{"title":"Capsaicin supplementation prevents western diet-induced hyperleptinemia by reducing endoplasmic reticulum stress in apolipoprotein E-deficient mice","authors":"Hyun Ju Kim","doi":"10.29219/fnr.v67.9610","DOIUrl":null,"url":null,"abstract":"<p style=\"color: #000000; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; font-weight: 400; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; white-space: normal; text-decoration-thickness: initial; text-decoration-style: initial; text-decoration-color: initial;\"><strong><em>Background</em></strong>: Endoplasmic reticulum (ER) stress implicated in leptin resistance in the diet-induced obesity, which can accelerate the development of atherosclerosis forms the background of this study.</p> <p style=\"color: #000000; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; font-weight: 400; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; white-space: normal; text-decoration-thickness: initial; text-decoration-style: initial; text-decoration-color: initial;\"><strong><em>Objective</em></strong>: This study aimed to investigate the effect of capsaicin on hyperleptinema by inhibiting ER stress in apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice fed a western diet (WD).</p> <p style=\"color: #000000; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; font-weight: 400; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; white-space: normal; text-decoration-thickness: initial; text-decoration-style: initial; text-decoration-color: initial;\"><strong><em>Design</em></strong>: ApoE <sup>-/-</sup> mice were assigned one of three experimental diets: WD (60% kcal from fat, <em>n</em> = 10), WD + 0.015% capsaicin (<em>n</em> = 10, w/w), and WD + 1% PBA (<em>n</em> = 10, w/w) for 12 weeks.</p> <p style=\"color: #000000; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; font-weight: 400; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; white-space: normal; text-decoration-thickness: initial; text-decoration-style: initial; text-decoration-color: initial;\"><strong><em>Results</em></strong>: In metabolic parameters, supplementation of dietary capsaicin displayed marked reduction of body weight gain and adipose tissue weight, plasma leptin, total cholesterol, and hepatic triglyceride levels without change in the plasma insulin level compared with WD fed ApoE-/- mice after 12 weeks. Capsaicin supplementation also attenuated the protein expression of ER stress markers such as eukaryotic translational initiation factor 2α and C/EBP homology protein in the liver, as well as glucose-related protein 78 localization in the aorta, indicating that capsaicin inhibits diet-induced hyperleptinemia in part by regulating the protein expression involved in ER stress.</p> <p style=\"color: #000000; font-family: 'Times New Roman'; font-size: medium; font-style: normal; font-variant-ligatures: normal; font-variant-caps: normal; font-weight: 400; letter-spacing: normal; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; widows: 2; word-spacing: 0px; -webkit-text-stroke-width: 0px; white-space: normal; text-decoration-thickness: initial; text-decoration-style: initial; text-decoration-color: initial;\"><strong><em>Conclusion</em></strong>: Capsaicin, therefore, may have potential as a therapeutic agent for individuals with diet-induced hyperleptinemia</p>","PeriodicalId":12119,"journal":{"name":"Food & Nutrition Research","volume":"9 1","pages":""},"PeriodicalIF":3.5000,"publicationDate":"2023-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food & Nutrition Research","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.29219/fnr.v67.9610","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
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Abstract
Background: Endoplasmic reticulum (ER) stress implicated in leptin resistance in the diet-induced obesity, which can accelerate the development of atherosclerosis forms the background of this study.
Objective: This study aimed to investigate the effect of capsaicin on hyperleptinema by inhibiting ER stress in apolipoprotein E-deficient (ApoE-/-) mice fed a western diet (WD).
Design: ApoE -/- mice were assigned one of three experimental diets: WD (60% kcal from fat, n = 10), WD + 0.015% capsaicin (n = 10, w/w), and WD + 1% PBA (n = 10, w/w) for 12 weeks.
Results: In metabolic parameters, supplementation of dietary capsaicin displayed marked reduction of body weight gain and adipose tissue weight, plasma leptin, total cholesterol, and hepatic triglyceride levels without change in the plasma insulin level compared with WD fed ApoE-/- mice after 12 weeks. Capsaicin supplementation also attenuated the protein expression of ER stress markers such as eukaryotic translational initiation factor 2α and C/EBP homology protein in the liver, as well as glucose-related protein 78 localization in the aorta, indicating that capsaicin inhibits diet-induced hyperleptinemia in part by regulating the protein expression involved in ER stress.
Conclusion: Capsaicin, therefore, may have potential as a therapeutic agent for individuals with diet-induced hyperleptinemia
期刊介绍：
Food & Nutrition Research is a peer-reviewed journal that presents the latest scientific research in various fields focusing on human nutrition. The journal publishes both quantitative and qualitative research papers.
Through an Open Access publishing model, Food & Nutrition Research opens an important forum for researchers from academic and private arenas to exchange the latest results from research on human nutrition in a broad sense, both original papers and reviews, including:
* Associations and effects of foods and nutrients on health
* Dietary patterns and health
* Molecular nutrition
* Health claims on foods
* Nutrition and cognitive functions
* Nutritional effects of food composition and processing
* Nutrition in developing countries
* Animal and in vitro models with clear relevance for human nutrition
* Nutrition and the Environment
* Food and Nutrition Education
* Nutrition and Economics
Research papers on food chemistry (focus on chemical composition and analysis of foods) are generally not considered eligible, unless the results have a clear impact on human nutrition.
The journal focuses on the different aspects of nutrition for people involved in nutrition research such as Dentists, Dieticians, Medical doctors, Nutritionists, Teachers, Journalists and Manufacturers in the food and pharmaceutical industries.
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