- Office: 210-562-4213
Other Website: https://www.uthscsa.edu/academics/biomedical-sciences/faculty/profile/4J911LKLR/Zang,-Mengwei
STRF-South Texas Research Facility
San Antonio, Texas 78229-3900
Mengwei Zang, MD, PhD
Professor of Molecular Medicine
The Ewing Halsell Distinguished Chair in Research
Associate Director of the MD/PhD Program at UT Health San Antonio
Sam and Ann Barshop Institute for Longevity and Aging Studies
|1984||MD||Medicine||Wannan Medical College
Anhui Province , China
|1987||MS||Pathophysiology||Henan Medical University
Henan Province , China
|1998||PhD||Pharmacology||Chinese Academy of Medical Sciences & Peking Union Medical College
Beijing , China
|1999||Postdoctoral Fellowship||Gastroenterology and Pharmacology||Mayo Clinic College of Medicine
Rochester , MN
|2003||Postdoctoral Fellowship||Diabetes and Signal Transduction||Boston University School of Medicine
Boston , MA
Our research focuses on the mechanisms by which nutrient sensors regulate nutrient metabolism and energy homeostasis. We seek to identify new molecular targets that could be leveraged in the management of obesity, type 2 diabetes, fatty liver disease, and other age-related metabolic diseases. Our research goals are:
- To characterize novel nutrient-sensing pathways involved in the regulation of lipid metabolism and energy homeostasis using nutritionally challenged models, metabolic disease mouse models, genetically modified mouse models, pharmacologically treated mouse models, as well as cell/molecular biology. Current efforts are focused on the molecular mechanism(s) by which vitamin A-related retinoic acid receptors and the hepatocyte-derived hormone, FGF21, regulate metabolic homeostasis and how this regulation affects the progression of Type 2 diabetes and age-related metabolic disease.
- To identify the regulation and function of nutrient sensing and to characterize its therapeutic potential on non-alcoholic fatty liver disease. Current efforts are focused on the role of SIRT1 and AMP-activated protein kinase in the regulation of lipid metabolism in non-alcoholic fatty liver disease.
- To define the molecular mechanisms underlying the pathogenesis of alcoholic liver disease. Current efforts are focused on the role of the nutrient sensing network in the development of alcoholic fatty liver and liver injury.
- To investigate the role of nutrient sensing in adipose tissue metabolism and dysfunction. Although adipose tissue fibrosis impairs adipocyte plasticity, little is known about how aberrant extracellular matrix remodeling of fat tissue is initiated during the development of obesity. Our recent studies demonstrate the critical role of AMPK and TGFβ1 in adipocytes in the regulation of extracellular matrix homeostasis and systemic glucose metabolism in obese mice and humans. Targeting the AMPK pathway, like the action of metformin, may provide an exciting new approach for treatment of obesity-induced adipose tissue fibrosis and other tissue fibrosis.
Department: Molecular Medicine
Where: Laboratory of Mengwei Zang, MD, PhD.
Barshop Institute for Longevity and Aging Studies/Department of Molecular Medicine
STRF-South Texas Research Facility
University of Texas Health Science Center at San Antonio – San Antonio, TX
Nature of Work: Two POST-DOCTORAL FELLOWS in Diabetes and Fatty Liver Disease
Two postdoctoral positions are available at Barshop Aging Institute of University of Texas Health Science Center at San Antonio, a leading institute in aging research, to work in the areas of signal transduction, cell metabolism, obesity, diabetes, fatty liver disease, and aging. Our ongoing research focuses on the nutrient regulation of glucose/lipid metabolism and energy balance, as well as the identification of new therapeutic mechanisms for fatty liver disease, diabetes and aging-related metabolic disease published in high impact journals (Li Y, et al. Cell Metabolism, 2011; Gastroenterology, 2014; Luo T, et al. Diabetes, 2016, Chen H, et al, Hepatology, 2018). We generate a variety of genetically modified mouse models and human disease-related animal models including obesity, diabetes, non-alcoholic fatty liver disease, and aging-related metabolic diseases. The ideal candidate are exceptionally motivated, creative, and committed to scientific discovery and have strong academic training in biochemistry, molecular and cell biology, and animal models.
For more information of the research work of Zang laboratory, please visit http://molecularmedicine.uthscsa.edu/FAC_Research.aspx?facID=210; http://gsbs.uthscsa.edu/faculty/mengwei-zang-m.d.-ph.d
Candidates with a strong background in metabolism, ER stress or autophagy biology are strongly encouraged to apply for the positions.
How to Apply:
To apply, please submit a cover letter to Dr. Mengwei Zang at email@example.com and attach: curriculum vitae, a one-page personal statement describing your scientific accomplishments and research interests, and contact information (including phone numbers) of three references.
Contact Name: Mengwei Zang
Contact Email: firstname.lastname@example.org
Job Number: 118
All postdoctoral appointments are designated as security sensitive positions. UT Health San Antonio is an Equal Employment Opportunity/Affirmative Action employer including protected veterans and persons with disabilities.
Dr. Zang received R01 and R21 research grants from the NIH in June 2019.
Naturally occurring protein could treat alcoholic liver disease
Published On: June 25, 2018
Shared by Will Sansom
Chronic alcohol drinking affects 16 million people in the United States, and one of the results is fatty liver damage leading to cirrhosis (scarring). Liver cirrhosis is the 12th-leading cause of death nationwide.
Researchers at UT Health San Antonio’s Sam & Ann Barshop Institute for Longevity & Aging Studies and Department of Molecular Medicine have identified a nutrient-sensing pathway that, if it can be blocked by pharmacological means, could either prevent this liver damage or be a treatment for it.
The scientists believed chronic alcohol consumption would increase activity of a nutrient sensor called mTORC1 and that this would play a role in alcoholic fatty liver, said Mengwei Zang, MD, PhD, associate professor of molecular medicine at UT Health San Antonio. Dr. Zang, the Ewing Halsell Distinguished Chair at the university, is the senior author of alcohol liver disease research published this year in the journal Hepatology.
To find out, the researchers measured liver mTORC1 levels in two groups of mice. Both groups drank a normal liquid diet for five days, with one group continuing on the normal diet for the duration of the study. The other group received a 5 percent ethanol liquid diet for 10 days and was allowed a one-time binging of the ethanol diet on day 16.
“We found exciting results—chronic alcohol consumption increased liver mTORC1 activity in mice and in patients,” Dr. Zang said.
Dr. Zang also reported that a protein called DEPTOR inhibits mTORC1 activity. Because DEPTOR is a naturally occurring protein in our bodies, she views it as a promising target of intervention to curb the fatty liver disease process.
Rapamycin is a compound that reduces mTORC1 activity. The UT Health San Antonio team, including first author Hanqing Chen, PhD, and second author Feng Shen, MD, PhD, conducted further studies in which they compared two groups of mice that were fed an ethanol liquid diet. One group additionally received rapamycin while the other did not. The rapamycin treatment group showed inhibited mTORC1 activity and decreased liver damage, Dr. Zang said.
“Based on these interesting findings, I hope in the future that we can target DEPTOR, perhaps with a pill, and treat alcoholic fatty liver disease,” she said.
Hepatic posttranscriptional network comprised of CCR4-NOT deadenylase and FGF21 maintains systemic metabolic homeostasis.
DEP domain-containing mTOR-interacting protein suppresses lipogenesis and ameliorates hepatic steatosis and acute-on-chronic liver injury in alcoholic liver disease.
Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating sirtuin 1 expression.
AMPK Activation by Metformin Suppresses Abnormal Extracellular Matrix Remodeling in Adipose Tissue and Ameliorates Insulin Resistance in Obesity.
The redox mechanism for vascular barrier dysfunction associated with metabolic disorders: Glutathionylation of Rac1 in endothelial cells.
Fibroblast growth factor 21 improves hepatic insulin sensitivity by inhibiting mammalian target of rapamycin complex 1 in mice.
Hepatic SIRT1 attenuates hepatic steatosis and controls energy balance in mice by inducing fibroblast growth factor 21.
Retinoic acid receptor β stimulates hepatic induction of fibroblast growth factor 21 to promote fatty acid oxidation and control whole-body energy homeostasis in mice.
AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin-resistant mice.
Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver.
SIRT1 regulates hepatocyte lipid metabolism through activating AMP-activated protein kinase.