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Huawei Zeng

Research Molecular Biologist

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Huawei Zeng, Ph.D.

 

Contact information

(701) 795-8465
huawei.zeng@usda.gov

Biography

Dr. Zeng was born and grew up in Xiamen, China. He obtained B.S. and M.S. degrees in Biology from Xiamen University. He attended the University of Wyoming, where he earned a Doctor of Philosophy degree in Molecular Biology in 1996. After graduation, Dr. Zeng spent three and half years as a postdoctoral researcher at the National Institutes of Health (Bethesda, MD) investigating steroid hormone-induced gene expression. Dr. Zeng joined the scientific staff of the USDA-ARS Grand Forks Human Nutrition Research Center (GFHNRC) as a Research Molecular Biologist in November1999.

Research Interests

Obesity related colon cancer is a significant global health concern and the impact of specific dietary components on colon cancer risk has been well recognized. Dr. Zeng's main area of research is to determine the molecular mechanisms of cancer-preventive nutrients in foods. This focus presently centers on dietary fiber / diet timing and gut microbiome, and the development of new molecular biomarkers for obesity related colon cancer prevention. Currently, Dr. Zeng is studying the effects of secondary bile acids and short chain fatty acids in the colon: a focus on colonic microbiome, cell proliferation, inflammation, and cancer.

Dr. Zeng is also investigating the impact of human genetic variation on optimal nutritional intake. Single nucleotide polymorphisms (SNPs) are a primary component of human genetic variation. To determine the diet that best fits certain SNPs, He examines the effects of hemochromatosis, selenoproteins and vitamin D receptor genotypes on the absorption and utilization of iron, selenium, calcium and other nutrients.

Research Accomplishments

Molecular Nutrition & Cancer Biology:

 

  • Demonstrated for the first time that through the activation of certain pro-apoptotic genes linked to p53, NFkB, and stress signal pathways, mice fed a selenium-enriched broccoli had stronger apoptotic ability in response to spontaneous colon tumor development caused by a genetic defect. This contributes to our incomplete knowledge about how nutrients affect gene expression and reduce obesity-related cancer risk. The findings are important because sensitive gene markers are needed to evaluate the anticancer effect of functional foods.
  • Demonstrated that both methylselenol and butyrate inhibit tumor cell migration and invasion, and that they exerted secondary cancer prevention through the inhibition of pro-MMP-2 activation. These findings provide the molecular evidence that secondary cancer prevention can be achieved by the high dietary intakes of selenium-enriched or high fiber foods. In addition, these data lay the groundwork for screening sensitive gene markers that are needed to evaluate the anticancer foods such as selenium-enriched or high fiber foods.
  • Determined the gut microbiome signature related to fatty liver, colonic inflammation in the context of obesity; and demonstrated that consumption of a high-fat diet increased colonic and liver inflammation which are associated with an increase of Lachnospiraceae, Streptococcaceae and Lactobacillus acidophilus bacteria. This work was the first to identify the connection of these three bacterial taxa and the colonic / liver inflammation. Because Lachnospiraceae, Streptococcaceae and Lactobacillus acidophilus are associated with colonic/liver inflammation, these findings provide the opportunity for the development of potential non-invasive markers for assessing the health status of the colon and liver.
  • Identified a potential pathway linking dietary fiber to cancer prevention; demonstrated that butyrate inhibits deoxycholic-acid resistant cell proliferation at the cellular and molecular level. These data provide a proof of concept that butyrate can protect against colon carcinogenesis through a specific targeting of DCA-resistant colonic cells. The finding provides new avenues to study dietary fiber and colon cancer prevention at the cellular and molecular levels.

  • Clinical Research
    Non-Assistance Cooperative Agreement (S)
     Accession Number:438433