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Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice

Sinapic acid (SA), a hydroxycinnamic acid, is known to confer protection against oxidative stress, inflammation, diabetes, and liver disease. However, the effectiveness of SA in improving obesity remains obscure. Therefore, this study evaluated anti-obesity efficacy of SA and to elucidate its mechan...

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Autores principales: Yoon, Hye Jin, Yoon, Dae Seong, Baek, Hea Ja, Kang, Beodeul, Jung, Un Ju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Food Science and Nutrition 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9843723/
https://www.ncbi.nlm.nih.gov/pubmed/36721747
http://dx.doi.org/10.3746/pnf.2022.27.4.407
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author Yoon, Hye Jin
Yoon, Dae Seong
Baek, Hea Ja
Kang, Beodeul
Jung, Un Ju
author_facet Yoon, Hye Jin
Yoon, Dae Seong
Baek, Hea Ja
Kang, Beodeul
Jung, Un Ju
author_sort Yoon, Hye Jin
collection PubMed
description Sinapic acid (SA), a hydroxycinnamic acid, is known to confer protection against oxidative stress, inflammation, diabetes, and liver disease. However, the effectiveness of SA in improving obesity remains obscure. Therefore, this study evaluated anti-obesity efficacy of SA and to elucidate its mechanism of action. Male mice were maintained for 16 weeks on high-fat diet (HFD) alone or with SA (0.004%, w/w) and bodyweight, fat mass, adipocyte size, food intake, and biochemical and molecular markers were evaluated. SA-supplemented mice demonstrated markedly decreased fat mass and adipocyte size compared to unsupplemented group, without any changes in bodyweight and food intake between the two groups. Plasma adipocytokines levels including leptin, resistin, monocyte chemoattractant protein (MCP)-1 and interleukin-6 were also markedly reduced by SA supplementation. SA tended to lower plasma insulin level and improved homeostatic index of insulin resistance and intraperitoneal glucose tolerance test in HFD-induced obese mice. The anti-adiposity effect of SA was maybe owing to down-regulation of the mRNA expression of lipogenic genes, including acetyl coenzyme A (CoA) carboxylase, fatty acid synthesis, stearoyl-CoA desaturase 1, and phosphatidate phosphatase, and peroxisome proliferator-activated receptor γ, a transcription factor responsible for governing lipid metabolism, in adipose tissues. SA significantly down-regulated pro-inflammatory nuclear factor kappa B, MCP-1, tumor necrosis factor-α, and Toll-like receptor 4 mRNA expression in adipose tissue. Thus, SA could be beneficial for the development of functional foods or herbal medications to combat obesity.
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spelling pubmed-98437232023-01-30 Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice Yoon, Hye Jin Yoon, Dae Seong Baek, Hea Ja Kang, Beodeul Jung, Un Ju Prev Nutr Food Sci Original Sinapic acid (SA), a hydroxycinnamic acid, is known to confer protection against oxidative stress, inflammation, diabetes, and liver disease. However, the effectiveness of SA in improving obesity remains obscure. Therefore, this study evaluated anti-obesity efficacy of SA and to elucidate its mechanism of action. Male mice were maintained for 16 weeks on high-fat diet (HFD) alone or with SA (0.004%, w/w) and bodyweight, fat mass, adipocyte size, food intake, and biochemical and molecular markers were evaluated. SA-supplemented mice demonstrated markedly decreased fat mass and adipocyte size compared to unsupplemented group, without any changes in bodyweight and food intake between the two groups. Plasma adipocytokines levels including leptin, resistin, monocyte chemoattractant protein (MCP)-1 and interleukin-6 were also markedly reduced by SA supplementation. SA tended to lower plasma insulin level and improved homeostatic index of insulin resistance and intraperitoneal glucose tolerance test in HFD-induced obese mice. The anti-adiposity effect of SA was maybe owing to down-regulation of the mRNA expression of lipogenic genes, including acetyl coenzyme A (CoA) carboxylase, fatty acid synthesis, stearoyl-CoA desaturase 1, and phosphatidate phosphatase, and peroxisome proliferator-activated receptor γ, a transcription factor responsible for governing lipid metabolism, in adipose tissues. SA significantly down-regulated pro-inflammatory nuclear factor kappa B, MCP-1, tumor necrosis factor-α, and Toll-like receptor 4 mRNA expression in adipose tissue. Thus, SA could be beneficial for the development of functional foods or herbal medications to combat obesity. The Korean Society of Food Science and Nutrition 2022-12-31 2022-12-31 /pmc/articles/PMC9843723/ /pubmed/36721747 http://dx.doi.org/10.3746/pnf.2022.27.4.407 Text en Copyright © 2022 by The Korean Society of Food Science and Nutrition. All rights Reserved. https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original
Yoon, Hye Jin
Yoon, Dae Seong
Baek, Hea Ja
Kang, Beodeul
Jung, Un Ju
Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title_full Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title_fullStr Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title_full_unstemmed Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title_short Dietary Sinapic Acid Alleviates Adiposity and Inflammation in Diet-Induced Obese Mice
title_sort dietary sinapic acid alleviates adiposity and inflammation in diet-induced obese mice
topic Original
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9843723/
https://www.ncbi.nlm.nih.gov/pubmed/36721747
http://dx.doi.org/10.3746/pnf.2022.27.4.407
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