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Shaodong Guo

Guo, Shaodong
Shaodong Guo
Associate Professor
123A Cater-Mattil
Undergraduate Education
Huazhong Agricultural University, 1989
B.S. in Agronomy
Graduate Education
Peking University, 1995
Ph.D. in Physiology
2015- American Diabetes Association Research Excellent Thomas R Lee Award
2015- American Diabetes Association Career Development Award
2007- American Diabetes Association Junior Faculty Award
1999- Travel Award of American 81st Annual Meeting of Endocrine Society
1999- Young Investigator Award, National Natural Science Foundation of China
1999- Young Investigator Award, Institute of Genetics and Developmental Biology of Chinese Academy of Sciences, Beijing, China
1995- Guanghua Scholarship for outstanding Ph.D. Student Award, Peking University, Beijing, China
Courses Taught
NUTR 481: Nutrition Seminar
MSCI 612: Current Topics in Cell Signaling
MSCI 601: Cell Biology
MPHY 631: Cardiovascular Science
MPHY 632: Cardiovascular Pathology

Research Interest

The long-term goal of our research is to study the molecular mechanisms of insulin signal transduction, insulin resistance and associated cardiovascular dysfunction, aiming at nutritional and therapeutic intervention for control of metabolic and cardiovascular disorders. My laboratory is focused on the study of cellular signaling and gene transcriptional regulation of metabolic homeostasis that are governed by the PI3K→Akt→FoxO pathway, with the hope of understanding how dysregulation of this pathway in insulin/IGF-1 action causes liver damage, cardiovascular dysfunction, and pancreatic beta cell failure, resulting in diabetes, obesity, and organ failure. Our research encompasses several areas. Firstly, we will decode the mechanism of insulin resistance and associated cardiovascular dysfunction. It is known that excess nutrients cause or accelerate insulin resistance, investigating how nutrient-mediated signaling activates intracellular mediators that attenuate the insulin→IRS→Akt→FoxO signaling pathway will provide a powerful platform for nutritional and therapeutic intervention for the treatment of diabetes and cardiovascular disorders. The discovery of bioactive compounds, functional food, peptides, nucleotides, or stem cells that increase gene expression of IRS or promote FoxO phosphorylation and ubiquitination will promote drug development and provide new insights on nutritional and therapeutic targets. Secondly, we will define the roles of FoxO proteins in insulin signaling and insulin resistance through creation of cell lines and animal models in which FoxO is either eliminated by a genetic “knock-out” or increased by overexpression. This will also include studies utilizing the technique of tissue specific gene inactivation or activation (knock-in) to determine the role of FoxO in various tissues, including classic and non-classic target tissues for insulin action, such as liver and heart. Lastly, we will explore the novel players mediating insulin actions, as well as other hormones including glucagon, in control of energy metabolism and survival. We have taken advantage of IRS and FoxO genetically engineered mouse and cell models with analyses in genomics, proteomics, and metabolomics, to better define the physiological connections between metabolic regulation and FoxO in intracellular signaling networks.


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  1. Pineda, SS, Chin, YK, Undheim, EAB, Senff, S, Mobli, M, Dauly, C et al.. Structural venomics reveals evolution of a complex venom by duplication and diversification of an ancient peptide-encoding gene. Proc. Natl. Acad. Sci. U.S.A. 2020;117 (21):11399-11408. doi: 10.1073/pnas.1914536117. PubMed PMID:32398368 .
  2. Chow, CY, Chin, YK, Walker, AA, Guo, S, Blomster, LV, Ward, MJ et al.. Venom Peptides with Dual Modulatory Activity on the Voltage-Gated Sodium Channel NaV1.1 Provide Novel Leads for Development of Antiepileptic Drugs. ACS Pharmacol Transl Sci. 2020;3 (1):119-134. doi: 10.1021/acsptsci.9b00079. PubMed PMID:32259093 PubMed Central PMC7088997.
  3. Li, X, Chan, LWC, Li, X, Liu, C, Yang, G, Gao, J et al.. Obesity-Induced Regulator of Calcineurin 1 Overexpression Leads to β-Cell Failure Through Mitophagy Pathway Inhibition. Antioxid. Redox Signal. 2020;32 (7):413-428. doi: 10.1089/ars.2019.7806. PubMed PMID:31822118 .
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