Chewing the fat for good health: ACSM3 deficiency exacerbates metabolic syndrome

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Abstract

The origin of metabolic syndrome, a pathophysiological condition facilitating cardiovascular disease, diabetes, and other comorbidities, remains poorly understood. Recent work by Xiao et al ( 2023) identifies the mitochondrial enzyme ACSM3 as a determinant of lipid homeostasis and hepatic health in mice and patients. Additionally, the authors identified deleterious downstream p38-MAPK signalling as a targetable feature of ACSM3 deficiency that may help to ameliorate metabolic syndrome.

Abstract

Recent work identifies mitochondrial acyl-CoA synthetase ACSM3 as a guardian of hepatic lipid processing and metabolic health in mice and patients.

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The Global Epidemic of the Metabolic Syndrome

Mohammad G. Saklayen (2018)

Metabolic syndrome, variously known also as syndrome X, insulin resistance, etc., is defined by WHO as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Though there is some variation in the definition by other health care organization, the differences are minor. With the successful conquest of communicable infectious diseases in most of the world, this new non-communicable disease (NCD) has become the major health hazard of modern world. Though it started in the Western world, with the spread of the Western lifestyle across the globe, it has become now a truly global problem. The prevalence of the metabolic syndrome is often more in the urban population of some developing countries than in its Western counterparts. The two basic forces spreading this malady are the increase in consumption of high calorie-low fiber fast food and the decrease in physical activity due to mechanized transportations and sedentary form of leisure time activities. The syndrome feeds into the spread of the diseases like type 2 diabetes, coronary diseases, stroke, and other disabilities. The total cost of the malady including the cost of health care and loss of potential economic activity is in trillions. The present trend is not sustainable unless a magic cure is found (unlikely) or concerted global/governmental/societal efforts are made to change the lifestyle that is promoting it. There are certainly some elements in the causation of the metabolic syndrome that cannot be changed but many are amenable for corrections and curtailments. For example, better urban planning to encourage active lifestyle, subsidizing consumption of whole grains and possible taxing high calorie snacks, restricting media advertisement of unhealthy food, etc. Revitalizing old fashion healthier lifestyle, promoting old-fashioned foods using healthy herbs rather than oil and sugar, and educating people about choosing healthy/wholesome food over junks are among the steps that can be considered.

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Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver?

Patricia Rada, Águeda González-Rodríguez, Carmelo García-Monzón … (2020)

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide. NAFLD stages range from simple steatosis (NAFL) to non-alcoholic steatohepatitis (NASH) which can progress to cirrhosis and hepatocellular carcinoma. One of the crucial events clearly involved in NAFLD progression is the lipotoxicity resulting from an excessive fatty acid (FFA) influx to hepatocytes. Hepatic lipotoxicity occurs when the capacity of the hepatocyte to manage and export FFAs as triglycerides (TGs) is overwhelmed. This review provides succinct insights into the molecular mechanisms responsible for lipotoxicity in NAFLD, including ER and oxidative stress, autophagy, lipoapotosis and inflammation. In addition, we highlight the role of CD36/FAT fatty acid translocase in NAFLD pathogenesis. Up-to-date, it is well known that CD36 increases FFA uptake and, in the liver, it drives hepatosteatosis onset and might contribute to its progression to NASH. Clinical studies have reinforced the significance of CD36 by showing increased content in the liver of NAFLD patients. Interestingly, circulating levels of a soluble form of CD36 (sCD36) are abnormally elevated in NAFLD patients and positively correlate with the histological grade of hepatic steatosis. In fact, the induction of CD36 translocation to the plasma membrane of the hepatocytes may be a determining factor in the physiopathology of hepatic steatosis in NAFLD patients. Given all these data, targeting the fatty acid translocase CD36 or some of its functional regulators may be a promising therapeutic approach for the prevention and treatment of NAFLD.

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Links between metabolic syndrome and metabolic dysfunction-associated fatty liver disease

Giovanni Targher, Jin-Wook Kim, Soo Kyung Lim (2021)

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Author and article information

Contributors

Brian J Altman:

ORCID: http://orcid.org/0000-0002-3954-4916

Brian_Altman@urmc.rochester.edu

Journal

Journal ID (nlm-ta): EMBO J

Journal ID (iso-abbrev): EMBO J

Title: The EMBO Journal

Publisher: Nature Publishing Group UK (London )

ISSN (Print): 0261-4189

ISSN (Electronic): 1460-2075

Publication date (Electronic): 23 January 2024

Publication date PMC-release: 23 January 2024

Publication date Collection: February 2024

Volume: 43

Issue: 4

Pages: 481-483

Affiliations

[1 ]Department of Biomedical Genetics, University of Rochester School of Medicine and Dentistry, ( https://ror.org/022kthw22) Rochester, NY USA

[2 ]Wilmot Cancer Institute, University of Rochester Medical Center, ( https://ror.org/00trqv719) Rochester, NY USA

[3 ]GRID grid.434675.7, ISNI 0000 0001 2159 4512, Member, Catalysts Program, The EMBO Journal, EMBO, ; Heidelberg, Germany

Author information

Juliana Cazarin http://orcid.org/0000-0002-5728-1857

Brian J Altman http://orcid.org/0000-0002-3954-4916

Article

Publisher ID: 37

DOI: 10.1038/s44318-024-00037-0

PMC ID: 10897420

PubMed ID: 38263332

SO-VID: b11418c4-1d54-46e3-8c9e-6441015597ec

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

History

Date received : 13 December 2023

Date accepted : 20 December 2023

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ScienceOpen disciplines: Molecular biology

Keywords: metabolism,molecular biology of disease

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ScienceOpen disciplines: Molecular biology

Keywords: metabolism, molecular biology of disease

Chewing the fat for good health: ACSM3 deficiency exacerbates metabolic syndrome

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Bioscientifica Open Endocrinology

Most cited references 11

The Global Epidemic of the Metabolic Syndrome

Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver?

Links between metabolic syndrome and metabolic dysfunction-associated fatty liver disease

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