# PCSK9 inhibitors improve lipid profile and hepatic steatosis surrogate indicators in patients with MAFLD and type 2 diabetes

**Authors:** Qingna Zhou, Xiaoxia Liu, Yunzhao Tang, Congqing Pan, Xuena Bi

PMC · DOI: 10.3389/fmed.2026.1756998 · 2026-03-05

## TL;DR

PCSK9 inhibitors improve liver health and cholesterol levels in patients with MAFLD and type 2 diabetes compared to standard treatment.

## Contribution

This study demonstrates that PCSK9 inhibitors provide greater improvement in hepatic steatosis and lipid profiles in MAFLD patients with T2DM.

## Key findings

- PCSK9i group showed greater reductions in TC and LDL-C compared to the control group.
- PCSK9i led to significant improvements in CAP and FLI, indicating reduced hepatic steatosis.
- The benefits of PCSK9i were independent of SGLT-2i therapy.

## Abstract

To investigate the impact of proprotein convertase subtilisin kexin type-9 inhibitor (PCSK9i) on patients with metabolic dysfunction-associated fatty liver disease (MAFLD) combined with type 2 diabetes mellitus (T2DM).

This retrospective study reviewed the clinical data of 60 inpatients with MAFLD combined with T2DM from the electronic medical record (EMR) system. According to the medical records, all patients were categorized into the Control group (n = 30, atorvastatin 20 mg QN) and the PCSK9i group (n = 30, evolocumab injection 140 mg Q2W in addition to atorvastatin). Body mass index (BMI), glycemic control, hepatic fibrosis and steatosis surrogate indicators such as aspartate aminotransferase to platelet ratio index (APRI), fibrosis-4 index (FIB-4), fatty liver index (FLI) and controlled attenuation parameter (CAP), and lipid profiles, including total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), were analyzed at baseline and the 12-week follow-up in both groups. Multivariable regression analyses for changes in hepatic fibrosis and steatosis surrogate indicators were performed.

At the 12-week follow-up, both groups exhibited significant reductions in lipid levels, with the PCSK9i group demonstrating greater decreases in TC (48.65 vs. 23.32%) and LDL-C (25.84 vs. 21.09%) compared to the Control group (P < 0.05). Meanwhile, the PCSK9i group exhibited significantly greater reductions in CAP (22.41 vs. 15.60%) and FLI (27.72 vs. 13.77%) in unadjusted analyses (both P < 0.05). Multivariable regression analyses demonstrated the superior improvement in CAP and FLI observed with PCSK9-i is independent of concomitant sodium-glucose co-transporter 2 inhibitor (SGLT-2i) therapy.

PCSK9i effectively reduced hepatic steatosis surrogate scores (FLI, CAP) and lipid levels (TC, LDL-C) in patients with MAFLD combined with T2DM.

## Linked entities

- **Proteins:** PCSK9 (proprotein convertase subtilisin/kexin type 9)
- **Chemicals:** atorvastatin (PubChem CID 60823)
- **Diseases:** type 2 diabetes mellitus (MONDO:0005148)

## Full-text entities

- **Genes:** PCSK9 (proprotein convertase subtilisin/kexin type 9) [NCBI Gene 255738] {aka FH3, FHCL3, HCHOLA3, LDLCQ1, NARC-1, NARC1}
- **Diseases:** fibrosis (MESH:D005355), T2DM (MESH:D003924), MAFLD (MESH:D005234), hepatic fibrosis (MESH:D008103)
- **Chemicals:** atorvastatin (MESH:D000069059), SGLT-2i (-), evolocumab (MESH:C577155), cholesterol (MESH:D002784), lipid (MESH:D008055), TG (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12999965/full.md

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Source: https://tomesphere.com/paper/PMC12999965