ArticleNutrition & metabolism2026
Ketosis elevates plasma concentrations of D-β-hydroxybutyryl-phenylalanine (BHB-Phe) in humans.
Article in Nutrition & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 4 registered trials, which are not on this map. Not yet cited in PubMed.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Metabolic Differences of an Oral and Intravenous Dose of 3-hydroxybutyrate (3-OHB).
The Effects of Ketogenic Diet on the Cardiac Substrate Metabolism and Brain Perfusion
3-hydroxybutyrate as a Meal Primer in Patients With Type 2 Diabetes
Pre-meals of 3-hydroxybutyrate for People With Type 2 Diabetes
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11 authors.
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Abstract
introductionβ-hydroxybutyrate (BHB), produced during ketosis, can conjugate with amino acids forming BHB-amino acids. D-BHB-phenylalanine (D-BHB-Phe) is the most abundant BHB-amino acid and has been shown to reduce appetite and induce weight loss in mice, but its function and regulation in humans remain unclear. The objective of this study was to determine whether D-BHB-Phe concentrations vary across different degrees and forms of ketosis in humans.
methodsPlasma D-BHB-Phe was measured in samples from four clinical cross-over trials (i) after 21 days on a ketogenic diet (n = 10), (ii) after oral consumption of 30 g ketone salt (KS) and 30 g ketone ester (KE) (n = 14), (iii) after oral KE at doses of 10, 20 and 40 g (n = 10) and (iv) after oral versus intravenous KS administration (n = 8).
resultsAfter 21 days of ketogenic dieting, plasma D-BHB-Phe became detectable (median 2.1 nmol/L; range 0.9-19.9), compared with near-undetectable concentrations during the standard diet (median 0; range 0-0.9; p = 0.005). Oral KS and KE increased D-BHB-Phe compared with placebo (intervention x time, p < 0.001). D-BHB-Phe rose dose-dependently after 10 g, 20 g, and 40 g of KE (intervention x time, p < 0.001). Oral KS induced higher peak concentrations of D-BHB-Phe (15.6 ± 6.4 nmol/L) compared with iso-ketotic intravenous KS infusion, which elicited only a modest peak (1.5 ± 0.3 nmol/L; intervention x time, p < 0.001). A positive association between the D-BHB and D-BHB-Phe concentration was observed in pooled analyses but was not consistent across cohorts.
conclusionD-BHB-Phe is inducible by ketosis in humans. Our findings suggest involvement of the splanchnic bed in its production and support further exploration of D-BHB-Phe's role in appetite regulation and metabolic health. CLINICAL TRIAL REGISTRATIONS: NCT05012748, NCT03935841, NCT05263401, NCT05581043.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.