{"title":"Capsaicin as an anti-obesity drug.","authors":"Felix W Leung","doi":"10.1007/978-3-0348-0828-6_7","DOIUrl":null,"url":null,"abstract":"<p><p>Laboratory studies support a role of capsaicin as an anti-obesity agent. Intestinal mucosal afferent nerves appear to play a role in controlling adipose tissue distribution between visceral and subcutaneous sites. Activation of the transient receptor potential vanilloid-1 channels by capsaicin prevents adipogenesis. A neurogenic mechanism modulates the regulation of fat metabolism by transient receptor potential vanilloid-1-sensitive sensory nerves. A neural pathway enables the selective activation of the central network that regulates brown adipose tissue sympathetic nerve activity in response to a specific stimulation of gastrointestinal transient receptor potential channels. Dietary capsaicin reduces metabolic dysregulation in obese/diabetic mice by enhancing expression of adiponectin and its receptor. The effects of capsaicin in adipose tissue and liver are related to its dual action on peroxisome proliferator-activated receptor alpha and transient receptor potential vanilloid-1 expression/activation. Local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation. Truncal vagotomy leads to significant reductions in both diet-induced weight gain and visceral abdominal fat deposition. Vagal de-afferentation leads to a more modest, but clinically and statistically significant, reduction in visceral abdominal fat. Thermogenesis and lipid metabolism-related proteins are altered upon capsaicin treatment in white adipose tissue. Capsaicin induces apoptosis and inhibits adipogenesis in preadipocytes and adipocytes. Epidemiologic data show that consumption of foods containing capsaicin is associated with a lower prevalence of obesity. Clinical evidence supports a role of capsaicin as an anti-obesity agent. Both oral and gastrointestinal exposure to capsaicin increase satiety and reduce energy and fat intake; the stronger reduction with oral exposure suggests a sensory effect of capsaicin. Bioactive components containing capsaicin may support weight maintenance after a hypocaloric diet. Capsaicin consumption 1 h before low intensity exercise is a valuable supplement for the treatment of individuals with hyperlipidemia and/or obesity because it improves lipolysis. Capsinoid ingestion increases energy expenditure through the activation of brown adipose tissue in humans. Capsinoid ingestion is associated with an increase in fat oxidation that is nearly significant; and two common genetic variants may be predictors of response. Further clinical research to develop convenient approaches for obese individuals to take advantage of this common dietary ingredient to prevent the onset or curtail the progression of obesity will be instructive and clinically relevant.</p>","PeriodicalId":20603,"journal":{"name":"Progress in drug research. Fortschritte der Arzneimittelforschung. Progres des recherches pharmaceutiques","volume":"68 ","pages":"171-9"},"PeriodicalIF":0.0000,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-0348-0828-6_7","citationCount":"70","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Progress in drug research. Fortschritte der Arzneimittelforschung. Progres des recherches pharmaceutiques","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-0348-0828-6_7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 70

Abstract

Laboratory studies support a role of capsaicin as an anti-obesity agent. Intestinal mucosal afferent nerves appear to play a role in controlling adipose tissue distribution between visceral and subcutaneous sites. Activation of the transient receptor potential vanilloid-1 channels by capsaicin prevents adipogenesis. A neurogenic mechanism modulates the regulation of fat metabolism by transient receptor potential vanilloid-1-sensitive sensory nerves. A neural pathway enables the selective activation of the central network that regulates brown adipose tissue sympathetic nerve activity in response to a specific stimulation of gastrointestinal transient receptor potential channels. Dietary capsaicin reduces metabolic dysregulation in obese/diabetic mice by enhancing expression of adiponectin and its receptor. The effects of capsaicin in adipose tissue and liver are related to its dual action on peroxisome proliferator-activated receptor alpha and transient receptor potential vanilloid-1 expression/activation. Local desensitization of the abdominal capsaicin-sensitive fibers attenuates the hypometabolic adaptation to food deprivation. Truncal vagotomy leads to significant reductions in both diet-induced weight gain and visceral abdominal fat deposition. Vagal de-afferentation leads to a more modest, but clinically and statistically significant, reduction in visceral abdominal fat. Thermogenesis and lipid metabolism-related proteins are altered upon capsaicin treatment in white adipose tissue. Capsaicin induces apoptosis and inhibits adipogenesis in preadipocytes and adipocytes. Epidemiologic data show that consumption of foods containing capsaicin is associated with a lower prevalence of obesity. Clinical evidence supports a role of capsaicin as an anti-obesity agent. Both oral and gastrointestinal exposure to capsaicin increase satiety and reduce energy and fat intake; the stronger reduction with oral exposure suggests a sensory effect of capsaicin. Bioactive components containing capsaicin may support weight maintenance after a hypocaloric diet. Capsaicin consumption 1 h before low intensity exercise is a valuable supplement for the treatment of individuals with hyperlipidemia and/or obesity because it improves lipolysis. Capsinoid ingestion increases energy expenditure through the activation of brown adipose tissue in humans. Capsinoid ingestion is associated with an increase in fat oxidation that is nearly significant; and two common genetic variants may be predictors of response. Further clinical research to develop convenient approaches for obese individuals to take advantage of this common dietary ingredient to prevent the onset or curtail the progression of obesity will be instructive and clinically relevant.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
辣椒素是一种抗肥胖药物。
实验室研究支持辣椒素作为抗肥胖剂的作用。肠粘膜传入神经似乎在控制内脏和皮下部位之间的脂肪组织分布中起作用。辣椒素激活瞬时受体电位vanililid -1通道可防止脂肪生成。一种神经源性机制通过瞬时受体电位香草素-1敏感感觉神经调节脂肪代谢。一种神经通路能够选择性激活中枢网络,该网络在胃肠道瞬时受体电位通道的特定刺激下调节棕色脂肪组织交感神经活动。膳食辣椒素通过增强脂联素及其受体的表达来减少肥胖/糖尿病小鼠的代谢失调。辣椒素在脂肪组织和肝脏中的作用与其对过氧化物酶体增殖物激活受体α和瞬时受体电位香草素-1表达/激活的双重作用有关。腹部辣椒素敏感纤维的局部脱敏减弱了对食物剥夺的低代谢适应。截尾迷走神经切开术可显著减少饮食引起的体重增加和内脏腹部脂肪沉积。迷走神经吸音减少导致腹部内脏脂肪的减少,虽然幅度不大,但在临床上和统计学上都有显著意义。白色脂肪组织中的产热和脂质代谢相关蛋白在辣椒素处理后发生改变。辣椒素诱导前脂肪细胞和脂肪细胞凋亡,抑制脂肪生成。流行病学数据显示,食用含有辣椒素的食物与肥胖率较低有关。临床证据支持辣椒素作为抗肥胖剂的作用。口服和胃肠道接触辣椒素都能增加饱腹感,减少能量和脂肪的摄入;口服接触辣椒素的效果更强,说明辣椒素有感官效应。含有辣椒素的生物活性成分可能有助于低热量饮食后的体重维持。在低强度运动前1小时摄入辣椒素对于治疗高脂血症和/或肥胖患者是一种有价值的补充,因为它能促进脂肪分解。摄入辣椒素通过激活人体棕色脂肪组织增加能量消耗。辣椒素的摄入与脂肪氧化的增加有关,这几乎是显著的;两种常见的基因变异可能是反应的预测因子。进一步的临床研究,为肥胖个体开发方便的方法,利用这种常见的饮食成分来预防肥胖的发生或减少肥胖的进展,将具有指导意义和临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Carbonic Anhydrase IX: Current and Emerging Therapies Targeting Carbonic Anhydrase Isozymes in the Treatment of Neurological Disorders Targeting Carbonic Anhydrase IX in Tumor Imaging and Theranostic Cancer Therapy Potential of Carbonic Anhydrase Inhibitors in the Treatment of Oxidative Stress and Diabetes Carbonic Anhydrase Inhibitors in Ophthalmology: Glaucoma and Macular Oedema
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1