Zhang T, Reid K, Acuff C G, Jin C B, Rockhold R W
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216.
Pharmacol Biochem Behav. 1994 May;48(1):57-61. doi: 10.1016/0091-3057(94)90498-7.
Ingestion of highly palatable diets (HPDs), rich in sucrose and fat, has been shown to lead to obesity and alterations in cardiovascular function in animal models. A hypothesis has been advanced which suggests that ingestion of an HPD increases hypothalamic beta-endorphin release, an effect which results in an increase in sympathetic nerve outflow during the development of obesity. The hypothesis was tested by chronic (10 weeks) feeding of male spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs) with the HPD or normal rat chow (ND). Cardiovascular function (systolic blood pressure, heart rate) and body weight gain were monitored during the feeding period. Pain sensitivity was tested weekly by measuring tail-flick latency. Body weight gain was greater in WKY rats than in SHRs, but ingestion of the HPD had no effect in either strain. Terminal organ analysis indicated differences between strains of SHRs and WKYs in the heart, the adrenal and pituitary glands, peri-testicular fat pad, and testis weights expressed by organ weight/body weight. The heart weight was greater in SHRs on the HPD than in SHRs on the ND. The ingestion of the HPD significantly increased blood pressure only in SHRs, following 10 weeks of dietary intervention. However, tail-flick latency was prolonged in both SHRs and WKYs during ingestion of the HPD. Increases in tail-flick latency suggest that the HPD increases brain opiate levels in both SHRs and WKYs. Exaggerated increases in heart weight and blood pressure were noted in SHRs following feeding with the HPD, indicating enhanced sensitivity of SHRs to HPD-induced hypertension.
在动物模型中，摄入富含蔗糖和脂肪的高适口性饮食（HPD）已被证明会导致肥胖和心血管功能改变。有人提出一种假说，即摄入HPD会增加下丘脑β-内啡肽的释放，这种效应会导致肥胖发展过程中交感神经输出增加。通过对雄性自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠（WKY）进行为期10周的慢性喂养，分别给予HPD或正常大鼠饲料（ND）来验证这一假说。在喂养期间监测心血管功能（收缩压、心率）和体重增加情况。每周通过测量甩尾潜伏期来测试疼痛敏感性。WKY大鼠的体重增加比SHR大鼠更多，但摄入HPD对两种品系的大鼠均无影响。终末器官分析表明，SHR和WKY品系在心脏、肾上腺、垂体、睾丸周围脂肪垫以及以器官重量/体重表示的睾丸重量方面存在差异。HPD喂养的SHR大鼠的心脏重量比ND喂养的SHR大鼠更大。经过10周的饮食干预后，仅SHR大鼠摄入HPD会显著升高血压。然而，在摄入HPD期间，SHR和WKY大鼠的甩尾潜伏期均延长。甩尾潜伏期延长表明HPD会增加SHR和WKY大鼠脑中阿片类物质的水平。喂食HPD后，SHR大鼠的心脏重量和血压出现过度增加，表明SHR对HPD诱导的高血压敏感性增强。
