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盧主欽

Juu-Chin Lu (盧主欽)

Appointments:Assistant Professor

Lab:Endocrine and Metabolism

Education:Ph.D.

School/Nation:University of Wisconsin-Madison/ USA

Tel:3687

Mail:juuchin@mail.cgu.edu.tw

Research websitehttp://juuchin.wix.com/cguwebsite

Laboratory personnel:

Postdoctoral fellow: 0;     Ph.D. student: 1;     Master student: 3;
Res. Assistant: 1;     Undergraduate: 1.

Research interests

Obesity is a well-described epidemic in the westernized countries including Taiwan. It has been linked to a variety of adverse health issues such as cardiovascular diseases, insulin resistance, type 2 diabetes (T2DM), and certain cancer. Obesity is characterized as the increase of body adipose (fat tissue) mass, which can be due to the enlargement of adipocyte (fat cell), the primary cell type in the adipose tissue. The enlargement of adipocyte (hypertrophy) has been linked to its abnormal function. Under the normal condition, the biological function of adipocytes is under the regulation of hormones, neuronal stimuli, and the nutrients. Insulin, the hormone secreted from pancreas, regulates adipocyte function by promoting glucose uptake and lipogenesis, and suppressing lipolysis, therefore regulates lipid and glucose homeostasis. The adipocytes were once considered only the place to store excess fat. However the discovery of many important adipocyte-secreted factors that regulate the whole-body physiology makes the researchers reconsider the adipose tissue as an endocrine organ. Among the secreted factors are peptide hormones (named adipokines) and lipokines, which can regulate the physiology and function of other tissues. Without the adipose tissue, excess fat will be stored in other tissues such as muscle and liver, leading to malfunction of these tissues. Moreover, the lack of adipose tissue also results in the absence of adipokines normally secreted by adipocytes, leading to abnormal regulation of other tissues. Therefore, the understanding of the biological function and regulation of adipocytes will not only provide information on the mechanism by which the adipose tissue regulates body metabolism, but also the therapeutic methods in treating diseases.

          We will use 3T3-L1 adipocytes, primary adipocyte culture, and the animal model to address the following questions:

  1)Molecular mechanism of insulin signaling and insulin action in adipocytes

  2)Molecular mechanism of the insulin-sensitizing drug thiazolidinediones (TZDs) in adipocytes

  3)Molecular mechanism and regulation of adipokine secretion

  4)The interaction of adipocytes and other tissues

Publications

1. Lu, J-C.*, Chiang, Y-T., Lin, Y-C., Chang, Y-T., Lu, C-Y., Chen, T-Y., and Yeh, C-S. (2016) Disruption of lipid raft function increases expression and secretion of monocyte chemoattractant protein-1 in 3T3-L1 adipocytes, PLoS One 11(12): e0169005. (*correspondence)

2. Chiang, N., Hsiao, Y-T., Yang, H-J., Lin, Y-C., Lu, J-C.*, and Wang, C-T.* (2014) Phosphomimetic mutation of cysteine string protein-α increases the rate of calcium- dependent exocytosis by modulating fusion pore dynamics in PC12 cells, PLoS One 9(6): e99180. (*correspondence)

3. Huang, C-Y., Chen, Y-L., Li, A-H., Lu, J-C., and Wang, H-L. (2014) Monocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons, J. Neuroinflam. 11(1): 7.

4. Huang, P-C., Hsiao, Y-T., Kao, S-Y., Chen, C-F., Chen, Y-C., Chiang, C-W., Lee, C-F., Lu, J-C., Chern, Y., and Wang, C-T. (2014) Adenosine A2A receptor up-regulates retinal wave frequency via starburst amacrine cells in the developing rat retina, PLoS One 9(4): e95090.

5. Lu, J-C., Hsiao, Y-T., Chiang, C-W., and Wang, C-T. (2014) GABBA receptor- mediated tonic depolarization in developing neural circuits, Mol. Neurobiol. 49:702- 723.

6. Lu, J-C.*, Chang, Y-T., Wang, C-T., Lin, Y-C., Lin, C-K., Wu, Z-S. (2013) Trichostatin A modulates thiazolidinedione-mediated suppression of tumor necrosis factor alpha-induced lipolysis in 3T3-L1 adipocytes, PLoS One 8(8): e71517. (*correspondence)

7. Chiang, C-W., Chen, Y-C., Lu, J-C., Hsiao, Y-T., Chang, C-W., Huang, P-C., Chang, Y-T., Chang, P. Y., Wang, C-T. (2012) Synaptotagmin I regulates patterned spontaneous activity in the developing rat retina via calcium binding to the C2AB domains, PLoS One 7(10): e47465.

8. Kao, D-J., Li, A.H., Chen, J-C., Luo, R-S., Chen, Y-L., Lu, J-C., Wang, H-L. (2012) CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons, J. Neuroinflamm. 9(1):189.

9. Piazza, T.M., Lu, J-C., Carver, K.C., and Schuler, L.A. (2009) SRC family kinases accelerate prolactin receptor internalization, modulating trafficking and signaling in breast cancer cells, Mol. Endocrinol. 23(2): 202-212.

10. Saberi, M., Woods, N-B., de Luca, C., Schenk, S., Lu, J-C., Bandyopadhyay, G., Verma, I.M., and Olefsky, J.M. (2009) Hematopoietic cell-specific deletion of Toll-like receptor 4 ameliorates hepatic and adipose tissue insulin resistance in high-fat-fed mice, Cell Metab. 10(5): 419-429.

11. Yoshizaki, T., Milne, J.C., Imamura, T., Schenk, S., Sonoda, N., Babendure, J.L., Lu, J-C., Smith, J.J., Jirousek, M.R., and Olefsky, J.M. (2009) SIRT1 exerts anti-inflammatory effects and improves insulin sensitivity in adipocytes, Mol. Cell. Biol. 29(5):1363-1374.

12. Sonoda, N., Imamura, T., Yoshizaki, T., Babendure, J.L., Lu, J-C., and Olefsky, J.M. (2008) Beta-Arrestin-1 mediates glucagons-like peptide-1 signaling to insulin secretion in cultured pancreatic b cells, Proc. Natl. Acad. Sci. USA 105(18): 6614-6619.

13. Kawamata, Y., Imamura, T., Babendure, J.L., Lu, J-C., Yoshizaki, T., and Olefsky, J.M. (2007) Tumor necrosis factor receptor-1 can function through a Galpha q/11/beta-arrestin-1 signaling complex. J. Biol. Chem. 282(39): 28549-28556.

14. Yoshizaki, T., Imamura, T., Babendure, J., Lu, J-C., Sonoda, N., and Olefsky, J.M. (2007) Myosin 5a is an insulin-stimulated Akt2 (protein kinase Bbeta) substrate modulating GLUT4 vesicle translocation. Mol. Cell. Biol. 27(14): 5172-5183.

15. Lu, J-C., Piazza, T.M., and Schuler, L.A. (2005) Proteasomes mediate prolactin-induced receptor downregulation and fragment generation in breast cancer, J. Biol. Chem. 280 (40):33909-33916.

 

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