# Leptin, vitamin D, and APRI values during the six months post-liver transplantation

**Authors:** Yasmine A. Algobashy, A. S. shehatta, Mabdel Wahab, Magdy M. Youssef

PMC · DOI: 10.1186/s12876-026-04640-9 · BMC Gastroenterology · 2026-02-20

## TL;DR

This study explores how leptin, vitamin D, and APRI values change after liver transplantation and their role in liver fibrosis progression.

## Contribution

The study identifies leptin and vitamin D as potential biomarkers for liver fibrosis and explores their relationship with extracellular matrix proteins.

## Key findings

- Serum leptin and APRI values decreased significantly after liver transplantation.
- Serum vitamin D levels increased significantly after liver transplantation.
- Leptin and vitamin D are linked to extracellular matrix proteins involved in liver fibrosis.

## Abstract

Liver fibrosis is a common outcome of chronic liver disease, characterized by accumulating extracellular matrix proteins. Aims: While the gold standard in the assessment of liver fibrosis remains liver biopsy, non-invasive methods have been increasingly used for estimating liver fibrosis. This study aims at contributing to our understanding of the role of leptin,vitamin D, APRI, and FIB-4 in the progression of liver disease. For this purpose, we evaluate the clinical significance of leptin, vitamin D, APRI, and FIB-4 in cirrhotic patients with different ratios of steatosis and in cirrhotic pateints with different grades of hepatocellular carcinoma. We compare the performance of simple biochemical scores (FIB-4 and APRI) with leptin and vitamin D. Also, We identified the proteins in the serum of liver fibrosis and showed the role of these proteins in the pathogenesis of liver fibrosis. Also, we identified the relationship between leptin and vitamin D with extracellular matrix proteins using bioinformatics analysis.

The current study included 50 liver fibrosis patients who underwent liver transplantation. We measured the levels of serum vitamin D and leptin in these patients at pre-LT and three- and six-months post-LT using enzyme-linked immunosorbent assay. We performed qualitative proteomic analysis to identify the proteins in the sera from patients with liver fibrosis. Among these proteins, there are extracellular matrix proteins. One-way ANOVA test was used.

We found that serum leptin levels and APRI values were significantly higher in liver fibrosis patients than in controls, after three- and six-months following LT serum leptin levels and APRI values significantly decreased. While serum vitamin D levels were significantly lower in liver fibrosis patients than in controls, after three- and six-months following LT, serum vitamin D levels significantly increased. ROC curves analysis showed that the area under the curve (AUC) of vitamin D and leptin was 1 and 0.997, respectively. Gene ontology analysis demonstrated that the proteins participate in a diverse array of biological processes, emphasizing the systemic effects of liver fibrosis disease. From the STRING database, the proteins are at least partially biologically connected, as a group with leptin and vitamin D explaining the promiscuous nature of leptin and vitamin D. This emphasized the role of leptin and vitamin D in accumulation and increased synthesis of extracellular matrix proteins that incorporated in the pathogenesis of liver fibrosis, and showed that the leptin and vitamin D are involved in the pathogenesis process where the total proteins are involved.

In summary, serum vitamin D and leptin could serve as a valuable supplemental biomarker for predicting the liver fibrosis.

## Linked entities

- **Chemicals:** leptin (PubChem CID 157010069)
- **Diseases:** hepatocellular carcinoma (MONDO:0007256)

## Full-text entities

- **Genes:** AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, ITIH4 (inter-alpha-trypsin inhibitor heavy chain 4) [NCBI Gene 3700] {aka GP120, H4P, IHRP, ITI-HC4, ITIHL1, PK-120}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, THPO (thrombopoietin) [NCBI Gene 7066] {aka CAMT2, MGDF, MKCSF, ML, MPLLG, THC9}, VTN (vitronectin) [NCBI Gene 7448] {aka V75, VN, VNT}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, ITIH1 (inter-alpha-trypsin inhibitor heavy chain 1) [NCBI Gene 3697] {aka H1P, IATIH, ITI-HC1, ITIH, SHAP}, ITIH3 (inter-alpha-trypsin inhibitor heavy chain 3) [NCBI Gene 3699] {aka H3P, ITI-HC3, SHAP}, ITIH2 (inter-alpha-trypsin inhibitor heavy chain 2) [NCBI Gene 3698] {aka H2P, ITI-HC2, SHAP}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, PPARA (peroxisome proliferator activated receptor alpha) [NCBI Gene 5465] {aka NR1C1, PPAR, PPAR-alpha, PPARalpha, hPPAR}, ITIH5 (inter-alpha-trypsin inhibitor heavy chain 5) [NCBI Gene 80760] {aka ITI-HC5, PP14776}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, LUM (lumican) [NCBI Gene 4060] {aka LDC, SLRR2D}, AMBP (alpha-1-microglobulin/bikunin precursor) [NCBI Gene 259] {aka A1M, EDC1, HCP, HI30, IATIL, ITI}, A2M (alpha-2-macroglobulin) [NCBI Gene 2] {aka A2MD, CPAMD5, FWP007, S863-7}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}
- **Diseases:** coagulation (MESH:D001778), tumor (MESH:D009369), cholestatic damage (MESH:D002779), Liver fibrosis (MESH:D008103), anorexia (MESH:D000855), hepatitis B and C (MESH:D006509), chronic inflammatory liver disease (MESH:D008107), hepatocyte injury (MESH:D014947), Fibrosis (MESH:D005355), complement (MESH:D007153), biliary atresia (MESH:D001656), cirrhotic (MESH:D000094724), viral infections (MESH:D014777), HCC (MESH:D006528), Primary biliary cholangitis (MESH:D008105), fibrotic tissues (MESH:D017695), hepatocyte damage (MESH:D020263), gastrointestinal bleeding (MESH:D006471), primary sclerosing cholangitis (MESH:D015209), Steatosis (MESH:D005234), alcoholic and non-alcoholic steatohepatitis (MESH:D005235), obesity (MESH:D009765), chronic liver damage (MESH:D056487), cholestatic liver injuries (MESH:D017093), liver carcinogenesis (MESH:D063646)
- **Chemicals:** Urea (MESH:D014508), TFA (MESH:D014269), ACN (MESH:C032159), acetone (MESH:D000096), BCA (-), Vitamin D (MESH:D014807), methanol (MESH:D000432), formic acid (MESH:C030544), DTT (MESH:D004229), fluoroacetic acid (MESH:C014815), FA (MESH:D005492), hyaluronan (MESH:D006820), IAA (MESH:D007460)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** C4-A

## Full text

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## Figures

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## References

3 references — full list in the complete paper: https://tomesphere.com/paper/PMC12930583/full.md

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Source: https://tomesphere.com/paper/PMC12930583