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Research Article

The Levels of Serum Leptin and TNF-α in Patients with Alcoholic Liver Disease in the Alcoholic Indian Population

, MBBS, , MSc MPhil, , MD, , MD, , PhD, , MD, , MD & , PhDORCID Icon show all
 

ABSTRACT

Alcoholic liver disease, resulting from chronic alcohol use, includes conditions like fatty liver, alcoholic hepatitis, and cirrhosis. This study assessed TNF-α and leptin levels in 45 alcoholic liver disease patients, explored their relationship, and examined the rs1137101 polymorphism in the leptin receptor gene. Participants (mean age 40.13 ± 10.36) had consumed alcohol for an average of 15.31 ± 9.49 years at a daily intake of 253.33 ± 118.25 mL. TNF-α increased with age, while no age-leptin correlation was observed. TNF-α and leptin showed a negative correlation. The study identified a 48% minor allele G frequency for rs1137101. The findings highlight a significant correlation between TNF-α and leptin levels in alcoholic liver disease, suggesting potential roles as inflammatory mediators. More prospective studies are needed to enhance our understanding of these factors and improve disease management, potentially reducing morbidity and mortality rates.

Acknowledgments

The author sincerely acknowledges Ms. K. Sevvanthi, Biostatistician, AVMC, and Dr. F. Anto Nazarene, M.D, NCD District Programme Officer for helping with statistical analysis.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Availability of data

Primary Data are available on request.

Ethical approval

This study was approved by the Institutional Human Ethical Committee of our institute (IHEC.No: AV/IEC/2022/052), and we obtained informed consent from all the subjects included in the study.

Consent to participate

All authors declared their consent to participate.

Consent to publish

All authors declare their consent to publish their work.

Abbreviation

TNF-α=

Tumor Necrosis Factor-alpha

LEPR=

Leptin receptor

SNP=

Single Nucleotide Polymorphism

RFLP=

Restriction Fragment Length Polymorphism

Additional information

Funding

The financial support for this study was provided by the Indian Council of Medical Research (ICMR) through the ICMR-STS grant (2022-01822), acknowledged by the author AA, and the ICMR Senior Research Fellowship (3/1//1(25)/2022-NCD-1), acknowledged by the author MM. Additionally, the study received financial support from the ICMR Adhoc Project No.5/4-35 5/1-6/2020-NCD-II Project.

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