An exercise-inducible metabolite that suppresses feeding and obesity
Open accessAbstract
Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases 1-5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear 6. Here we show that exercise stimulates the production of N-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity. The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and other immune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure. Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training. Last, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species. These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.
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A recent study revealed that lactate reduced appetite via N-lactoyl-phenylalanine (Lac-Phe) and exerted neuroplastic effects through the BDNF pathway.
“A recent study revealed that lactate reduced appetite via N-lactoyl-phenylalanine (Lac-Phe) and exerted neuroplastic effects through the BDNF pathway [58].”
From High-intensity interval training or lactate administration combined with aerobic training enhances visceral fat loss while promoting VMH neuroplasticity in female rats (2024) · cites this paper as [58]
The 'Lac-Phe suppresses feeding and obesity' section reports that Lac-Phe reduced food intake in diet-induced obese mice, while lactate alone had no effect. The Discussion says Lac-Phe’s downstream mediators in the brain remain unidentified; the paper does not establish neuroplastic effects through a BDNF pathway. Page numbers are unavailable in our copy. (LLM, conf=0.91)
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“One latest evidence published in Nature detected that exercise–inducible metabolite can control food intake and influence systemic energy balance, which might partially support the mediation effects of dietary from the mechanism perspective (72).”
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Cooperative nutrient scavenging is an evolutionary advantage in cancer
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“In fact, previous evidence indicates that stromal cells – specially macrophages - display high levels of CNDP2 (Li et al , 2022).”
Exercise-induced hypothalamic neuroplasticity: Implications for energy and glucose metabolism
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BackgroundInfluentialPlasma Proteomic Kinetics in Response to Acute Exercise
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“On average, participants achieved an adequate level of exercise stress, as demonstrated by percent-predicted peak heart rate of 90% (14) and METs of 9.”
BackgroundDietary timing enhances exercise by modulating fat-muscle crosstalk via adipocyte AMPKα2 signaling
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“Acute Lac-Phe injection reduces food intake in diet-induced obese mice by ~ 50% and daily injections reduce body weight by ~ 7% over a 10-day period (Li et al., 2022).”
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“16 It is synthesized through the condensation of lactic acid from skeletal muscles and phenylalanine in the body, catalyzed by the cytoplasmic enzyme carnosine dipeptidase 2 (CNDP2).”
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“Recently, exercise was reported to increase both the human and racehorse plasma metabolite, N - lactoyl-phenylalanine (Lac-Phe), which suppressed feeding and obesity in mice ( 71 ).”
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“86 Legaard et al. 87 conducted a 16-week intervention study focusing on the effects of dietary changes coupled with exercise in patients diagnosed with T2D within the preceding 7 years.”
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BackgroundResultInfluentialA diverse proteome is present and enzymatically active in metabolite extracts
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Self-citationThe clinical relevance of novel biomarkers as outcome parameter in adults with phenylketonuria
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“23,49 The N-lactoyl-Phe concentrations correlated strongly with lactate concentrations, but normalized more slowly than lactate.”
InfluentialHow can physical activity facilitate a sustainable future? Reducing obesity and chronic disease
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METTL3 Is Essential for Exercise Benefits in Diabetic Cardiomyopathy
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Self-citationLactate-Mediated Signaling in the Brain—An Update
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“This product of conjugation of Lac with phenylalanine is formed in the periphery when Lac levels are increased by exercise in mice, humans and racehorses, and can suppress food consumption [66].”
BackgroundThe Power and Connection of the Six Pillars
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“Lac-Phe was found to increase with exercise, and reduced food intake and appetite.(5)”
BackgroundQuantitative challenges and their bioinformatic solutions in mass spectrometry-based metabolomics
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Molecular Insights From Multiomics Studies of Physical Activity
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Hallmarks of the metabolic secretome
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SLC17A1/3 transporters mediate renal excretion of Lac-Phe in mice and humans
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“First, CNDP2 is an intracellular, cytosolic enzyme, yet Lac-Phe is enriched in the conditioned medium of cultured cells 9 .”
InfluentialSelf-citationABHD7-mediated depalmitoylation of lamin A promotes myoblast differentiation
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“76 Recent studies have associated lac-AAs with various physiological and pathological conditions, including exercise, 77 prediabetes and diabetes, 47 appetite suppression, 37 and poor outcomes in septic shock.”
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“Indeed, a recent study highlighted that exercise-induced lactate is used as a precursor for the synthesis of N-lactoyl-phenylalanine, a metabolite shown to possess anorexic properties in rodents following pharmacological administration (Li et al., 2022).”
- Authors
- Li, V. L., He, Y., Contrepois, K., Liu, H., Kim, J. T., Wiggenhorn, A. L., Tanzo, J. T., Tung, A. S.-H., Lyu, X., Zushin, P.-J. H., Jansen, R. S., Michael, B., Loh, K. Y., Yang, A. C., Carl, C. S., Voldstedlund, C. T., Wei, W., Terrell, S. M., Moeller, B. C., Arthur, R. M., Wallis, G. A., van de Wetering, K., Stahl, A., Kiens, B., Richter, E. A., Banik, S. M., Snyder, M. P., Xu, Y., & Long, J. Z.
- Affiliations
- Stanford Medicine (US)
- Baylor College of Medicine (US)
- University of California, Berkeley (US)
- Radboud University Nijmegen (NL)
- Stanford University (US)
- University of California, San Francisco (US)
- University of Copenhagen (DK)
- University of California, Davis (US)
- University of Birmingham (GB)
- Corresponding author
- Xu, Yong
- Long, Jonathan Z.
- ORCID
- Li, Veronica L.
- He, Yang
- Contrepois, Kévin
- Liu, Hailan
- Kim, Joon T.
- Wiggenhorn, Amanda L.
- Tanzo, Julia T.
- Tung, Alan Sheng-Hwa
- Lyu, Xuchao
- Zushin, Peter-James H.
- Jansen, Robert S.
- Michael, Basil
- Loh, Kang Yong
- Yang, Andrew C.
- Carl, Christian S.
- Voldstedlund, Christian T.
- Wei, Wei
- Terrell, Stephanie M.
- Moeller, Benjamin C.
- Wallis, Gareth A.
- van de Wetering, Koen
- Stahl, Andreas
- Kiens, Bente
- Richter, Erik A.
- Banik, Steven M.
- Snyder, Michael P.
- Xu, Yong
- Long, Jonathan Z.
- Venue
- Nature
- Published
- 2022-06-15
- Volume
- 606
- Issue
- 7915
- Pages
- 785-790
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC9767481
- OpenAlex
- W4282972916
- Cited by
- 331
- References
- 31
- Citations by year
- 2026: 69 · 2025: 91 · 2024: 86 · 2023: 61 · 2022: 24
- FWCI
- 34.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (publishedVersion, other-oa)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
- PubMed Central (acceptedVersion)
- Digital Commons-TMC (Texas Medical Center) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- U.S. Department of Agriculture (51000-064-01S)
- American Heart Association (20POST35120600)
- Novo Nordisk
- Novo Nordisk Fonden (NNF18OC0034072, NNF17OC0027274)
- Ono Pharma Foundation
- National Institutes of Health (DK130541, 51000-064-01S, DK113954)
- National Institute of General Medical Sciences (T32GM113854)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK124265, R01DK120858, R01DK118940, P01DK113954, R01DK126830, R01DK117281, R01DK115761, DP1DK130641, R01DK109934, P30DK020579)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR072695)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- physical activity, feeding inhibition, obesity, dietary intake, energy balance, lactate, phenylalanine, CNDP2, macrophages, monocytes, glucose homeostasis, diet-induced obesity, exercise training, racehorses
- MeSH terms
- Animals, Body Weight, Diabetes Mellitus, Type 2, Disease Models, Animal, Eating, Energy Metabolism, Feeding Behavior, Glucose, Obesity, Phenylalanine, Physical Conditioning, Animal, Lactic Acid, Adiposity, Mice
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