Circulating Ism1 Reduces the Risk of Type 2 Diabetes but not Diabetes-Associated NAFLD
Editorial on the Research Topic
The roles and mechanisms of hepatokines, adipokines and myokines in the development of non-alcoholic fatty liver disease (NAFLD)
Nonalcoholic fatty liver disease (NAFLD), which is characterized by excessive triglyceride (TG) accumulation in hepatocytes, have become a serious health problem worldwide (1). Due to the changes of life style, such as overnutrition and lack of exercise, the prevalence of NAFLD is increasing year by year. NAFLD can further progress to nonalcoholic steatohepatitis (NASH) liver fibrosis, and hepatocellular carcinoma (2). Besides, both human studies and animal experiments have shown that NAFLD is strongly associated with systemic metabolic disorders, including hyperglycemia, insulin resistance and dyslipidemia (3). However, until now, there is no FDA-approved drugs for treating NAFLD and NASH. Therefore, a better understanding the molecular mechanisms of NAFLD and NASH remains urgent.
Decades of studies have demonstrated that cytokines derived from metabolic organs, including liver, adipose tissues and skeletal muscles, play crucial role in the regulation of hepatic and systemic lipid homeostasis (4). These organokines, termed as hepatokines, adipokines and myokines, could modulate lipid synthesis, oxidation and transport through autocrine, paracrine and endocrine manners. For instance, the role and mechanisms of hepatokine FGF21, adipokine adiponectin, and myokine Irisin in the development of NAFLD have been well-acknowledged (5–8). More importantly, these studies have provided potential therapeutic targets for the treatment of NAFLD and NASH.
Therefore, at this stage, we set up a Research Topic entitled “The Roles and Mechanisms of Hepatokines, Adipokines and Myokines in the Development of Non-Alcoholic Fatty Liver Disease (NAFLD)” in the Frontiers in Endocrinology. Through this Research Topic, we aimed to further establish the roles of hepatokines, adipokines and myokines in NAFLD and NASH. In this collection, Guo et al., identified dysregulated myokines in the development of NAFLD and NASH through comprehensive transcriptome profiling. Mao et al., identified adipokines and hepatokines associated with high-salt-diet in mice. Wang et al., analyzed the relationship between circulating Ism1 and diabetes and diabetes-associated NAFLD. Gao et al., provided a novel view on endoplasmic reticulum-related and secretome gene in NAFLD progression.
Overall, these studies together identified some new cytokines associated with NAFLD pathogenesis, which further strengthened our understanding of metabolic liver disease. However, intensive work is still required, such as investigations into the roles and mechanisms of these cytokines through genetic models, translational studies in human subjects, and screening potential therapeutic target for treatment. We hope that more and more studies on this Research Topic would help us better understand the molecular mechanisms of NAFLD development and identify more therapeutic targets for its treatment.
Author contributions
The author confirms being the sole contributor of this work and has approved it for publication.
Funding
This study was supported by the National Key Research and Development Program of China (No. 2018YFA0800402).
Conflict of interest
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
1. Paik JM, Kabbara K, Eberly KE, Younossi Y, Henry L, Younossi ZM, et al. Global burden of NAFLD and chronic liver disease among adolescents and young adults. Hepatology (2022) 75(5):1204–17. doi: 10.1002/hep.32228
2. Loomba R, Friedman SL, Shulman GI. Mechanisms and disease consequences of nonalcoholic fatty liver disease. Cell (2021) 184(10):2537–64. doi: 10.1016/j.cell.2021.04.015
3. Tilg H, Moschen AR, Roden M. NAFLD and diabetes mellitus. Nat Rev Gastroenterol Hepatol (2017) 14(1):32–42. doi: 10.1038/nrgastro.2016.147
4. Santos JPMD, Maio MC, Lemes MA, Laurindo LF, Haber JFDS, Bechara MD, et al. Non-alcoholic steatohepatitis (NASH) and organokines: What is now and what will be in the future. Int J Mol Sci (2022) 23(1):498. doi: 10.3390/ijms23010498
5. Flippo KH, Potthoff MJ. Metabolic messengers: FGF21. Nat Metab (2021) 3(3):309–17. doi: 10.1038/s42255-021-00354-2
6. Straub LG, Scherer PE. Metabolic messengers: Adiponectin. Nat Metab (2019) 1(3):334–9. doi: 10.1038/s42255-019-0041-z
7. Wang X, Mao L, Li C, Hui Y, Yu Z, Sun M, et al. The potential role of FNDC5/irisin in various liver diseases: awakening the sleeping beauties. Expert Rev Mol Med (2022) 24:e23. doi: 10.1017/erm.2022.19
Keywords: adipokine, hepatokines, myokines, nonalcoholic fatty live disease, liver
Citation: Lu Y (2022) Editorial: The roles and mechanisms of hepatokines, adipokines and myokines in the development of non-alcoholic fatty liver disease (NAFLD). Front. Endocrinol. 13:1074842. doi: 10.3389/fendo.2022.1074842
Received: 20 October 2022; Accepted: 07 December 2022;
Published: 16 December 2022.
Edited and Reviewed by:
Ralf Jockers, Université de Paris, FranceCopyright © 2022 Lu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Yan Lu, lu.yan2@zs-hospital.sh.cn