Haiwei Gu obtained his doctorate from Purdue University (2003-2008). Gu received his postdoctoral training focused on LCxLC in the University of Minnesota (2009-2011). From 2011-2017, Gu worked as a research faculty in the Northwest Metabolomics Research Center (NW-MRC) in the University of Washington. Between 2017-2021, Gu was an assistant professor in the College of Health Solutions, Arizona State University. Gu was an associate professor in the Florida International University from 2021-2023. Currently, Gu is an associate professor at Arizona State University. Metabolomics research in the Gu Lab has focused on the development of advanced analytical tools and statistical methodologies for profiling metabolites and metabolic pathways in complex biological systems, and their applications to study diseases, nutrition, drug toxicity, environment, etc.
Education
Ph.D. Chemical Physics/Bioanalytical Chemistry, Purdue University, West Lafayette, Indiana 2003-2008
B.S., Applied Physics, University of Science and Technology of China, Hefei, P. R. China, 1999-2003
My research interests focus on biomarker discovery and systems biology studies using multi-omics approaches, mainly including metabolomics, lipidomics, transcriptomics, and microbiomics. I am working closely with a number of biological and clinical researchers in various studies for identifying metabolic markers and investigating metabolic mechanisms.
Title: Targeting Whole-body Fatty Acid Metabolism in Alzheimer’s Disease, with Special Interest in Lauric acid
Major goal: We hypothesize that whole-body metabolic reprogramming, including fatty acid metabolism, is profoundly involved in AD development and progression. The overall objective of this study (short-term goal) is to further collect validation and mechanistic data in human subjects, and to establish whether 3xTg mice reproduce abnormalities of fatty acid metabolism along the gut-liver-brain axis, making them useful for exploration of mechanisms and testing of potential treatments.
Title: Developmental PBDE exposure, gut microbiome, and diabetes
Major goal: We hypothesize that early life PBDE exposure causes acute and persistent dysbiosis, which upsets the balance between endogenous PXR activation (by indoles) vs. xenobiotic PXR activation (by PBDEs), leading to the delayed onset of diabetes. We seek to establish a causal relationship between developmental PBDE exposure, a change in gut microbiome, selective PXR modulation (sPXRm), and diabetes later in life using humanized PXR-transgenic (hPXR-TG) mice.
Title: Acceleration of Circulatory and Neurological Aging due to Wildfire Exposures
Major goal: The major goals of this project are to assess whether inhaled pollutants accelerate vascular neurological aging by augmentation of aging-related circulatory proteins and peptide fragments that: 1) compromise blood brain barrier integrity and alter microglial function; and 2) promote a reduced metabolic, senescent cellular phenotype that may be reversible with treatment of NAD+ boosting compounds.
