A STUDY OF CORRELATION BETWEEN NON-ALCOHOLIC FATTY LIVER DISEASE AND SERUM LIPOPROTEIN A LEVEL

Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with significant implications for cardiovascular health. Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein associated with atherosclerosis and cardiovascular risk. However, its relationship with NAFLD remains unclear. Some studies suggest an inverse association, where lower Lp(a) levels correlate with increased hepatic fat accumulation and advanced fibrosis. Other studies report no significant association or even elevated Lp(a) levels in NAFLD patients. Given these inconsistencies, the role of Lp(a) in NAFLD pathogenesis, progression, and cardiovascular risk requires further investigation. This review highlights current evidence, explores potential mechanisms linking Lp(a) to liver metabolism, and discusses its potential as a biomarker for NAFLD severity and related complications. Future studies with larger, well-defined cohorts and mechanistic insight are needed to establish the clinical relevance of Lp(a) in NAFLD.

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Publication Details

Published
2025-03-30
DOI
https://doi.org/10.53555/jw67nq08
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
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article

A STUDY OF CORRELATION BETWEEN NON-ALCOHOLIC FATTY LIVER DISEASE AND SERUM LIPOPROTEIN A LEVEL

Dr Sriharsha Kulkarni
Liver Disease Diagnosis and Treatment
article

A STUDY OF CORRELATION BETWEEN NON-ALCOHOLIC FATTY LIVER DISEASE AND SERUM LIPOPROTEIN A LEVEL

Dr Sriharsha Kulkarni
article en

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with significant implications for cardiovascular health. Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein associated with atherosclerosis and cardiovascular risk. However, its relationship with NAFLD remains unclear. Some studies suggest an inverse association, where lower Lp(a) levels correlate with increased hepatic fat accumulation and advanced fibrosis. Other studies report no significant association or even elevated Lp(a) levels in NAFLD patients. Given these inconsistencies, the role of Lp(a) in NAFLD pathogenesis, progression, and cardiovascular risk requires further investigation. This review highlights current evidence, explores potential mechanisms linking Lp(a) to liver metabolism, and discusses its potential as a biomarker for NAFLD severity and related complications. Future studies with larger, well-defined cohorts and mechanistic insight are needed to establish the clinical relevance of Lp(a) in NAFLD.

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