ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Calpain inhibition by calpeptin modulates adipocyte lipid metabolism and secretome-mediated inflammatory crosstalk with hepatocytes.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveCalpeptin, a calpain inhibitor with potential for treating inflammatory diseases, reduces extracellular vesicle (EV) secretion. While adipose tissue is a recognized target of calpeptin, its effects on lipid metabolism remain unknown. We investigated calpeptin's impact on fatty acid (FA) profiles and metabolic pathways in human Simpson-Golabi-Behmel Syndrome adipocytes and their EVs.
methodsAdipocytes were treated with 25 or 50 µM calpeptin, and EVs were isolated from conditioned media (CM) by ultracentrifugation. Immortalized human hepatocytes (IHHs) were pre-treated with 0 or 400 µM palmitic acid (PA) and subsequently exposed to CM from calpeptin-treated adipocytes. Total lipid FA composition was determined by gas chromatography-mass spectrometry, and gene expression with RNA-sequencing and qPCR, followed by univariate and multivariate statistics and pathway analyses.
resultsCalpeptin reduced EV secretion and arachidonic acid proportions in adipocytes, while also perturbing key metabolic pathways, including those of the dietarily essential polyunsaturated FAs (PUFAs). Potential biomarker candidates associated with calpeptin included C20-22 PUFAs (adipocytes) and 23:0 (EVs). Both PA and the secretome from calpeptin-treated adipocytes induced pro-inflammatory responses in IHHs.
conclusionThe findings suggest that calpeptin may modulate adipocyte lipid metabolism and EV secretion, with associated inflammatory responses in hepatocytes likely mediated by adipocyte‑derived secreted factors. These observations warrant further investigation into the potential adverse effects of calpeptin in the context of metabolic diseases.
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