Duca Frank A, Swartz Timothy D, Covasa Mihai
UMR 1319 MICALIS, Institut National de la Recherche Agronomique, Centre de Recherche de Jouy-, Jouy-en-Josas, France; AgroParisTech, Jouy-en-Josas, France.
UMR 1319 MICALIS, Institut National de la Recherche Agronomique, Centre de Recherche de Jouy-, Jouy-en-Josas, France; AgroParisTech, Jouy-en-Josas, France; Department of Basic Medical Sciences, College of Osteopathic Medicine, Western University of Health Sciences, Pomona, California, United States of America; Department of Human Health and Development, University of Suceava, Suceava, Romania.
PLoS One. 2014 Oct 20;9(10):e111232. doi: 10.1371/journal.pone.0111232. eCollection 2014.
Increased orosensory stimulation from palatable diets and decreased feedback from gut signals have been proposed as contributing factors to obesity development. Whether altered taste functions associated with obesity are common traits or acquired deficits to environmental factors, such as a high-energy (HE)-diet, however, is not clear. To address this, we examined preference and sensitivity of increasing concentrations of sucrose solutions in rats prone (OP) and resistant (OR) to obesity during chow and HE feeding and measured lingual gene expression of the sweet taste receptor T1R3. When chow-fed, OP rats exhibited reduced preference and acceptance of dilute sucrose solutions, sham-fed less sucrose compared to OR rats, and had reduced lingual T1R3 gene expression. HE-feeding abrogated differences in sucrose preference and intake and lingual T1R3 expression between phenotypes. Despite similar sucrose intakes however, OP rats consumed significantly more total calories during 48-h two-bottle testing compared to OR rats. The results demonstrate that OP rats have an innate deficit for sweet taste detection, as illustrated by a reduction in sensitivity to sweets and reduced T1R3 gene expression; however their hyperphagia and subsequent obesity during HE-feeding is most likely not due to altered consumption of sweets.
美味饮食带来的口部感觉刺激增加以及肠道信号反馈减少，被认为是导致肥胖的因素。然而，与肥胖相关的味觉功能改变是常见特征还是由环境因素（如高能饮食）导致的后天缺陷，目前尚不清楚。为了解决这个问题，我们研究了在正常饮食和高能饮食期间，肥胖易感（OP）和肥胖抵抗（OR）大鼠对不同浓度蔗糖溶液的偏好和敏感度，并检测了甜味受体T1R3的舌部基因表达。在正常饮食时，OP大鼠对稀释蔗糖溶液的偏好和接受度降低，假饲时摄入的蔗糖比OR大鼠少，且舌部T1R3基因表达降低。高能饮食消除了两种表型之间在蔗糖偏好、摄入量和舌部T1R3表达上的差异。然而，尽管蔗糖摄入量相似，但在48小时双瓶测试中，OP大鼠比OR大鼠消耗的总热量显著更多。结果表明，OP大鼠在甜味检测方面存在先天性缺陷，表现为对甜味的敏感度降低和T1R3基因表达减少；然而，它们在高能饮食期间的食欲亢进及随后的肥胖很可能并非由于对甜食的摄入量改变所致。
