![\"Excessive](\"https:\/\/themedicinereview.com\/\/en\/wp-content\/uploads\/shared\/wine-2789265_640.jpg\")
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Excessive alcohol consumption disrupts liver metabolism early and promotes fibrosis. Excessive alcohol consumption causes progressive damage to the liver, ranging from fat accumulation to advanced fibrosis and then cirrhosis. A recent study analyzed the molecular changes associated with these different stages in adults with a history of excessive alcohol consumption. The results reveal that disruptions in fat and sugar metabolism appear as early as the first stages of the disease, long before fibrosis becomes severe.<\/p>\n
Researchers examined liver samples from 50 individuals, divided into three groups: no fibrosis, mild to moderate fibrosis, and advanced fibrosis or cirrhosis. They observed that, from the early stages, certain genes involved in glucose and lipid metabolism\u2014such as those regulating fat production or sugar response\u2014show reduced activity. This early decline suggests that the liver gradually loses its ability to normally process nutrients, which could make cells more vulnerable to damage and promote the accumulation of scar tissue.<\/p>\n
As fibrosis worsens, the changes become more pronounced. Genes linked to the formation of the extracellular matrix, a network of proteins that supports cells, are strongly activated. Among these, those encoding collagen, a key protein in scar tissue, show a significant increase in expression. At the same time, genes involved in inflammation, such as those producing pro-inflammatory signals, are also overexpressed. These changes reflect the liver’s response to chronic inflammation and cell destruction, typical of advanced disease stages.<\/p>\n
Another notable aspect is the progressive suppression of metabolic pathways. In advanced stages, genes responsible for fatty acid and steroid metabolism are strongly inhibited. This indicates that the liver, already weakened by fibrosis, also loses its ability to process fats and other essential substances. This dual impairment\u2014both structural and functional\u2014further worsens liver dysfunction.<\/p>\n
Two proteins, galectin-3 and S100A4, stand out in particular. Galectin-3 is a protein that binds to sugars and plays a role in activating immune cells and fibrosis formation. S100A4, on the other hand, is associated with the activation of hepatic stellate cells, which are primarily responsible for producing scar tissue. Levels of these two proteins increase with the severity of fibrosis, and their heightened presence in liver samples confirms their involvement in disease progression. Their detection could thus serve as a marker to assess the severity of fibrosis.<\/p>\n
These findings show that alcohol-related liver disease follows a precise molecular pattern. From the earliest stages, metabolism is disrupted, and as fibrosis worsens, the liver’s repair mechanisms become excessive, leading to an accumulation of scar tissue that permanently alters its structure and function. These results open avenues for identifying new markers or therapeutic targets to better manage patients before the damage becomes irreversible.<\/p>\n
Excessive alcohol consumption disrupts liver metabolism early and promotes fibrosis. Excessive alcohol consumption causes progressive damage to the liver, ranging from fat accumulation to advanced fibrosis and then cirrhosis. A recent study analyzed the molecular changes associated with these different stages in adults with a history of excessive alcohol consumption. The results reveal that disruptions in fat and sugar metabolism appear as early as the first stages of the disease, long before fibrosis becomes severe.<\/p>\n
Researchers examined liver samples from 50 individuals, divided into three groups: no fibrosis, mild to moderate fibrosis, and advanced fibrosis or cirrhosis. They observed that, from the early stages, certain genes involved in glucose and lipid metabolism show reduced activity. This early decline suggests that the liver gradually loses its ability to normally process nutrients, which could make cells more vulnerable to damage and promote the accumulation of scar tissue.<\/p>\n
As fibrosis worsens, the changes become more pronounced. Genes linked to the formation of the extracellular matrix, a network of proteins that supports cells, are strongly activated. Among these, those encoding collagen, a key protein in scar tissue, show a significant increase in expression. At the same time, genes involved in inflammation are also overexpressed. These changes reflect the liver’s response to chronic inflammation and cell destruction, typical of advanced disease stages.<\/p>\n
Another notable aspect is the progressive suppression of metabolic pathways. In advanced stages, genes responsible for fatty acid and steroid metabolism are strongly inhibited. This indicates that the liver, already weakened by fibrosis, also loses its ability to process fats and other essential substances. This dual impairment\u2014both structural and functional\u2014further worsens liver dysfunction.<\/p>\n
Two proteins, galectin-3 and S100A4, stand out in particular. Galectin-3 is a protein that binds to sugars and plays a role in activating immune cells and fibrosis formation. S100A4 is associated with the activation of hepatic stellate cells, which are primarily responsible for producing scar tissue. Levels of these two proteins increase with the severity of fibrosis, and their heightened presence in liver samples confirms their involvement in disease progression. Their detection could thus serve as a marker to assess the severity of fibrosis.<\/p>\n
These findings show that alcohol-related liver disease follows a precise molecular pattern. From the earliest stages, metabolism is disrupted, and as fibrosis worsens, the liver’s repair mechanisms become excessive, leading to an accumulation of scar tissue that permanently alters its structure and function.<\/p>\n
DOI:<\/strong> https:\/\/doi.org\/10.1007\/s11033-026-11955-z<\/a><\/p>\n Title:<\/strong> Multiplexed targeted mRNA profiling of alcohol-related liver disease reveals stage-specific dysregulation of signaling pathways<\/p>\n Journal:<\/strong> Molecular Biology Reports<\/p>\n Publisher:<\/strong> Springer Science and Business Media LLC<\/p>\n Authors:<\/strong> Dusan Rasic; Maja Thiele; Peter Andersen; Aleksander Krag; S\u00f6nke Detlefsen<\/p>\n","protected":false},"excerpt":{"rendered":" Excessive alcohol consumption disrupts liver metabolism early and promotes fibrosis Excessive alcohol consumption disrupts liver metabolism early and promotes fibrosis. Excessive alcohol consumption causes progressive damage to the liver, ranging from fat accumulation to advanced fibrosis and then cirrhosis. A recent study analyzed the molecular changes associated with these different stages in adults with a… Continue reading Excessive alcohol consumption disrupts liver metabolism early and promotes fibrosis<\/span><\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[2],"tags":[],"class_list":["post-67","post","type-post","status-publish","format-standard","hentry","category-health","entry"],"_links":{"self":[{"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/posts\/67","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/comments?post=67"}],"version-history":[{"count":1,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/posts\/67\/revisions"}],"predecessor-version":[{"id":68,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/posts\/67\/revisions\/68"}],"wp:attachment":[{"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/media?parent=67"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/categories?post=67"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/themedicinereview.com\/en\/wp-json\/wp\/v2\/tags?post=67"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}