ArticleEuropean journal of clinical nutrition2026
Evidence of docosahexaenoic acid deficiency in maple syrup urine disease: insights from plasma long-chain polyunsaturated fatty acid status.
Article in European journal of clinical 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
backgroundMaple syrup urine disease (MSUD) is an inherited metabolic disorder requiring protein restriction, often limiting intake of animal-derived foods. This raises concerns about long-chain polyunsaturated fatty acid (LC-PUFA) status. The primary aim of this study is to evaluate plasma n-3 and n-6 fatty acid levels in MSUD patients.
methodsThis single-center, cross-sectional study included 16 MSUD patients and 22 unaffected siblings sharing a similar household and environmental background. Dietary intake was recorded and plasma fatty acid profiles were analyzed.
resultsDietary assessments revealed significantly lower intakes of total fat and cholesterol (both p < 0.001) and n-3 PUFAs (p = 0.036) in MSUD patients, with alpha-linolenic acid (ALA) intake as the only individual LC-PUFA significantly reduced (p = 0.048). Plasma analysis showed significantly lower docosahexaenoic acid (DHA) levels in patients despite similar dietary DHA intake (p < 0.001), while arachidonic acid and mead acid were significantly elevated (both p < 0.001). Although plasma DHA concentrations showed a moderate positive correlation with dietary ALA intake (r = 0.516, p = 0.041), regression analysis showed that neither dietary ALA intake (B = 0.005, p = 0.584) nor the dietary n-6/n-3 PUFA ratio (B = -0.552, p = 0.706) independently predicted plasma DHA levels. In the MSUD group, plasma DHA levels were positively associated with dietary leucine intake (r = 0.635, p = 0.008) and plasma isoleucine concentrations (r = 0.524, p = 0.037).
conclusionOur findings provide evidence of DHA deficiency in MSUD patients, which may result from both inadequate dietary intake and changes in n-3 PUFA metabolism, highlighting the need to investigate additional contributing mechanisms.
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