Heidi Coia1, Ning Ma2, Yanqi Hou3, Eva Permaul4, Deborah L Berry5, M Idalia Cruz6, Evan Pannkuk7, Michael Girgis8, Zizhao Zhu9, Yichen Lee10, Olga Rodriquez11, Amrita Cheema12, Fung-Lung Chung13. 1. Department of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC 20057, USA. Electronic address: hgc10@georgetown.edu. 2. Department of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC 20057, USA. Electronic address: nm758@georgetown.edu. 3. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: hou_yanqi@163.com. 4. Department of Pathology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: permaule@gmail.com. 5. Department of Pathology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: dlb82@georgetown.edu. 6. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: cruzi@georgetown.edu. 7. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: elp44@georgetown.edu. 8. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: mg1773@georgetown.edu. 9. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: zz207@georgetown.edu. 10. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: yl285@georgetown.edu. 11. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: Olga.Rodriquez@georgetown.edu. 12. Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: ack27@georgetown.edu. 13. Department of Biochemistry & Molecular Biology, Georgetown University Medical Center, Washington, DC 20057, USA; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA. Electronic address: flc6@georgetown.edu.
Abstract
BACKGROUND & AIMS: Obesity is a major cause of non-alcoholic fatty liver disease (NAFLD). NAFLD is an epidemic affecting nearly 34% of the adult population in the US. As a chronic inflammatory disease, NAFLD influences the immune system by dysregulating T-cell activity. Remedies for the adverse effects on the immune system are urgently needed. We studied Theaphenon E (TE), a standardized formulation of green tea extract, on the adverse effects of NAFLD in C57BL/6J mice fed a high fat diet (HFD). METHODS: Mice received HFD, low fat diet (LFD) or HFD+2% TE for 35 weeks. Hepatic lipid accumulation, cell proliferation, apoptosis and CD4+T lymphocytes were measured throughout the bioassay. The hepatic composition of fatty acids was determined. The effects of epigallocatechin gallate (EGCG) metabolites on lipid accumulation in mouse and primary human liver cells were studied. RESULTS: Unlike mice receiving HFD, mice on HFD+2% TE maintained normal liver to body weight ratios with low levels of alanine and aspartate aminotransferase (ALT and AST). Hepatic lipid accumulation was observed in HFD mice, accompanied by increased proliferation, reduced apoptosis and loss of CD4+ T lymphocytes. TE significantly inhibited lipid accumulation, decreased proliferation, induced apoptosis and increased CD4+ T cell survival in HFD mice. It was found that the EGCG metabolite EGC-M3 reduced lipid accumulation in mouse and human hepatocytes. Linoleic acid showed the largest increase (2.5-fold) in livers of mice on a HFD and this increase was significantly suppressed by TE. CONCLUSIONS: Livers of HFD-fed mice showed lipid accumulation, increased proliferation, reduced apoptosis, elevated linoleic acid and loss of CD4+ T cells. TE effectively ameliorated all of these adverse effects. Published by Elsevier Ltd.
BACKGROUND & AIMS: Obesity is a major cause of non-alcoholic fatty liver disease (NAFLD). NAFLD is an epidemic affecting nearly 34% of the adult population in the US. As a chronic inflammatory disease, NAFLD influences the immune system by dysregulating T-cell activity. Remedies for the adverse effects on the immune system are urgently needed. We studied Theaphenon E (TE), a standardized formulation of green tea extract, on the adverse effects of NAFLD in C57BL/6J mice fed a high fat diet (HFD). METHODS: Mice received HFD, low fat diet (LFD) or HFD+2% TE for 35 weeks. Hepatic lipid accumulation, cell proliferation, apoptosis and CD4+T lymphocytes were measured throughout the bioassay. The hepatic composition of fatty acids was determined. The effects of epigallocatechin gallate (EGCG) metabolites on lipid accumulation in mouse and primary human liver cells were studied. RESULTS: Unlike mice receiving HFD, mice on HFD+2% TE maintained normal liver to body weight ratios with low levels of alanine and aspartate aminotransferase (ALT and AST). Hepatic lipid accumulation was observed in HFD mice, accompanied by increased proliferation, reduced apoptosis and loss of CD4+ T lymphocytes. TE significantly inhibited lipid accumulation, decreased proliferation, induced apoptosis and increased CD4+ T cell survival in HFD mice. It was found that the EGCG metabolite EGC-M3 reduced lipid accumulation in mouse and human hepatocytes. Linoleic acid showed the largest increase (2.5-fold) in livers of mice on a HFD and this increase was significantly suppressed by TE. CONCLUSIONS: Livers of HFD-fed mice showed lipid accumulation, increased proliferation, reduced apoptosis, elevated linoleic acid and loss of CD4+ T cells. TE effectively ameliorated all of these adverse effects. Published by Elsevier Ltd.
Entities:
Keywords:
CD4+T cells; Linoleic acid; Non-alcoholic fatty liver disease; Prevention by green tea
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