Suppr超能文献

肥胖的发展与每餐摄入的卡路里增加有关,而不是与每天摄入的卡路里有关。一项关于高脂肪饮食诱导的年轻大鼠肥胖的研究。

Development of obesity is associated with increased calories per meal rather than per day. A study of high-fat diet-induced obesity in young rats.

机构信息

Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Laboratory Center, Erling Skjalgssons gate 1, 7006, Trondheim, Norway.

出版信息

Obes Surg. 2009 Oct;19(10):1430-8. doi: 10.1007/s11695-009-9863-1. Epub 2009 Jun 9.

Abstract

BACKGROUND

We challenge the current belief that obesity is a result of overnutrition by studying a rodent model of human obesity.

METHODS

Male Sprague-Dawley rats at 3 weeks of age were fed with a mixed normal diet of 10% fat and high-fat diet of 60% fat (50:50) for 2 weeks and then turned to 100% high-fat diet until 43 weeks of age. Body weight gain was recorded, and food intake, eating behavior, and metabolic variables were measured by a comprehensive laboratory animal monitoring system. Body composition was determined by dual-energy X-ray absorptiometry. Ghrelin/obestatin-producing A-like cells in the stomach were analyzed by immunohistochemistry.

RESULTS

Rats on high-fat diet were overweight at 9 weeks of age and later became obese characterized by increased body weight and excess fat deposition. There were no obesity-prone, obesity middle tertile, and obesity-resistant subgroups in rats on high-fat diet. The young rats on high-fat diet, even before becoming overweight (i.e., 8 weeks), consumed larger portion of meal (kilocalorie per meal) and ate faster but less frequent than the rats on normal diet. Obese rats had reduced food intake (expressed as gram per 100-g body weight per 24 h), unchanged calorie intake (kilocalorie per 100-g body weight per 24 h), and energy expenditure (kilocalorie per hour per 100-g body weight), and increased number of A-like cells in the stomach.

CONCLUSION

Large size of meal, but not overnutrition, appears to be responsible for high-fat diet-induced obesity in rats. We propose a consideration that prevention strategies for obesity epidemic should strongly focus on meal size at early childhood and adolescence.

摘要

背景

我们通过研究人类肥胖的啮齿动物模型,对肥胖是由营养过剩引起的这一现有观点提出了挑战。

方法

3 周龄雄性 Sprague-Dawley 大鼠最初给予含 10%脂肪的混合正常饮食和含 60%脂肪的高脂肪饮食(50:50)2 周,然后转为 100%高脂肪饮食,直至 43 周龄。记录体重增加,采用综合实验室动物监测系统测量食物摄入量、摄食行为和代谢变量。通过双能 X 射线吸收法测定身体成分。采用免疫组织化学法分析胃中产生 ghrelin/obestatin 的 A 样细胞。

结果

高脂肪饮食组大鼠 9 周龄时超重,随后肥胖,表现为体重增加和脂肪沉积过多。高脂肪饮食组大鼠中没有肥胖易感亚组、肥胖中值亚组和肥胖抵抗亚组。高脂肪饮食的年轻大鼠,甚至在超重之前(即 8 周时),每餐的进食量(每餐的千卡数)更大,进食速度更快,但进食频率较低。肥胖大鼠的食物摄入量(每 100 克体重 24 小时的克数)减少,热量摄入量(每 100 克体重 24 小时的千卡数)不变,能量消耗(每 100 克体重每小时的千卡数)增加,胃中 A 样细胞数量增加。

结论

大餐量,而不是营养过剩,似乎是高脂肪饮食引起大鼠肥胖的原因。我们提出一种考虑,即肥胖流行的预防策略应在儿童和青少年早期阶段重点关注餐量。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验