Lei Yin

Lei Yin, PhD

Associate Professor of Molecular and Integrative Physiology
Accepting new students?
Yes
Trainings and Identities:
MORE Mentor Training, CMB DEI Month Book Club, Bystander Training, Self-Identified: Female, Working Mother
Research Interests:
Hepatic lipid metabolism; Circadian rhythm; post-translational modifications; Non-Alcoholic fatty liver disease

I firmly believe the importance of diversity, equity and inclusion in my laboratory. I believe that not only my students and research staff have a job, but they have the same ability to get promoted, to contribute and have the same impact — in the world and in the workplace — as their peers.”

Our lab is interested in understanding molecular mechanisms and pathophysiological significance of liver lipid metabolism and chronic metabolic liver diseases, such as liver insulin resistance, Non-Alcoholic fatty liver disease and drug-induced liver injury. The long-term goal is to gain in-depth understanding about the molecular mechanisms responsible for onset and progression of NAFLD/NASH and at the same time identify potential therapeutic targets to treat NASH. Both in vivo mouse models and in vitro biochemical, cell biology and pharmacology approaches are employed in our studies. We have successfully established experimental platforms and obtained a variety of expertise in studying liver lipogenesis, fatty acid oxidation, liver steatosis and fibrosis, liver injury, transcriptional regulation, and protein post-translational modifications.

The specific research areas include (1) The role and regulation of transcription factor ChREBP in hepatic lipid metabolism and diet-induced NAFLD/NASH; (2) Function and regulation of circadian proteins in the crosstalk between hepatocyte and non-hepatocytes (immune cells and hepatic stellate cells); (3) Impact of brown adipose tissue on hepatic lipid metabolism and diet-induced NAFLD; (4) Identification of novel post-translational regulators during the pathogenesis of diet-induced hepatic insulin resistance and fatty liver disease.

Recent Publications:

1. D. Zhang, X. Tong, K. VanDommelen, N. Gupta N, K. Stamper K, G. Brady, Z Meng, J. Lin, L. Rui L, MB. Omary, and L. Yin. Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatoxicity. J. Clin Invest 2017 127(7):2855-2867 PMCID: PMC5490767

2. D. Zhang, S.Wang, E. Ospina, O. Shanbandrd, D. Lank, J. Akakpo, Z. Zhao, M. Yang, J. Wu, H. Jaeschke, P. Saha, X. Tong and L. Yin. Fructose protects against Acetaminophen-induced hepatoxicity mainly via activating the ChREBPa-FGF21 axis in mice. Hepatology Communication (Accepted in Jan. 2021)

3. D. Zhang, X. Tong, B. Nelson, E. Jin, J. Sit, N. Charney, M. Yang, MB. Omary, and L. Yin. The hepatic BMAL1/AKT/lipogenesis axis protects against alcoholic liver disease in mice via promoting PPARalpha pathway Hepatology 2018 68(3);883-896 PMCID:PMC6428639

4. M. Yang, D. Zhang, Z. Zhao, J. Sit, K. Zhang, O. Shabandra, L. Yin*, X. Tong. Hepatic E4BP4 induction promotes lipid accumulation via suppressing AMPK signaling in response to chemical or diet-induced ER stress. FASEB J 2020 (Accepted) * co-corresponding author

5. X. Tong, D. Zhang, N. Charney, E. Jin, K. Stamper, N. Gupta, J. Saldate, L. Yin. DDB1-mediated CRY1 degradation promotes FOXO1-driven gluconeogenesis in liver. Diabetes 2017 (66): 2571-2582. PMCID: PMC5606320

6. X. Tong, D. Zhang, O. Shanbandrd, E. Jin, K. Stamper, L. Yin. DDB1 E3 ligase controls dietary fructose induced ChREBP stabilization and liver steatosis via CRY1. Metabolism 2020 (107):154222. PMCID: PMC7282961