DEVELOPMENT AND CHARACTERIZATION OF A PURIFIED DIET TO IDENTIFY OBESITY-SUSCEPTIBLE AND RESISTANT RAT-POPULATIONS

被引:57
作者
LAUTERIO, TJ
BOND, JP
ULMAN, EA
机构
[1] EASTERN VIRGINIA MED SCH, DEPT PHYSIOL, NORFOLK, VA 23501 USA
[2] DEPT VET AFFAIRS MED CTR, HAMPTON, VA 23667 USA
[3] RES DIETS INC, NEW BRUNSWICK, NJ 08901 USA
关键词
DIET-INDUCED OBESITY; FEED EFFICIENCY; RATS; RESISTERS AND GAINERS; GLUCOSE CONCENTRATIONS;
D O I
10.1093/jn/124.11.2172
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
A purified moderately high fat diet has been developed to examine diet-induced obesity in rats. Male Sprague-Dawley rats were fed this or an AIN-76A diet for 15 wk and energy metabolism indices were monitored. Food intake, body weight and water. balance indices were recorded on a weekly or daily basis. Over the 15-wk period, rats fed the experimental diet diverged into two groups differing in the rate of body weight gain. Animals were labeled as ''gainers'' or ''resisters'' depending on their susceptibility to obesity. Following the dietary period, rats were decapitated and trunk blood was collected for glucose and insulin measurements. Gainers consumed slightly more energy than resisters over the experimental period (P < 0.05), but due to greater fecal energy loss, absorbed energy did not differ. Hence gainers became obese without significantly altered energy retention. Urinary creatinine, urea nitrogen and water balance were not different between the groups and consequently could not explain body weight differences. Further, gainers had significantly greater plasma glucose concentration than controls, indicating a potential for these animals to become diabetic. Results suggest metabolic differences must account for the divergence in weight gain observed in the two groups. The dietary model characterized in this study should provide a useful tool to study diet-induced obesity and to determine its underlying mechanism.
引用
收藏
页码:2172 / 2178
页数:7
相关论文
共 33 条
[1]  
Bieri JG, 1980, J NUTR, V110, P1726, DOI [10.1093/jn/110.8.1726, DOI 10.1093/JN/110.8.1726]
[2]  
BJORNTORP P, 1988, DIABETES METAB REV, V4, P615, DOI 10.1002/dmr.5610040607
[3]   GENETIC AND NONGENETIC DETERMINANTS OF REGIONAL FAT DISTRIBUTION [J].
BOUCHARD, C ;
DESPRES, JP ;
MAURIEGE, P .
ENDOCRINE REVIEWS, 1993, 14 (01) :72-93
[4]   CURRENT UNDERSTANDING OF THE ETIOLOGY OF OBESITY - GENETIC AND NONGENETIC FACTORS [J].
BOUCHARD, C .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1991, 53 (06) :S1561-S1565
[5]  
COLDITZ GA, 1992, AM J CLIN NUTR, V55, P503
[6]   WEIGHT AS A RISK FACTOR FOR CLINICAL DIABETES IN WOMEN [J].
COLDITZ, GA ;
WILLETT, WC ;
STAMPFER, MJ ;
MANSON, JE ;
HENNEKENS, CH ;
ARKY, RA ;
SPEIZER, FE .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1990, 132 (03) :501-513
[7]   ENERGY-EXPENDITURE IN RATS WITH DIET-INDUCED OBESITY [J].
CORBETT, SW ;
STERN, JS ;
KEESEY, RE .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1986, 44 (02) :173-180
[8]  
FOLCH J, 1957, J BIOL CHEM, V226, P497
[9]  
JAMES WPT, 1976, LANCET, V2, P770
[10]   SEX-DIFFERENCES IN THE EFFECTS OF HIGH-FAT FEEDING ON BEHAVIOR AND CARCASS COMPOSITION [J].
JEN, KLC ;
GREENWOOD, MRC ;
BRASEL, JA .
PHYSIOLOGY & BEHAVIOR, 1981, 27 (01) :161-166