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Visfatin is released from 3T3-L1 adipocytes via a non-classical pathway
Masaki Tanaka1, Maiko Nozaki, Atsunori Fukuhara
1Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka, Japan.
Biochemical and Biophysical Research Communications
|June 5, 2007
Summary
Visfatin, a protein linked to obesity, is released from adipocytes through a novel pathway. This mechanism bypasses the typical endoplasmic reticulum-Golgi secretion route and microvesicles.
Area of Science:
- Biochemistry
- Cell Biology
- Metabolic Research
Background:
- Visfatin is a secretory protein with insulin-mimetic and pro-inflammatory effects.
- Elevated plasma visfatin and adipose tissue mRNA are observed in obesity.
- The mechanism of visfatin release from adipocytes is not well understood.
Purpose of the Study:
- To investigate the mechanism of visfatin release from adipocytes.
- To determine the subcellular localization and secretion pathway of visfatin.
Main Methods:
- 3T3-L1 adipocytes were cultured and treated with Brefeldin A and Monensin.
- Subcellular fractionation was performed to isolate cellular components.
- Visfatin release into the culture medium was quantified.
Main Results:
- Visfatin was abundantly released into the culture medium from 3T3-L1 adipocytes.
- Subcellular fractionation revealed visfatin localization in the cytosol.
- Inhibitors of ER-Golgi-dependent secretion did not affect visfatin release.
- Visfatin was not released via microvesicles.
Conclusions:
- Visfatin release from adipocytes occurs independently of the classical ER-Golgi pathway.
- The findings suggest a novel, non-conventional secretion mechanism for visfatin.
- Further research is needed to elucidate the precise pathway of visfatin secretion.
