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  • Commentary   
  • J Obes Metab 2022, Vol 5(2): 119
  • DOI: 10.4172/jomb.1000119

A Cross-Sectional study of Serum Methionine Metabolites and Non-Alcoholic Fatty Liver Disease

Zongtao Chen*
Health Management Center, First Affiliated Hospital of Army Medical University, Chongqing, China
*Corresponding Author: Zongtao Chen, Health Management Center, First Affiliated Hospital of Army Medical University, Chongqing, China, Email: zongtao.c@gmail.com

Received: 13-Apr-2022 / Manuscript No. jomb-22-60732 / Editor assigned: 15-Apr-2022 / PreQC No. jomb-22-60732 (PQ) / Reviewed: 29-Apr-2022 / QC No. jomb-22-60732 / Revised: 04-May-2022 / Manuscript No. jomb-22-60732 (R) / Accepted Date: 09-May-2022 / Published Date: 11-May-2022 DOI: 10.4172/jomb.1000119

Description

Non-alcoholic fatty liver disease (NAFLD) has been emerging as the leading chronic liver disease and a significant global health burden gradually, affecting up to 25% of the world population. In China, the prevalence of NAFLD reached 32.9% in 2018. And the incidence has risen substantially over the past decades, from 4.6% in 2011-2013 to 5.2% in 2014-2016. NAFLD, ranging from isolated hepatic steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis, is viewed as the hepatic manifestation of metabolic syndrome. The progression of NAFLD is often unpredictable and asymptomatic, which makes it easy to be ignored. Therefore, it is necessary to identify new biomarkers in terms of the prediction of the occurrence and development of NAFLD.

Methionine cycle is a key thing of one-carbon metabolism which performs an essential function in an extensive vary of metabolic diseases. At this aspect, intermediate metabolites, consisting of S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH) and homocysteine (Hcy), have been acquired first-rate attention. As the direct metabolite of methionine, SAM is the familiar methyl donor for mobile methylation. SAH, as a predominant by-product of methylation, is the powerful comments inhibitor of SAM-dependent methyltransferases. Elevated plasma SAH concentrations had been related with a multiplied danger of cardiovascular occasions in coronary angiography patients [1 ]. Moreover, S-adenosylmethionine/ S-adenosylhomocysteine (SAM/SAH) ratio is regarded as the methylation practicable or potential index. A low ratio used to be related with improved dangers of metabolic ailments such as continual kidney sickness and cardiovascular disease. Hcy is produced from SAH by way of reversible response of SAH hydrolase (SAHH), and for this reason is intrinsically associated to mobile methylation popularity as well. Hyperhomocysteinemia may additionally be implicated in the improvement of many metabolic diseases, such as weight problems and type 2 diabetes, and a latest find out about indicated that excessive plasma. Hcy degree should irritate insulin resistance and vascular endothelial dysfunction in sufferers with type 2 diabetes. Studies have proven that methionine metabolism is tremendously energetic in the hepatocytes and serum methionine degrees had been correlated with hepatic methionine metabolism activity. Thus, serum methionine metabolites may also be the indications of liver methionine metabolism.

The mechanisms by means of which improved serum methionine metabolites such as SAH and Hcy had been positively related with the presence of NAFLD may want to be as follows. It has been said that increased methionine metabolites ought to disrupt the methylation of a range of substances, along with PC and SREBPs. Hepatic PC is produced by SAM-dependent methylation of phosphatidylethanolamine. PC performs a critical position in keeping hepatic lipid homeostasis by using regulating lipid transport [2 ]. Decreased PC degree weakens the meeting and secretion of lipoproteins especially low-density lipoprotein which impairs lipid excretion and in addition hurries up intracellular lipid droplet accumulation in the liver. An epidemiological find out about additionally confirmed that contributors with hepatic steatosis had 25% much less PC in the liver than the regular population. On the different hand, SREBP-1, a transcription thing regulating lipogenesis gene in mammals, can be activated via low PC stage in a comments mechanism. Activated SREBP-1 consequently upregulates genes worried in lipid biosynthesis, boosting lipid droplet formation and main to lipid accumulation in hepatocytes as well. Therefore, no longer solely impaired lipid excretion however additionally multiplied lipogenesis can promote the prevalence of NAFLD. In addition, greater SAH or Hcy ought to promote the development of infection in the liver. Arumugam et al. [3 ] mentioned that expanded SAH expanded the launch of pro-inflammatory cytokines from adipocytes. Powell et al. [4 ] confirmed that expanded Hcy brought on oxidative stress and recruited inflammatory cells in the liver of rats.

This learns has several limitations. Firstly, the cross-sectional design can’t make clarify the causal inference. Whether methionine metabolites are bystanders, causal elements or consequences of NAFLD can’t be answered from the outcomes of this cross-sectional study and potential research are warranted. Secondly, on the grounds that all find out about individuals had been voluntarily recruited, there is achievable for choice bias. Thirdly, NAFLD was once identified non-invasively as gorgeous for epidemiological research generally. Nevertheless, in contrast to liver biopsy, ultrasonography can’t furnish histological statistics to similarly discover the affiliation between methionine metabolites and NASH [5 ]. Lastly, all learn about individuals had been solely Chinese, which restricts the generalizability to different ethnic populations. In this cross-sectional find out about of middle-aged and elderly Chinese, serum SAH and Hcy tiers might also be positively related with the threat of NAFLD prevalence, and SAM/SAH ratio may also be inversely associated to NAFLD.

Acknowledgement

I would like to acknowledge Health Management Center, First Affiliated Hospital of Army Medical University, Chongqing, China for providing an opportunity to do research.

Conflict of Interest

No potential conflicts of interest relevant to this article were reported.

References

  1. Arumugam MK, Chava S, Rasineni K, Paal MC, Donohue T, et al. (2021) Elevated S-adenosylhomocysteine induces adipocyte dysfunction to promote alcohol-associated liver steatosis. Sci Rep 11: 14693.
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  3. Matte C, Stefanello FM, Mackedanz V, Pederzolli CD, Lamers ML, et al. (2009) Homocysteine induces oxidative stress, inflammatory infiltration, fibrosis and reduces glycogen/glycoprotein content in liver of rats. Int J Dev Neurosci 27: 337-344. 
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  5. Zhou J, Zhou F, Wang W, Zhang XJ, Ji XY, et al. (2020) Epidemiological features of NAFLD from 1999 to 2018 in China. Hepatology 71: 1851-1864. 
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  7. Powell EE, Wong VWS, Rinella M (2021) Non-alcoholic fatty liver disease. Lancet 397: 2212-2224. 
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  9. Ducker GS, Rabinowitz JD (2017) One-carbon metabolism in health and disease. Cell Metab 25: 27-42. 
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Citation: Chen Z (2022) A Cross-Sectional study of Serum Methionine Metabolites and Non-Alcoholic Fatty Liver Disease. J Obes Metab 5: 119. DOI: 10.4172/jomb.1000119

Copyright: © 2022 Chen Z. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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