Conventional kinesin KIF5B mediates adiponectin secretion in 3T3-L1 adipocytes.
Insulin stimulates adiponectin secretion and glucose transporter type 4 (GLUT4) translocation in adipocyte to regulate metabolism homeostasis. Similar to GLUT4 translocation, intracellular trafficking and release of adiponectin in adipocytes relies on the trans-Golgi network and endosomal system. Recent studies show that the heavy chain of conventional kinesin (KIF5B) mediates GLUT4 translocation in murine 3T3-L1 adipocytes, however, the motor machinery involved in mediating intracellular trafficking and release of adiponectin is unknown. Here, we examined the role of KIF5B in the regulation of adiponectin secretion. The KIF5B level was up-regulated during 3T3-L1 adipogenesis. This increase in cytosolic KIF5B was synchronized with the induction of adiponectin. Endogenous KIF5B and adiponectin were partially colocalized at the peri-nuclear and cytosolic regions. In addition, adiponectin-containing vesicles were co-immunoprecipitated with KIF5B. Knockdown of KIF5B resulted in a marked inhibition of adiponectin secretion and overexpression of KIF5B enhanced adiponectin release, whereas leptin secretion was not affected by changes in KIF5B expression. These data suggest that the secretion of adiponectin, but not leptin, is dependent on functional KIF5B.
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China. Electronic address: juzi.cui@gmail.com.
Ju
J
Cui
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Jing
J
Pang
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Ya-Jun
YJ
Lin
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Ping
P
Jiang
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Huan
H
Gong
Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Zai
Z
Wang
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Jian
J
Li
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China.
Jian-Ping
JP
Cai
School of Biomedical Sciences and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Pokfulam, Hong Kong; The Centre for Synthetic Biology Engineering Research, Shenzhen Institutes of Advanced Technology, Shenzhen, China. Electronic address: jdhuang@hku.hk.
Jian-Dong
JD
Huang
The Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Beijing, China. Electronic address: tmzhang126@126.com.
Tie-Mei
TM
Zhang
D041721:3T3-L1 Cells; D021581:Active Transport, Cell Nucleus; D017667:Adipocytes / Q000166:cytology / Q000378:metabolism*; D050156:Adipogenesis / Q000235:genetics / Q000502:physiology; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002454:Cell Differentiation; D055785:Gene Knockdown Techniques; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D016547:Kinesins / Q000235:genetics / Q000378:metabolism*; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D051379:Mice
D052242:Adiponectin; C499919:Adipoq protein, mouse; D051275:Glucose Transporter Type 4; D020738:Leptin; C495693:Slc2a4 protein, mouse; C475469:Kif5b protein, mouse; D016547:Kinesins
3T3-L1 cell; Adipocyte; Adiponectin secretion; KIF5B