ArticleFrontiers in nutrition2026
Bioavailable human metabolites of a keratin-derived hydrolysate promote primary human dermal fibroblast activities and protect against oxidative stress-related damages.
Article in Frontiers in nutrition, 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
Introduction: Nutricosmetic strategies may support skin homeostasis by modulating dermal fibroblast function. Poultry feather keratin hydrolysates are a sustainable source of amino acids and low-molecular weight peptides. We investigated whether bioavailable human metabolites generated after ingestion of a keratin-derived hydrolysate (Kera‑Diet®) influence primary human dermal fibroblasts and protect against oxidative stress-related damage. Methods: Ten healthy fasted men ingested 5,000 mg Kera‑Diet®. Plasma amino acids were quantified over 240 min (UPLC-MS) to identify the absorption peak and to collect paired naïve human serum (NHS, pre-ingestion) and enriched human serum (EHS, peak time). Fibroblasts were incubated with NHS or EHS to assess viability, migration (scratch assay), and hydration markers (glycosaminoglycans and hyaluronan). Oxidative stress was induced with H₂O₂ and endpoints included ROS (DCF‑DA), apoptosis (caspase‑3), ER stress (XBP1 mRNA), and senescence (β‑galactosidase). Results: Circulating amino acids peaked at ~20 min post‑ingestion. Compared with NHS, EHS increased glycosaminoglycans (+11%) and hyaluronan release (+43%) and enhanced early migration. Under oxidative stress, Kera‑Diet® (in vitro) and EHS (ex vivo) mitigated cell stress by reducing ROS, caspase‑3 activity, XBP1 induction, and senescence, while preserving viability. Discussion: Bioavailable metabolites produced after oral keratin hydrolysate intake promote fibroblast anabolic/repair functions and blunt oxidative stress-linked ER stress, senescence, and apoptosis, supporting keratin hydrolysate-based nutritional approaches for skin health.
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