ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2025
Apremilast attenuates hepatic steatosis and metabolic dysfunction in a murine model of MASLD: Implications for patients with Psoriatic disease.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Repurposing apremilast for alzheimer's disease: multitarget modulation of cAMP‑PI3K/Akt-GSK‑3β and NF‑κB signaling.Metabolic brain disease · 2026Review
- Imbalance of TCA-related miRNA-mRNA networks involving IDH2, SDHA, SDHC, and SUCLG1 drives psoriasis development.Frontiers in physiology · 2026Article
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19 authors.
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Abstract
backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a major cause of morbidity, linked to obesity, type 2 diabetes, and cardiovascular disease. Psoriatic disease (PsD), a chronic inflammatory condition, often coexists with MASLD, exacerbating systemic inflammation and cardiometabolic risk. Apremilast, a selective PDE4 inhibitor approved for PsD, may provide additional metabolic benefits by improving weight, lipid metabolism, and insulin sensitivity.
objectiveTo evaluate the effects of apremilast on metabolic dysfunction, hepatic steatosis, and systemic inflammation in PsD patients with metabolic comorbidities, and to investigate mechanistic impact in a murine model of diet-induced MASLD.
methodsTwenty PsD patients treated with apremilast were stratified by metabolic comorbidities. Glucose metabolism and liver function were monitored for 6 months. In parallel, C57BL/6 J mice were fed chow or GAN diet. After 14 weeks, apremilast (10 mg/kg/day) was administered for two weeks. Body weight, adiposity, liver biomarkers, insulin resistance, histology, and proteomics were evaluated.
resultsIn PsD patients with comorbidities, apremilast reduced fasting insulin, HOMA-IR, transaminases, and the hepatic steatosis index. GAN-fed mice developed steatosis, increased fat mass, and elevated alanine aminotransferase (ALT) and HOMA-IR levels. Apremilast reduced body weight, ALT, insulin resistance, and hepatic fat. Histology confirmed a decrease in fibrosis. Proteomic profiling showed modulation of inflammatory, fibrotic, and lipid metabolic pathways, partially reversing GAN-induced proinflammatory signatures in liver, adipose tissue, and muscle.
conclusionsApremilast ameliorates hepatic dysfunction, improves insulin sensitivity, and reduces systemic metabolic dysfunction in a murine MASLD model. These findings support its therapeutic potential in PsD patients with metabolic disease, offering both anti-inflammatory and metabolic benefits.
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