Hankir, M. K., Seyfried, F., Hintschich, C. A., Diep, T.-A., Kleberg, K., Kranz, M., Deuther-Conrad, W., Tellez, L. A., Rullmann, M., Patt, M., Teichert, J., Hesse, S., Sabri, O., Brust, P., Hansen, H. S., de Araujo, I. E., Krügel, U., & Fenske, W. K. (2017). Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats. Cell Metabolism, 25(2), 335-344. https://doi.org/10.1016/j.cmet.2016.12.006
Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats. / Hankir, Mohammed K; Seyfried, Florian; Hintschich, Constantin A et al.
In:
Cell Metabolism, Vol. 25, No. 2, 07.02.2017, p. 335-344.
Research output: Contribution to journal › Journal article › Research › peer-review
Hankir, MK, Seyfried, F, Hintschich, CA, Diep, T-A, Kleberg, K, Kranz, M, Deuther-Conrad, W, Tellez, LA, Rullmann, M, Patt, M, Teichert, J, Hesse, S, Sabri, O, Brust, P, Hansen, HS, de Araujo, IE, Krügel, U & Fenske, WK 2017, 'Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats', Cell Metabolism, vol. 25, no. 2, pp. 335-344. https://doi.org/10.1016/j.cmet.2016.12.006
Hankir MK, Seyfried F, Hintschich CA, Diep TA, Kleberg K, Kranz M et al. Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats. Cell Metabolism. 2017 Feb 7;25(2):335-344. doi: 10.1016/j.cmet.2016.12.006
Hankir, Mohammed K ; Seyfried, Florian ; Hintschich, Constantin A et al. / Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats. In: Cell Metabolism. 2017 ; Vol. 25, No. 2. pp. 335-344.
@article{a83e83e125c443f891713daec7b6d321,
title = "Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats",
abstract = "Bariatric surgery remains the single most effective long-term treatment modality for morbid obesity, achieved mainly by lowering caloric intake through as yet ill-defined mechanisms. Here we show in rats that Roux-en-Y gastric bypass (RYGB)-like rerouting of ingested fat mobilizes lower small intestine production of the fat-satiety molecule oleoylethanolamide (OEA). This was associated with vagus nerve-driven increases in dorsal striatal dopamine release. We also demonstrate that RYGB upregulates striatal dopamine 1 receptor (D1R) expression specifically under high-fat diet feeding conditions. Mechanistically, interfering with local OEA, vagal, and dorsal striatal D1R signaling negated the beneficial effects of RYGB on fat intake and preferences. These findings delineate a molecular/systems pathway through which bariatric surgery improves feeding behavior and may aid in the development of novel weight loss strategies that similarly modify brain reward circuits compromised in obesity.",
keywords = "Journal Article",
author = "Hankir, {Mohammed K} and Florian Seyfried and Hintschich, {Constantin A} and Thi-Ai Diep and Karen Kleberg and Mathias Kranz and Winnie Deuther-Conrad and Tellez, {Luis A} and Michael Rullmann and Marianne Patt and Jens Teichert and Swen Hesse and Osama Sabri and Peter Brust and Hansen, {Harald S} and {de Araujo}, {Ivan E} and Ute Kr{\"u}gel and Fenske, {Wiebke K}",
note = "Copyright {\textcopyright} 2017 Elsevier Inc. All rights reserved.",
year = "2017",
month = feb,
day = "7",
doi = "10.1016/j.cmet.2016.12.006",
language = "English",
volume = "25",
pages = "335--344",
journal = "Cell Metabolism",
issn = "1550-4131",
publisher = "Cell Press",
number = "2",
}
TY - JOUR
T1 - Gastric Bypass Surgery Recruits a Gut PPAR-α-Striatal D1R Pathway to Reduce Fat Appetite in Obese Rats
AU - Hankir, Mohammed K
AU - Seyfried, Florian
AU - Hintschich, Constantin A
AU - Diep, Thi-Ai
AU - Kleberg, Karen
AU - Kranz, Mathias
AU - Deuther-Conrad, Winnie
AU - Tellez, Luis A
AU - Rullmann, Michael
AU - Patt, Marianne
AU - Teichert, Jens
AU - Hesse, Swen
AU - Sabri, Osama
AU - Brust, Peter
AU - Hansen, Harald S
AU - de Araujo, Ivan E
AU - Krügel, Ute
AU - Fenske, Wiebke K
N1 - Copyright © 2017 Elsevier Inc. All rights reserved.
PY - 2017/2/7
Y1 - 2017/2/7
N2 - Bariatric surgery remains the single most effective long-term treatment modality for morbid obesity, achieved mainly by lowering caloric intake through as yet ill-defined mechanisms. Here we show in rats that Roux-en-Y gastric bypass (RYGB)-like rerouting of ingested fat mobilizes lower small intestine production of the fat-satiety molecule oleoylethanolamide (OEA). This was associated with vagus nerve-driven increases in dorsal striatal dopamine release. We also demonstrate that RYGB upregulates striatal dopamine 1 receptor (D1R) expression specifically under high-fat diet feeding conditions. Mechanistically, interfering with local OEA, vagal, and dorsal striatal D1R signaling negated the beneficial effects of RYGB on fat intake and preferences. These findings delineate a molecular/systems pathway through which bariatric surgery improves feeding behavior and may aid in the development of novel weight loss strategies that similarly modify brain reward circuits compromised in obesity.
AB - Bariatric surgery remains the single most effective long-term treatment modality for morbid obesity, achieved mainly by lowering caloric intake through as yet ill-defined mechanisms. Here we show in rats that Roux-en-Y gastric bypass (RYGB)-like rerouting of ingested fat mobilizes lower small intestine production of the fat-satiety molecule oleoylethanolamide (OEA). This was associated with vagus nerve-driven increases in dorsal striatal dopamine release. We also demonstrate that RYGB upregulates striatal dopamine 1 receptor (D1R) expression specifically under high-fat diet feeding conditions. Mechanistically, interfering with local OEA, vagal, and dorsal striatal D1R signaling negated the beneficial effects of RYGB on fat intake and preferences. These findings delineate a molecular/systems pathway through which bariatric surgery improves feeding behavior and may aid in the development of novel weight loss strategies that similarly modify brain reward circuits compromised in obesity.
KW - Journal Article
U2 - 10.1016/j.cmet.2016.12.006
DO - 10.1016/j.cmet.2016.12.006
M3 - Journal article
C2 - 28065827
SN - 1550-4131
VL - 25
SP - 335
EP - 344
JO - Cell Metabolism
JF - Cell Metabolism
IS - 2
ER -
