The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans. / Mandøe, Mette J.; Hansen, Katrine B.; Hartmann, Bolette; Rehfeld, Jens F.; Holst, Jens J.; Hansen, Harald S.

I: The American Journal of Clinical Nutrition, Bind 102, Nr. 3, 2015, s. 548-555.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Mandøe, MJ, Hansen, KB, Hartmann, B, Rehfeld, JF, Holst, JJ & Hansen, HS 2015, 'The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans.', The American Journal of Clinical Nutrition, bind 102, nr. 3, s. 548-555. https://doi.org/10.3945/ajcn.115.106799

APA

Mandøe, M. J., Hansen, K. B., Hartmann, B., Rehfeld, J. F., Holst, J. J., & Hansen, H. S. (2015). The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans. The American Journal of Clinical Nutrition, 102(3), 548-555. https://doi.org/10.3945/ajcn.115.106799

Vancouver

Mandøe MJ, Hansen KB, Hartmann B, Rehfeld JF, Holst JJ, Hansen HS. The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans. The American Journal of Clinical Nutrition. 2015;102(3):548-555. https://doi.org/10.3945/ajcn.115.106799

Author

Mandøe, Mette J. ; Hansen, Katrine B. ; Hartmann, Bolette ; Rehfeld, Jens F. ; Holst, Jens J. ; Hansen, Harald S. / The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans. I: The American Journal of Clinical Nutrition. 2015 ; Bind 102, Nr. 3. s. 548-555.

Bibtex

@article{7c4a19ebee44420a8532e3d75c97181f,
title = "The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans.",
abstract = "Background: Dietary triglycerides can, after digestion, stimulate the intestinal release of incretin hormones through activation of G protein-coupled receptor (GPR) 119 by 2-monoacylglycerol and by the activation of fatty acid receptors for long- and short-chain fatty acids. Medium-chain fatty acids do not stimulate the release of intestinal hormones. Objective: To dissect the mechanism of fat-induced glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) release in humans, we compared the effects of tributyrin (contg. short-chain fatty acids; i.e., butyric acid), olive oil [contg. long-chain fatty acids; e.g., oleic acid plus 2-oleoyl glycerol (2-OG)], and 1,3-dioctanoyl-2-oleoyl glycerol (C8-dietary oil), which is digested to form medium-chain fatty acids (i.e., octanoic acid) and 2-OG. Design: In a randomized, single-blinded crossover study, 12 healthy white men [mean age: 24 y; BMI (in kg/m2): 22] were given the following 4 meals on 4 different days: 200 g carrots + 6.53 g tributyrin, 200 g carrots + 13.15 g C8-dietary oil, 200 g carrots + 19 g olive oil, or 200 g carrots. All of the lipids totaled 0.0216 mol. Main outcome measures were incremental areas under the curve for total GLP-1, GIP, and cholecystokinin (CCK) in plasma. Results: C8-dietary oil and olive oil showed the same GLP-1 response [583 ± 101 and 538 ± 71 (pmol/L) × 120 min; P = 0.733], whereas the GIP response was higher for olive oil than for C8-dietary oil [3293 ± 404 and 1674 ± 270 (pmol/L) × 120 min; P = 0.002]. Tributyrin and carrots alone resulted in no increase in any of the measured hormones. Peptide YY (PYY) and neurotensin responses resembled those of GLP-1. Only olive oil stimulated CCK release. Conclusions: Under our study conditions, 2-OG and GPR119 activation can fully explain the olive oil-induced secretion of GLP-1, PYY, and neurotensin. In contrast, both oleic acid and 2-OG contributed to the GIP response. Dietary butyrate did not stimulate gut hormone secretion. Olive oil-derived oleic acid seems to be fully responsible for olive oil-induced CCK secretion. [on SciFinder(R)]",
author = "Mand{\o}e, {Mette J.} and Hansen, {Katrine B.} and Bolette Hartmann and Rehfeld, {Jens F.} and Holst, {Jens J.} and Hansen, {Harald S.}",
note = "M1 - Copyright (C) 2015 American Chemical Society (ACS). All Rights Reserved. CAPLUS AN 2015:1600066(Journal)",
year = "2015",
doi = "10.3945/ajcn.115.106799",
language = "English",
volume = "102",
pages = "548--555",
journal = "American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "3",

}

RIS

TY - JOUR

T1 - The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans.

AU - Mandøe, Mette J.

AU - Hansen, Katrine B.

AU - Hartmann, Bolette

AU - Rehfeld, Jens F.

AU - Holst, Jens J.

AU - Hansen, Harald S.

N1 - M1 - Copyright (C) 2015 American Chemical Society (ACS). All Rights Reserved. CAPLUS AN 2015:1600066(Journal)

PY - 2015

Y1 - 2015

N2 - Background: Dietary triglycerides can, after digestion, stimulate the intestinal release of incretin hormones through activation of G protein-coupled receptor (GPR) 119 by 2-monoacylglycerol and by the activation of fatty acid receptors for long- and short-chain fatty acids. Medium-chain fatty acids do not stimulate the release of intestinal hormones. Objective: To dissect the mechanism of fat-induced glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) release in humans, we compared the effects of tributyrin (contg. short-chain fatty acids; i.e., butyric acid), olive oil [contg. long-chain fatty acids; e.g., oleic acid plus 2-oleoyl glycerol (2-OG)], and 1,3-dioctanoyl-2-oleoyl glycerol (C8-dietary oil), which is digested to form medium-chain fatty acids (i.e., octanoic acid) and 2-OG. Design: In a randomized, single-blinded crossover study, 12 healthy white men [mean age: 24 y; BMI (in kg/m2): 22] were given the following 4 meals on 4 different days: 200 g carrots + 6.53 g tributyrin, 200 g carrots + 13.15 g C8-dietary oil, 200 g carrots + 19 g olive oil, or 200 g carrots. All of the lipids totaled 0.0216 mol. Main outcome measures were incremental areas under the curve for total GLP-1, GIP, and cholecystokinin (CCK) in plasma. Results: C8-dietary oil and olive oil showed the same GLP-1 response [583 ± 101 and 538 ± 71 (pmol/L) × 120 min; P = 0.733], whereas the GIP response was higher for olive oil than for C8-dietary oil [3293 ± 404 and 1674 ± 270 (pmol/L) × 120 min; P = 0.002]. Tributyrin and carrots alone resulted in no increase in any of the measured hormones. Peptide YY (PYY) and neurotensin responses resembled those of GLP-1. Only olive oil stimulated CCK release. Conclusions: Under our study conditions, 2-OG and GPR119 activation can fully explain the olive oil-induced secretion of GLP-1, PYY, and neurotensin. In contrast, both oleic acid and 2-OG contributed to the GIP response. Dietary butyrate did not stimulate gut hormone secretion. Olive oil-derived oleic acid seems to be fully responsible for olive oil-induced CCK secretion. [on SciFinder(R)]

AB - Background: Dietary triglycerides can, after digestion, stimulate the intestinal release of incretin hormones through activation of G protein-coupled receptor (GPR) 119 by 2-monoacylglycerol and by the activation of fatty acid receptors for long- and short-chain fatty acids. Medium-chain fatty acids do not stimulate the release of intestinal hormones. Objective: To dissect the mechanism of fat-induced glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) release in humans, we compared the effects of tributyrin (contg. short-chain fatty acids; i.e., butyric acid), olive oil [contg. long-chain fatty acids; e.g., oleic acid plus 2-oleoyl glycerol (2-OG)], and 1,3-dioctanoyl-2-oleoyl glycerol (C8-dietary oil), which is digested to form medium-chain fatty acids (i.e., octanoic acid) and 2-OG. Design: In a randomized, single-blinded crossover study, 12 healthy white men [mean age: 24 y; BMI (in kg/m2): 22] were given the following 4 meals on 4 different days: 200 g carrots + 6.53 g tributyrin, 200 g carrots + 13.15 g C8-dietary oil, 200 g carrots + 19 g olive oil, or 200 g carrots. All of the lipids totaled 0.0216 mol. Main outcome measures were incremental areas under the curve for total GLP-1, GIP, and cholecystokinin (CCK) in plasma. Results: C8-dietary oil and olive oil showed the same GLP-1 response [583 ± 101 and 538 ± 71 (pmol/L) × 120 min; P = 0.733], whereas the GIP response was higher for olive oil than for C8-dietary oil [3293 ± 404 and 1674 ± 270 (pmol/L) × 120 min; P = 0.002]. Tributyrin and carrots alone resulted in no increase in any of the measured hormones. Peptide YY (PYY) and neurotensin responses resembled those of GLP-1. Only olive oil stimulated CCK release. Conclusions: Under our study conditions, 2-OG and GPR119 activation can fully explain the olive oil-induced secretion of GLP-1, PYY, and neurotensin. In contrast, both oleic acid and 2-OG contributed to the GIP response. Dietary butyrate did not stimulate gut hormone secretion. Olive oil-derived oleic acid seems to be fully responsible for olive oil-induced CCK secretion. [on SciFinder(R)]

U2 - 10.3945/ajcn.115.106799

DO - 10.3945/ajcn.115.106799

M3 - Journal article

VL - 102

SP - 548

EP - 555

JO - American Journal of Clinical Nutrition

JF - American Journal of Clinical Nutrition

SN - 0002-9165

IS - 3

ER -

ID: 150703261