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An exercise-inducible metabolite that suppresses feeding and obesity.
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; Arthur, Rick M; 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.
Afiliação
  • Li VL; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • He Y; Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Contrepois K; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Liu H; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
  • Kim JT; Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
  • Wiggenhorn AL; Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Tanzo JT; Stanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
  • Tung AS; Stanford Diabetes Research Center, Stanford University, Stanford, CA, USA.
  • Lyu X; Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
  • Zushin PH; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Jansen RS; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Michael B; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Loh KY; Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Yang AC; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Carl CS; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Voldstedlund CT; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Wei W; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Terrell SM; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Moeller BC; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Arthur RM; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Wallis GA; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
  • van de Wetering K; Department of Nutrition and Toxicology, University of California Berkeley, Berkeley, CA, USA.
  • Stahl A; Netherlands Cancer Institute, Amsterdam, Netherlands.
  • Kiens B; Department of Microbiology, Radboud University, Nijmegen, Netherlands.
  • Richter EA; Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Banik SM; Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Snyder MP; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Xu Y; Department of Anatomy and the Bakar Aging Research Institute, University of California San Francisco, San Francisco, CA, USA.
  • Long JZ; August Krogh Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
Nature ; 606(7915): 785-790, 2022 06.
Article em En | MEDLINE | ID: mdl-35705806
Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases1-5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear6. 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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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fenilalanina / Condicionamento Físico Animal / Ingestão de Alimentos / Comportamento Alimentar / Obesidade Limite: Animals Idioma: En Revista: Nature Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
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PubMed Links
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fenilalanina / Condicionamento Físico Animal / Ingestão de Alimentos / Comportamento Alimentar / Obesidade Limite: Animals Idioma: En Revista: Nature Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Estados Unidos