin [VerfasserIn]

Links:

Volltext

Themen:

FNDC5 protein, mouse
Fibronectins
Glucose
IY9XDZ35W2
Journal Article
Recombinant Proteins
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 19.07.2016

Date Revised 13.11.2018

published: Electronic-eCollection

Citation Status MEDLINE

doi:

10.1371/journal.pone.0147480

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM256739811