Non-Alcoholic Fatty Liver Disease: Pathophysiology, Diagnosis, and Emerging Therapies

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Autore principale: Amit Namde*, Amey Dhuri, Nutan Gaikwad, Rini Punathil, Dr. Kamlesh Soni
Natura: Recurso digital
Pubblicazione: Zenodo 2025
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author Amit Namde*, Amey Dhuri, Nutan Gaikwad, Rini Punathil, Dr. Kamlesh Soni
author_facet Amit Namde*, Amey Dhuri, Nutan Gaikwad, Rini Punathil, Dr. Kamlesh Soni
contents <p><span lang="EN-US">Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disorder worldwide, affecting nearly one-fourth of the global population. It encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), progressive fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). NAFLD is strongly linked with obesity, insulin resistance, type 2 diabetes mellitus, and dyslipidaemia, making it a hepatic manifestation of metabolic syndrome. The disease pathogenesis involves excessive hepatic lipid accumulation driven by increased fatty acid uptake, de novo lipogenesis, impaired fatty acid oxidation, and defective lipid export, ultimately leading to lipo-toxicity, oxidative stress, inflammation, and fibrosis. Diagnosis traditionally relies on liver biopsy, but non-invasive biomarkers and imaging modalities are increasingly employed. Lifestyle modification through diet and exercise remains the cornerstone of management, while pharmacological options such as pioglitazone and vitamin E are recommended in selected patients. Emerging therapies, including FXR agonists (obeticholic acid), PPAR ligands (elafibranor), and GLP-1 receptor agonists (liraglutide, semaglutide, resmetirom), hold promise for disease modification. Despite advances, no FDA-approved drug is yet available, highlighting the urgent need for effective therapies. This review summarises the molecular mechanisms, diagnostic strategies, current management, and future therapeutic perspectives in NAFLD.</span></p>
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spellingShingle Non-Alcoholic Fatty Liver Disease: Pathophysiology, Diagnosis, and Emerging Therapies
Amit Namde*, Amey Dhuri, Nutan Gaikwad, Rini Punathil, Dr. Kamlesh Soni
Non-alcoholic fatty liver disease, NASH, Lipotoxicity, Insulin resistance, FXR agonists, GLP-1 receptor agonists, Metabolic syndrome.
<p><span lang="EN-US">Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common chronic liver disorder worldwide, affecting nearly one-fourth of the global population. It encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), progressive fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). NAFLD is strongly linked with obesity, insulin resistance, type 2 diabetes mellitus, and dyslipidaemia, making it a hepatic manifestation of metabolic syndrome. The disease pathogenesis involves excessive hepatic lipid accumulation driven by increased fatty acid uptake, de novo lipogenesis, impaired fatty acid oxidation, and defective lipid export, ultimately leading to lipo-toxicity, oxidative stress, inflammation, and fibrosis. Diagnosis traditionally relies on liver biopsy, but non-invasive biomarkers and imaging modalities are increasingly employed. Lifestyle modification through diet and exercise remains the cornerstone of management, while pharmacological options such as pioglitazone and vitamin E are recommended in selected patients. Emerging therapies, including FXR agonists (obeticholic acid), PPAR ligands (elafibranor), and GLP-1 receptor agonists (liraglutide, semaglutide, resmetirom), hold promise for disease modification. Despite advances, no FDA-approved drug is yet available, highlighting the urgent need for effective therapies. This review summarises the molecular mechanisms, diagnostic strategies, current management, and future therapeutic perspectives in NAFLD.</span></p>
title Non-Alcoholic Fatty Liver Disease: Pathophysiology, Diagnosis, and Emerging Therapies
topic Non-alcoholic fatty liver disease, NASH, Lipotoxicity, Insulin resistance, FXR agonists, GLP-1 receptor agonists, Metabolic syndrome.
url https://doi.org/10.5281/zenodo.17313048