Juu-Chin Lu
JobTitle： Ph.D.
CurrentJob： Associate Professor
E-mail： juuchin@mail.cgu.edu.tw
Phone： 032118800#3687
Education： University of Wisconsin-Madison/ USA
Expertise： Endocrine and Metabolism
Website： https://pure.lib.cgu.edu.tw/zh/persons/juu-chin-lu-2/
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, and type 2 diabetes (T2DM). 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 regulations 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 adipose tissue was once considered only for the storage of excess fat. However, the discovery of many important adipocyte-secreted factors, which 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 TZDs (Thiazolidinediones) in adipocytes
3. The molecular mechanism and regulation of adipokine release
4. The interaction of adipocytes and other tissues
List of Publications (2019-present):
1. Hsiao, Y-T., Su, Y-L., Chen, P-C., Huang, C-T., Hsieh, Y-Y., Chiang, N., Lin, Y-C., Lu, J-C.*, and Wang, C-T.*, 2025, October, Deficiency of PKA-mediated SNAP-25b phosphorylation destabilizes exocytotic fusion pores and reduces the interactions of t-SNAREs, Journal of Physiology 603(20):6073-6105. (*correspondence)
2. Wu, Y-Y., Huang, Y-Y., and Lu, J-C.*, 2025, August, PKD and scaffold protein NHERF1 mediate hypoxia-induced gene expression in 3T3-L1 adipocytes, Journal of Molecular Endocrinology 75:e250011. (*corresponding author)
3. Chiang, Y-T., Wu, Y-Y., Lin, Y-C., Huang, Y-Y., and Lu, J-C.*, 2023, September, Cyclodextrin-mediated cholesterol depletion induces adiponectin secretion in 3T3-L1 adipocytes, International Journal of Molecular Sciences 24(19):14718. (*correspondence)
4. Wang, H-L., Cheng, Y-C., Yeh, T-H., Liu, H-F., Weng, Y-H., Shen, R-S., Chen, Y-C., Lu, J-C., Hwang, T-L., Wei, K-C., Liu, Y-C., Wang, Y-T., Hsu, C-C., Chiu, T-J., and Chiu, C-C., 2023, June, HCH6-1, an antagonist of formyl peptide receptor-1, exerts anti-neuroinflammatory and neuroprotective effects in cellular and animal models of Parkinson’s disease, Biochemical Pharmacology 212:115524.
5. Chiu, C-C., Weng, Y-H., Yeh, T-H., Lu, J-C., Shen, W-S., Li, A.H., Chen, Y-L., Wei, K-C., and Wang, H-L.*, 2023, May, Deficiency of RAB39B Activates ER Stress-Induced Pro-apoptotic Pathway and Causes Mitochondrial Dysfunction and Oxidative Stress in Dopaminergic Neurons by Impairing Autophagy and Upregulating α-Synuclein, Molecular Neurobiology 60(5):2706-2728.
6. Chen, C-F., Wo, R.R., Huang, C-T., Cheng, T-L., Lu, J-C., and Wang, C-T.*, (2022) Phosphorylation of cysteine string protein-a regulates the frequency of cholinergic waves via starburst amacrine cells, Visual Neuroscience, 39:E003.
7. Lu, J-C.*, Lu, C-Y., and Wu, Y-Y. (2021) THRAP3 depletion reduces PPARγ mRNA and anti-inflammatory action in 3T3-L1 adipocytes, Journal of Molecular Endocrinology. 67(3): 149-159. (*correspondence)
8. Yang, H-J., Chen, P-C., Huang, C-T., Cheng, T-L., Hsu, S-P., Chen, C-Y., Lu, J-C.*, and Wang, C-T.* (2021) The synaptic vesicle-specific phosphoprotein Synapsin Ia regulates the kinetics of dense-core vesicle release, The Journal of Neuroscience, 41(13):2828-2841. (*correspondence)
9. Hsiao, Y-T., Shu, W-C., Chen, P-C., Yang, H-J., Chen, H-Y., Hsu, S-P., Huang, Y-T., Yang, C-C., Chen, Y-J., Yu, N-Y., Liou, S-Y., Chiang, N., Huang, C-T., Cheng, T-L., Cheung, L-Y., Lin, Y-C., Lu, J-C.*, and Wang, C-T.* (2019) February, Presynaptic SNAP-25 regulates retinal waves and retinogeniculate projection via phosphorylation, Proc. Natl. Acad. Sci. USA, 116(8):3262-3267. (*correspondence)