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PTER is a N-acetyltaurine hydrolase that regulates feeding and obesity.
Wei, Wei; Lyu, Xuchao; Markhard, Andrew L; Fu, Sipei; Mardjuki, Rachel E; Cavanagh, Peter E; Zeng, Xianfeng; Rajniak, Jakub; Lu, Nannan; Xiao, Shuke; Zhao, Meng; Moya-Garzon, Maria Dolores; Truong, Steven D; Chou, Jonathan Chiu-Chun; Wat, Lianna W; Chidambaranathan-Reghupaty, Saranya; Coassolo, Laetitia; Xu, Duo; Shen, Fangfang; Huang, Wentao; Ramirez, Cuauhtemoc B; Jang, Cholsoon; Li, Lingyin; Svensson, Katrin J; Fischbach, Michael A; Long, Jonathan Z.
Afiliação
  • Wei W; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Lyu X; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Markhard AL; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Fu S; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Mardjuki RE; Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
  • Cavanagh PE; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Zeng X; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Rajniak J; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Lu N; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Xiao S; Department of Biology, Stanford University, Stanford, CA, USA.
  • Zhao M; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Moya-Garzon MD; Department of Biochemistry, Stanford University, Stanford, CA, USA.
  • Truong SD; Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Chou JC; Department of Biochemistry, Stanford University, Stanford, CA, USA.
  • Wat LW; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Chidambaranathan-Reghupaty S; Department of Bioengineering, Stanford University, Stanford, CA, USA.
  • Coassolo L; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Xu D; Department of Bioengineering, Stanford University, Stanford, CA, USA.
  • Shen F; Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA.
  • Huang W; Wu Tsai Neurosciences Institute, Stanford University School of Medicine, Stanford, CA, USA.
  • Ramirez CB; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Jang C; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
  • Li L; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Svensson KJ; Stanford Diabetes Research Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Fischbach MA; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Long JZ; Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
Nature ; 633(8028): 182-188, 2024 Sep.
Article em En | MEDLINE | ID: mdl-39112712
ABSTRACT
Taurine is a conditionally essential micronutrient and one of the most abundant amino acids in humans1-3. In endogenous taurine metabolism, dedicated enzymes are involved in the biosynthesis of taurine from cysteine and in the downstream metabolism of secondary taurine metabolites4,5. One taurine metabolite is N-acetyltaurine6. Levels of N-acetyltaurine are dynamically regulated by stimuli that alter taurine or acetate flux, including endurance exercise7, dietary taurine supplementation8 and alcohol consumption6,9. So far, the identities of the enzymes involved in N-acetyltaurine metabolism, and the potential functions of N-acetyltaurine itself, have remained unknown. Here we show that the body mass index associated orphan enzyme phosphotriesterase-related (PTER)10 is a physiological N-acetyltaurine hydrolase. In vitro, PTER catalyses the hydrolysis of N-acetyltaurine to taurine and acetate. In mice, PTER is expressed in the kidney, liver and brainstem. Genetic ablation of Pter in mice results in complete loss of tissue N-acetyltaurine hydrolysis activity and a systemic increase in N-acetyltaurine levels. After stimuli that increase taurine levels, Pter knockout mice exhibit reduced food intake, resistance to diet-induced obesity and improved glucose homeostasis. Administration of N-acetyltaurine to obese wild-type mice also reduces food intake and body weight in a GFRAL-dependent manner. These data place PTER into a central enzymatic node of secondary taurine metabolism and uncover a role for PTER and N-acetyltaurine in body weight control and energy balance.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Taurina / Peso Corporal / Ingestão de Alimentos / Hidrolases / Obesidade Limite: Animals / Female / Humans / Male Idioma: En Revista: Nature Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Taurina / Peso Corporal / Ingestão de Alimentos / Hidrolases / Obesidade Limite: Animals / Female / Humans / Male Idioma: En Revista: Nature Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos