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N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis

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Harvard

Grevengoed, TJ, Trammell, SAJ, McKinney, MK, Petersen, N, Cardone, RL, Svenningsen, JS, Ogasawara, D, Nexøe-Larsen, CC, Knop, FK, Schwartz, TW, Kibbey, RG, Cravatt, BF & Gillum, MP 2019, 'N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis' Proceedings of the National Academy of Sciences of the United States of America, bind 116, nr. 49, s. 24770-24778. https://doi.org/10.1073/pnas.1916288116

APA

Grevengoed, T. J., Trammell, S. A. J., McKinney, M. K., Petersen, N., Cardone, R. L., Svenningsen, J. S., ... Gillum, M. P. (2019). N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis. Proceedings of the National Academy of Sciences of the United States of America, 116(49), 24770-24778. https://doi.org/10.1073/pnas.1916288116

CBE

Grevengoed TJ, Trammell SAJ, McKinney MK, Petersen N, Cardone RL, Svenningsen JS, Ogasawara D, Nexøe-Larsen CC, Knop FK, Schwartz TW, Kibbey RG, Cravatt BF, Gillum MP. 2019. N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis. Proceedings of the National Academy of Sciences of the United States of America. 116(49): 24770-24778. https://doi.org/10.1073/pnas.1916288116

MLA

Vancouver

Author

Grevengoed, Trisha J ; Trammell, Samuel A J ; McKinney, Michele K ; Petersen, Natalia ; Cardone, Rebecca L ; Svenningsen, Jens S ; Ogasawara, Daisuke ; Nexøe-Larsen, Christina C ; Knop, Filip K ; Schwartz, Thue W ; Kibbey, Richard G ; Cravatt, Benjamin F ; Gillum, Matthew P. / N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis. I: Proceedings of the National Academy of Sciences of the United States of America. 2019 ; Bind 116, Nr. 49. s. 24770-24778.

Bibtex

@article{a6ea5a152bee495c99c1b5951ae6c759,
title = "N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis",
abstract = "Fatty acid amide hydrolase (FAAH) degrades 2 major classes of bioactive fatty acid amides, the N-acylethanolamines (NAEs) and N-acyl taurines (NATs), in central and peripheral tissues. A functional polymorphism in the human FAAH gene is linked to obesity and mice lacking FAAH show altered metabolic states, but whether these phenotypes are caused by elevations in NAEs or NATs is unknown. To overcome the problem of concurrent elevation of NAEs and NATs caused by genetic or pharmacological disruption of FAAH in vivo, we developed an engineered mouse model harboring a single-amino acid substitution in FAAH (S268D) that selectively disrupts NAT, but not NAE, hydrolytic activity. The FAAH-S268D mice accordingly show substantial elevations in NATs without alterations in NAE content, a unique metabolic profile that correlates with heightened insulin sensitivity and GLP-1 secretion. We also show that N-oleoyl taurine (C18:1 NAT), the most abundant NAT in human plasma, decreases food intake, improves glucose tolerance, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice. Together, these data suggest that NATs act as a class of lipid messengers that improve postprandial glucose regulation and may have potential as investigational metabolites to modify metabolic disease.",
keywords = "Fatty acid amide hydrolase, Lipid signaling, Metabolism, N-acyl taurines",
author = "Grevengoed, {Trisha J} and Trammell, {Samuel A J} and McKinney, {Michele K} and Natalia Petersen and Cardone, {Rebecca L} and Svenningsen, {Jens S} and Daisuke Ogasawara and Nex{\o}e-Larsen, {Christina C} and Knop, {Filip K} and Schwartz, {Thue W} and Kibbey, {Richard G} and Cravatt, {Benjamin F} and Gillum, {Matthew P}",
year = "2019",
month = "12",
day = "3",
doi = "10.1073/pnas.1916288116",
language = "English",
volume = "116",
pages = "24770--24778",
journal = "National Academy of Sciences. Proceedings",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "49",

}

RIS

TY - JOUR

T1 - N-acyl taurines are endogenous lipid messengers that improve glucose homeostasis

AU - Grevengoed, Trisha J

AU - Trammell, Samuel A J

AU - McKinney, Michele K

AU - Petersen, Natalia

AU - Cardone, Rebecca L

AU - Svenningsen, Jens S

AU - Ogasawara, Daisuke

AU - Nexøe-Larsen, Christina C

AU - Knop, Filip K

AU - Schwartz, Thue W

AU - Kibbey, Richard G

AU - Cravatt, Benjamin F

AU - Gillum, Matthew P

PY - 2019/12/3

Y1 - 2019/12/3

N2 - Fatty acid amide hydrolase (FAAH) degrades 2 major classes of bioactive fatty acid amides, the N-acylethanolamines (NAEs) and N-acyl taurines (NATs), in central and peripheral tissues. A functional polymorphism in the human FAAH gene is linked to obesity and mice lacking FAAH show altered metabolic states, but whether these phenotypes are caused by elevations in NAEs or NATs is unknown. To overcome the problem of concurrent elevation of NAEs and NATs caused by genetic or pharmacological disruption of FAAH in vivo, we developed an engineered mouse model harboring a single-amino acid substitution in FAAH (S268D) that selectively disrupts NAT, but not NAE, hydrolytic activity. The FAAH-S268D mice accordingly show substantial elevations in NATs without alterations in NAE content, a unique metabolic profile that correlates with heightened insulin sensitivity and GLP-1 secretion. We also show that N-oleoyl taurine (C18:1 NAT), the most abundant NAT in human plasma, decreases food intake, improves glucose tolerance, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice. Together, these data suggest that NATs act as a class of lipid messengers that improve postprandial glucose regulation and may have potential as investigational metabolites to modify metabolic disease.

AB - Fatty acid amide hydrolase (FAAH) degrades 2 major classes of bioactive fatty acid amides, the N-acylethanolamines (NAEs) and N-acyl taurines (NATs), in central and peripheral tissues. A functional polymorphism in the human FAAH gene is linked to obesity and mice lacking FAAH show altered metabolic states, but whether these phenotypes are caused by elevations in NAEs or NATs is unknown. To overcome the problem of concurrent elevation of NAEs and NATs caused by genetic or pharmacological disruption of FAAH in vivo, we developed an engineered mouse model harboring a single-amino acid substitution in FAAH (S268D) that selectively disrupts NAT, but not NAE, hydrolytic activity. The FAAH-S268D mice accordingly show substantial elevations in NATs without alterations in NAE content, a unique metabolic profile that correlates with heightened insulin sensitivity and GLP-1 secretion. We also show that N-oleoyl taurine (C18:1 NAT), the most abundant NAT in human plasma, decreases food intake, improves glucose tolerance, and stimulates GPR119-dependent GLP-1 and glucagon secretion in mice. Together, these data suggest that NATs act as a class of lipid messengers that improve postprandial glucose regulation and may have potential as investigational metabolites to modify metabolic disease.

KW - Fatty acid amide hydrolase

KW - Lipid signaling

KW - Metabolism

KW - N-acyl taurines

UR - http://www.scopus.com/inward/record.url?scp=85076052418&partnerID=8YFLogxK

U2 - 10.1073/pnas.1916288116

DO - 10.1073/pnas.1916288116

M3 - Journal article

VL - 116

SP - 24770

EP - 24778

JO - National Academy of Sciences. Proceedings

JF - National Academy of Sciences. Proceedings

SN - 0027-8424

IS - 49

ER -

ID: 58436211