Contact

Department

Cellular and Integrative Physiology

Teppei Fujikawa, Ph.D.

Assistant Professor

Education

B.Sc. Kyoto University, 2003
Ph.D. Kyoto University, 2008

Research

 Visit our lab website for more details

Our scientific interest is to unravel the mechanism by which the central nervous system (CNS) regulates whole body metabolic homeostasis such as glucose and fat metabolism, energy expenditure, and food intake. Obesity and metabolic diseases have been increasing at the alarming rate and threating our health and economy over the world. Understanding the mechanism underlying the regulation of metabolism is a fundamental step towards to designing new treatments for obesity and its associated diseases, and many other metabolic diseases. To unravel the mechanism by which the CNS regulates metabolism, we will utilize a variety of technique including, but not limited, generating transgenic animals, optogenetics, chemogenetics, in situ hybridization, immunohistochemistry, and biochemical assay. Currently, our lab is focused on two projects

1) The CNS regulates metabolic adaptations to high physical activity

Most, if not all, animals have evolved in the environment in which high physical activity is required in order to seek food for surviving. Our genetics is optimized to this metabolically challenging environment, and not ready for our modern sedentary lifestyle. Human and rodents studies have shown that high physical activity or exercise training can dramatically improve metabolism. A part of beneficial effects of exercise on metabolism results from metabolic adaptations to exercise such as increases the metabolic capacity of the skeletal muscle. Our lab will investigate the contributions of the CNS to metabolic adaptations to exercise.

2) The CNS regulates glucose metabolism independently of insulin

Insulin, which is secreted from pancreatic beta-cells, is essential for life. In fact, a person who lacks insulin develops severe disease, type 1 diabetes mellitus (T1DM). Insulin treatment has been saving the life of T1DM patients, yet the treatment is not still perfect. For instance, T1DM patients have a higher risk of cardiovascular diseases compared to same age of non-T1DM subjects. Previously we found that the CNS has a capability to regulate glucose metabolism independently of insulin. Our aim is to unravel the precise neuronal and molecular mechanism by which the CNS regulates glucose metabolism without insulin.

If you are interested in our lab and would like to join the team, please contact fujikawa@uthscsa.edu

Lab Members

 Nancy Gonzalez
Research Assistant – Senior
Postdoctoral Fellow

Publications

Fujikawa T, Castorena CM, Pearson M, Kusminski CM, Ahmed N, Battiprolu PK, Kim KW, Lee S, Hill JA, Scherer PE, Holland WL, Elmquist JK. SF-1 expression in the hypothalamus is required for beneficial metabolic effects of exercise. eLife. 2016; 5. PMID: 27874828

Fujikawa, T. *, and Coppari, R. *, Living without insulin: the role of leptin signaling in the hypothalamus. Front Neurosci, (2015) 9, 108. *co-corresponding author

Williams, K.W., Liu, T., Kong, X., Fukuda, M., Deng, Y., Berglund, E.D., Deng, Z., Gao, Y., Liu, T., Sohn, J.-W., Jia, L., Fujikawa, T., Kohno, D., Sccotte, M., Lee, S., Lee, S., Sun, K., Chang, Y., Scherer, P.E., and Elmquist, J.K., Xbp1s in Pomc neurons connects ER stress with energy balance and glucose homeostasis. Cell metabolism, (2014) 20, 471-482.

Fujikawa, T. * and Coppari, R. *, Hypothalamic-mediated control of glucose balance in the presence and absence of insulin. Aging, (2014) 6, 92-97. *co-corresponding author

Asterholm, I.W., Rutkowski, J.M., Fujikawa, T., Cho, Y.R., Fukuda, M., Tao, C., Wang, Z.V., Gupta, R.K., Elmquist, J.K., and Scherer, P.E., Elevated resistin levels induce central leptin resistance and increased atherosclerotic progression in mice. Diabetologia, (2014) 57, 1209-1218.

Fujikawa T, Berglund ED, Patel VR, Ramadori G, Vianna CR, Vong L, Thorel F, Chera S, Herrera PL, Lowell BB, Elmquist JK, Baldi P, Coppari R. Leptin engages a hypothalamic neurocircuitry to permit survival in the absence of insulin. Cell Metab. 2013 Sep 3;18(3):431-44. doi: 10.1016/j.cmet.2013.08.004. PubMed PMID: 24011077; PubMed Central PMCID: PMC3890693.

Fujikawa, T., Berglund, E.D., Patel, V.R., Ramadori, G., Vianna, C.R., Vong, L., Thorel, F., Chera, S., Herrera, P.L., Lowell, B.B., Elmquist, J.K., Baldi, P., and Coppari, R., Leptin engages a hypothalamic neurocircuitry to permit survival in the absence of insulin. Cell metabolism, (2013) 18: p.431-444

Choi, Y.H.*, Fujikawa,T.* (co-first author), Lee, J., Reuter, A., and Kim, K.W., Revisiting the Ventral Medial Nucleus of the Hypothalamus: The Roles of SF-1 Neurons in Energy Homeostasis. Front Neurosci, (2013) 7: p. 71.

Yamada, H., Iwaki, Y., Kitaoka, R., Fujitani, M., Shibakusa, T., Fujikawa, T., Matsumura, S., Fushiki, T., and Inoue, K., Blood lactate functions as a signal for enhancing fatty acid metabolism during exercise via TGF-beta in the brain. J Nutr Sci Vitaminol (Tokyo), (2012) 58(2): p. 88-95.

Ramadori, G., Fujikawa, T., Anderson, J., Berglund, E.D., Frazao, R., Michan, S., Vianna, C.R., Sinclair, D.A., Elias, C.F., and Coppari, R., SIRT1 deacetylase in SF1 neurons protects against metabolic imbalance. Cell metabolism, (2011). 14(3): p. 301-12.

Miyaki, T., Fujikawa, T., Kitaoka, R., Hirano, N., Matsumura, S., Fushiki, T., and Inoue, K., Noradrenergic projections to the ventromedial hypothalamus regulate fat metabolism during endurance exercise. Neuroscience, (2011) 190: p. 239-50.

Ramadori, G., Fujikawa, T., Fukuda, M., Anderson, J., Morgan, D.A., Mostoslavsky, R., Stuart, R.C., Perello, M., Vianna, C.R., Nillni, E.A., Rahmouni, K., and Coppari, R., SIRT1 deacetylase in POMC neurons is required for homeostatic defenses against diet-induced obesity. Cell metabolism, (2010) 12(1): p. 78-87.

Kitaoka, R., Fujikawa, T., Miyaki, T., Matsumura, S., Fushiki, T., and Inoue, K., Increased Noradrenergic Activity in the Ventromedial Hypothalamus during Treadmill Running in Rats. J Nutr Sci Vitaminol (Tokyo), (2010) 56(3): p. 185-90.

Fujikawa, T., Fujita, R., Iwaki, Y., Matsumura, S., Fushiki, T., and Inoue, K., Inhibition of fatty acid oxidation activates transforming growth factor-beta in cerebrospinal fluid and decreases spontaneous motor activity. Physiology & behavior, (2010) 101(3): p. 370-5.

Fujikawa, T., Chuang, J.C., Sakata, I., Ramadori, G., and Coppari, R., Leptin therapy improves insulin-deficient type 1 diabetes by CNS-dependent mechanisms in mice. Proc Natl Acad Sci U S A, (2010) 107(40): p. 17391-6.

Ramadori, G., Gautron, L., Fujikawa, T., Vianna, C.R., Elmquist, J.K., and Coppari, R., Central administration of resveratrol improves diet-induced diabetes. Endocrinology, (2009) 150(12): p. 5326-33.

Matsumura, S., Shibakusa, T., Fujikawa, T., Yamada, H., Matsumura, K., Inoue, K., and Fushiki, T., Intracisternal administration of transforming growth factor-beta evokes fever through the induction of cyclooxygenase-2 in brain endothelial cells. American journal of physiology. Regulatory, integrative and comparative physiology, (2008) 294(1): p. R266-75.

Matsumura, S., Shibakusa, T., Fujikawa, T., Yamada, H., Inoue, K., and Fushiki, T., Increase in transforming growth factor-beta in the brain during infection is related to fever, not depression of spontaneous motor activity. Neuroscience, (2007) 144(3): p. 1133-4o.

Fujikawa, T., Matsumura, S., Yamada, H., Inoue, K., and Fushiki, T., Transforming growth factor-beta in the brain enhances fat oxidation via noradrenergic neurons in the ventromedial and paraventricular hypothalamic nucleus. Brain Res, (2007) 1173: p. 92-101

Fujikawa, T., Castorena, C.M., Pearson, M., Kusminski, C.M., Ahmed, N., Battiprolu, P.K., Kim, K.W., Lee, S., Hill, J.A., Scherer, P.E., Holland, L.W., and Elmquist, K.J., SF-1 Expression in the Hypothalamus is Required for Beneficial Metabolic Effects of Exercise. eLife, (2016) Nov 22;5

Anderson, G.A., Ramadori, G., Ioris, M.R., Galiè, M., Berglund, D.E., Coate, C. K., Fujikawa, T., Pucciarelli, S., Moreschini, B., Amici, A., Andreani, C., and Coppari, R., Enhanced insulin sensitivity in skeletal muscle and liver by physiological overexpression of SIRT6. Molecular metabolism, (2015) 4, 846-56.