Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use

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Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use. / Worthmann, Anna; Ridder, Julius; Piel, Sharlaine Y L; Evangelakos, Ioannis; Musfeldt, Melina; Voß, Hannah; O'Farrell, Marie; Fischer, Alexander W; Adak, Sangeeta; Sundd, Monica; Siffeti, Hasibullah; Haumann, Friederike; Kloth, Katja; Bierhals, Tatjana; Heine, Markus; Pertzborn, Paul; Pauly, Mira; Scholz, Julia-Josefine; Kundu, Suman; Fuh, Marceline M; Neu, Axel; Tödter, Klaus; Hempel, Maja; Knippschild, Uwe; Semenkovich, Clay F; Schlüter, Hartmut; Heeren, Joerg; Scheja, Ludger; Kubisch, Christian; Schlein, Christian.

in: NAT COMMUN, Jahrgang 15, Nr. 1, 02.01.2024, S. 45.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Worthmann, A, Ridder, J, Piel, SYL, Evangelakos, I, Musfeldt, M, Voß, H, O'Farrell, M, Fischer, AW, Adak, S, Sundd, M, Siffeti, H, Haumann, F, Kloth, K, Bierhals, T, Heine, M, Pertzborn, P, Pauly, M, Scholz, J-J, Kundu, S, Fuh, MM, Neu, A, Tödter, K, Hempel, M, Knippschild, U, Semenkovich, CF, Schlüter, H, Heeren, J, Scheja, L, Kubisch, C & Schlein, C 2024, 'Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use', NAT COMMUN, Jg. 15, Nr. 1, S. 45. https://doi.org/10.1038/s41467-023-44364-y

APA

Worthmann, A., Ridder, J., Piel, S. Y. L., Evangelakos, I., Musfeldt, M., Voß, H., O'Farrell, M., Fischer, A. W., Adak, S., Sundd, M., Siffeti, H., Haumann, F., Kloth, K., Bierhals, T., Heine, M., Pertzborn, P., Pauly, M., Scholz, J-J., Kundu, S., ... Schlein, C. (2024). Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use. NAT COMMUN, 15(1), 45. https://doi.org/10.1038/s41467-023-44364-y

Vancouver

Bibtex

@article{eff16cba5c44448a84f71118cdaef214,
title = "Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use",
abstract = "Dietary polyunsaturated fatty acids (PUFA) are increasingly recognized for their health benefits, whereas a high production of endogenous fatty acids - a process called de novo lipogenesis (DNL) - is closely linked to metabolic diseases. Determinants of PUFA incorporation into complex lipids are insufficiently understood and may influence the onset and progression of metabolic diseases. Here we show that fatty acid synthase (FASN), the key enzyme of DNL, critically determines the use of dietary PUFA in mice and humans. Moreover, the combination of FASN inhibition and PUFA-supplementation decreases liver triacylglycerols (TAG) in mice fed with high-fat diet. Mechanistically, FASN inhibition causes higher PUFA uptake via the lysophosphatidylcholine transporter MFSD2A, and a diacylglycerol O-acyltransferase 2 (DGAT2)-dependent incorporation of PUFA into TAG. Overall, the outcome of PUFA supplementation may depend on the degree of endogenous DNL and combining PUFA supplementation and FASN inhibition might be a promising approach to target metabolic disease.",
keywords = "Mice, Humans, Animals, Lipogenesis, Fatty Acids, Omega-3/pharmacology, Fatty Acids, Unsaturated, Triglycerides/metabolism, Fatty Acids, Diet, High-Fat/adverse effects, Metabolic Diseases",
author = "Anna Worthmann and Julius Ridder and Piel, {Sharlaine Y L} and Ioannis Evangelakos and Melina Musfeldt and Hannah Vo{\ss} and Marie O'Farrell and Fischer, {Alexander W} and Sangeeta Adak and Monica Sundd and Hasibullah Siffeti and Friederike Haumann and Katja Kloth and Tatjana Bierhals and Markus Heine and Paul Pertzborn and Mira Pauly and Julia-Josefine Scholz and Suman Kundu and Fuh, {Marceline M} and Axel Neu and Klaus T{\"o}dter and Maja Hempel and Uwe Knippschild and Semenkovich, {Clay F} and Hartmut Schl{\"u}ter and Joerg Heeren and Ludger Scheja and Christian Kubisch and Christian Schlein",
note = "{\textcopyright} 2024. The Author(s).",
year = "2024",
month = jan,
day = "2",
doi = "10.1038/s41467-023-44364-y",
language = "English",
volume = "15",
pages = "45",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Fatty acid synthesis suppresses dietary polyunsaturated fatty acid use

AU - Worthmann, Anna

AU - Ridder, Julius

AU - Piel, Sharlaine Y L

AU - Evangelakos, Ioannis

AU - Musfeldt, Melina

AU - Voß, Hannah

AU - O'Farrell, Marie

AU - Fischer, Alexander W

AU - Adak, Sangeeta

AU - Sundd, Monica

AU - Siffeti, Hasibullah

AU - Haumann, Friederike

AU - Kloth, Katja

AU - Bierhals, Tatjana

AU - Heine, Markus

AU - Pertzborn, Paul

AU - Pauly, Mira

AU - Scholz, Julia-Josefine

AU - Kundu, Suman

AU - Fuh, Marceline M

AU - Neu, Axel

AU - Tödter, Klaus

AU - Hempel, Maja

AU - Knippschild, Uwe

AU - Semenkovich, Clay F

AU - Schlüter, Hartmut

AU - Heeren, Joerg

AU - Scheja, Ludger

AU - Kubisch, Christian

AU - Schlein, Christian

N1 - © 2024. The Author(s).

PY - 2024/1/2

Y1 - 2024/1/2

N2 - Dietary polyunsaturated fatty acids (PUFA) are increasingly recognized for their health benefits, whereas a high production of endogenous fatty acids - a process called de novo lipogenesis (DNL) - is closely linked to metabolic diseases. Determinants of PUFA incorporation into complex lipids are insufficiently understood and may influence the onset and progression of metabolic diseases. Here we show that fatty acid synthase (FASN), the key enzyme of DNL, critically determines the use of dietary PUFA in mice and humans. Moreover, the combination of FASN inhibition and PUFA-supplementation decreases liver triacylglycerols (TAG) in mice fed with high-fat diet. Mechanistically, FASN inhibition causes higher PUFA uptake via the lysophosphatidylcholine transporter MFSD2A, and a diacylglycerol O-acyltransferase 2 (DGAT2)-dependent incorporation of PUFA into TAG. Overall, the outcome of PUFA supplementation may depend on the degree of endogenous DNL and combining PUFA supplementation and FASN inhibition might be a promising approach to target metabolic disease.

AB - Dietary polyunsaturated fatty acids (PUFA) are increasingly recognized for their health benefits, whereas a high production of endogenous fatty acids - a process called de novo lipogenesis (DNL) - is closely linked to metabolic diseases. Determinants of PUFA incorporation into complex lipids are insufficiently understood and may influence the onset and progression of metabolic diseases. Here we show that fatty acid synthase (FASN), the key enzyme of DNL, critically determines the use of dietary PUFA in mice and humans. Moreover, the combination of FASN inhibition and PUFA-supplementation decreases liver triacylglycerols (TAG) in mice fed with high-fat diet. Mechanistically, FASN inhibition causes higher PUFA uptake via the lysophosphatidylcholine transporter MFSD2A, and a diacylglycerol O-acyltransferase 2 (DGAT2)-dependent incorporation of PUFA into TAG. Overall, the outcome of PUFA supplementation may depend on the degree of endogenous DNL and combining PUFA supplementation and FASN inhibition might be a promising approach to target metabolic disease.

KW - Mice

KW - Humans

KW - Animals

KW - Lipogenesis

KW - Fatty Acids, Omega-3/pharmacology

KW - Fatty Acids, Unsaturated

KW - Triglycerides/metabolism

KW - Fatty Acids

KW - Diet, High-Fat/adverse effects

KW - Metabolic Diseases

U2 - 10.1038/s41467-023-44364-y

DO - 10.1038/s41467-023-44364-y

M3 - SCORING: Journal article

C2 - 38167725

VL - 15

SP - 45

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -