The role of microRNA-33 as a key regulator in hepatic lipogenesis signaling and a potential serological biomarker for NAFLD with excessive dietary fructose consumption in C57BL/6N mice

Author:

Pan Jeong Hoon12345,Cha Hanvit6789,Tang Jingsi123410,Lee Seoyoon6789,Lee Suk Hee1112131415,Le Brandy516174,Redding Mersady C.516174,Kim Sangyub1819204,Batish Mona2116174,Kong Byungwhi C.22234,Lee Jin Hyup6789,Kim Jae Kyeom12345ORCID

Affiliation:

1. School of Human Environmental Sciences

2. University of Arkansas

3. Fayetteville

4. USA

5. Department of Behavioral Health and Nutrition

6. Department of Food and Biotechnology

7. Korea University

8. Sejong 30019

9. Republic of Korea.

10. Department of Animal Science

11. Department of Molecular Medicine

12. Cell and Matrix Research Institute

13. School of Medicine

14. Kyungpook National University

15. Daegu 41944

16. University of Delaware

17. Newark

18. Department of Pharmacology

19. Penn State University

20. Hershey

21. Department of Molecular and Medical Sciences

22. Department of Poultry Science

Abstract

Fructose-induced hepatic miR-33 suppression lead to fatty liver via upregulation of SREBP1. Additionally, fructose-induced hepatic ferroptosis may cause a spill-over of miR-33 into blood stream, which could be a potential serological biomarker for fructose-induced NAFLD.

Funder

Arkansas Biosciences Institute

University of Delaware

China Scholarship Council

National Research Foundation of Korea

Publisher

Royal Society of Chemistry (RSC)

Subject

General Medicine,Food Science

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