Diet-induced obesity in the Sprague–Dawley rat: dietary manipulations and their effect on hypothalamic neuropeptide energy balance systems

2005 ◽  
Vol 33 (5) ◽  
pp. 1068-1072 ◽  
Author(s):  
J.G. Mercer ◽  
Z.A. Archer

The SD (Sprague–Dawley) rat model of DIO (diet-induced obesity) is reported to exhibit a clear segregation into susceptible and resistant subpopulations shortly after transfer to a HE (high energy) diet. This does not appear to be the case for rats sourced in the U.K., where body weight gain on obesogenic HE diet is normally distributed, as might be anticipated for a polygenic trait in an outbred population. Many of the energy balance effects of dietary manipulation in this model (e.g. supplementation of HE diet with the liquid diet, Ensure; energy intake and defence of body weight following withdrawal of obesogenic diet) appear to be characteristics of the diets being manipulated rather than subject traits. The activities of energy balance-related hypothalamic signals are affected by diet and the development of DIO, but may not be able to differentiate between different diets and the relative levels of obesity that develop.

2004 ◽  
Vol 286 (4) ◽  
pp. R669-R677 ◽  
Author(s):  
Qinmin Zhang ◽  
Michael G. Tordoff

Recent epidemiological and animal studies have led to the hypothesis that low dietary calcium intakes contribute to obesity. Here, we evaluated whether calcium influenced the body weight of normal-weight and obese rodents. All experiments involved female C57BL/6J mice or Sprague-Dawley rats fed normal- or high-energy-density diets (3.8 or 4.7 kcal/g). Calcium intake was manipulated by allowing mice to drink sweetened 30 mM CaCl2 solution or feeding mice and rats diets differing in calcium content (0.2%, 0.6%, or 1.8% Ca2+). Blood samples were taken from rats to confirm that the diets had their intended effects on metabolism. There were no effects of the calcium manipulations on energy intake, body weight, or carcass fat content and no simple relation between calciotropic hormones and body weight. One experiment found a significant decrease in body weight gain of lean and obese rats fed the 1.8% Ca2+ diet, but we suspect that this was due to forced consumption of the unpalatable diet, reducing growth. These studies provide little support for the hypothesis that dietary calcium contributes to the etiology or maintenance of obesity.


2003 ◽  
Vol 285 (4) ◽  
pp. R791-R799 ◽  
Author(s):  
Chantal Michel ◽  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell

To assess the interaction between stress and energy homeostasis, we immobilized male Sprague-Dawley rats prone to diet-induced obesity (DIO) or diet resistance (DR) once for 20 min and then fed them either low-fat (4.5%) chow or a medium-fat (31%), high-energy (HE) diet for 9 days. Stressed, chow-fed DIO rats gained less, while stressed DIO rats on HE diet gained more body weight and had higher feed efficiency and plasma leptin levels than unstressed controls. Neither stress nor diet affected DR body weight gain. While stress-induced plasma corticosterone levels did not differ between phenotypes, DIO rats were initially more active in an open field and had higher hippocampal dentate gyrus and CA1 glucocorticoid receptor (GR) mRNA than DR rats, regardless of prior stress or diet. HE diet intake was associated with raised dentate gyrus and CA1 GR and amygdalar central nucleus (CeA) corticotropin-releasing hormone (CRH) mRNA expression, while stress was associated with reduced hypothalamic dorsomedial nucleus Ob-R mRNA and CeA CRH specifically in DIO rats fed HE diet. Thus a single stress triggers a complex interaction among weight gain phenotype, diet, and stress responsivity, which determines the body weight and adiposity of a given individual.


1989 ◽  
Vol 61 (3) ◽  
pp. 445-452 ◽  
Author(s):  
Christopher J. H. Woodward ◽  
Peter W. Emery

1. Sprague–Dawley rats were given corticosterone for 4 to 14 d either by subcutaneous injection (50 mg/kg body-weight per d) or as a higher dose in the diet (1 g/kg diet). Energy balance was calculated using the comparative carcass technique.2. Corticosterone significantly suppressed growth rate by at least 50% (P < 0·001 in all experiments). The reduction in growth was more marked in males than in females.3. Hormone treatment significantly reduced metabolizable intake (kJ/d) in males but not in females. Expressed relative to either metabolic body size (kg body-weight0·75) or fat-free mass, metabolizable intake tended to be increased in the treated groups.4. Energy expenditure, calculated as the difference between metabolizable intake and gain and expressed as kJ/d, did not differ between treated and control rats. Relative to either metabolic body size or fat-free mass, expenditure was consistently increased in treated rats. This change was statistically significant in five of the eight comparisons.5. The corticosterone-treated rat is characterized by high energy intake and expenditure relative to its body size and growth rate. Alterations in the relative sizes of different lean tissues may contribute to these changes.


1994 ◽  
Vol 267 (2) ◽  
pp. R527-R535 ◽  
Author(s):  
B. E. Levin

For assessment of the effect of diet cycling on body weight gain patterns, 3-mo-old male Sprague-Dawley rats were either cycled from chow to a high-energy condensed milk (CM) diet, back to chow, and then back to CM diet at 3-mo intervals (cyclers) or were fed chow to 9 mo of age and then CM diet for 3 mo (noncyclers). Nine of 21 cyclers developed diet-induced obesity (DIO), gaining 36, 59, and 281% more weight than chow-fed controls (CF) at each cycle, respectively. Twelve cycled rats were diet-resistant (DR) with comparable weight gain to CF rats after the first CM diet and chow cycles. However, they gained 202% more than CF rats and 50% more, with 29% heavier retroperitoneal fat pads, than noncycled DR rats after their second CM diet cycle begun at 9 mo of age. Enhanced weight gain in DR cyclers was probably due to enhanced food efficiency in the last few weeks of CM diet intake. Plasma insulin levels were 70% higher in cycled vs. noncycled DIO and DR rats, and both were higher than CF rats. Unlike 6-mo-old DR rats in a prior study, 12-mo-old noncycled DR rats after 3 mo on CM diet here had 45-172% higher alpha 2-adrenoceptors binding in 6 of 17 brain areas than noncycled DIO and/or CF rats. Thus age, diet cycling, and brain alpha 2-adrenoceptors interact to affect long-term changes in weight gain and metabolism.


Endocrinology ◽  
2003 ◽  
Vol 144 (12) ◽  
pp. 5347-5352 ◽  
Author(s):  
Bénédicte Prunet-Marcassus ◽  
Mathieu Desbazeille ◽  
Arnaud Bros ◽  
Katie Louche ◽  
Philippe Delagrange ◽  
...  

2002 ◽  
Vol 282 (1) ◽  
pp. R46-R54 ◽  
Author(s):  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell

Sprague-Dawley rats selectively bred for diet-induced obesity (DIO) or diet resistance (DR) were characterized on diets of differing energy content and palatability. Over 10 wk, DR rats on a high-energy (HE) diet (31% fat) gained weight similarly to DR rats fed chow (4.5% fat), but they became obese on a palatable liquid diet (Ensure). DIO rats gained 22% more weight on an HE diet and 50% more on Ensure than chow-fed DIO rats. DIO body weight gains plateaued when switched from HE diet to chow. But, Ensure-fed DIO rats switched to chow spontaneously reduced their intake and weight to that of rats switched from HE diet to chow. They also reduced their hypothalamic proopiomelanocortin and dynorphin but not neuropeptide Y mRNA expression by 17–40%. When reexposed to Ensure after 7 wk, they again overate and matched their body weights to rats maintained on Ensure throughout. All Ensure-fed rats had a selective reduction in dynorphin mRNA in the ventromedial hypothalamic nucleus. Thus genetic background, diet composition, and palatability interact to produce disparate levels of defended body weight and central neuropeptide expression.


2018 ◽  
Vol 29 (5) ◽  
pp. 553-563 ◽  
Author(s):  
Shakthi R.K. Devan ◽  
Surendar Arumugam ◽  
Ganesh Shankar ◽  
Suresh Poosala

AbstractBackgroundThe prevalence of obesity is reported to be increasing owing to the high intake of dietary fat and is a predisposing risk factor with associated complex metabolic syndromes in the human population. Preclinical rodent models play a pivotal role in understanding the pathogenesis of obesity and development of new treatment strategies for humans. High-fat-diet (HFD)-induced rodents are used for chronic obesity models owing to their quick adaptation to high-fat diets and rapid body weight gain and different rats (Wistar Sprague-Dawley and Lewis) have been used by various researchers. However, the selection of appropriate stock contributes to the translation of clinically linked disease phenotypes to preclinical animal models.MethodsThe study was conducted using two commonly used rat stocks Hsd:Sprague-Dawley (SD) and Crl:Charles River (CD) to develop a chronic high-fat-diet-induced obesity model (DIO) to explore the underlying mechanisms of obesity and its utilization in drug discovery and development during preclinical stages. In addition two high-fat diets of different composition were evaluated (D12327; 40% kcal fat and D12492; 60% kcal fat) for their potential to induce obesity using these two stocks.ResultsA differential sensitivity to HFD was observed in body weight gain fat mass composition and obesity-linked symptoms such as impaired glucose tolerance insulin and leptin levels. The comparative research findings of Hsd:SD and Crl:CD rat stocks suggested that Crl:CD rats are more prone to diet-induced obesity and its associated complications.ConclusionsCrl:CD rats were found to be a suitable model for obesity over Hsd:SD when considering the important hallmarks of metabolic disorders that may be utilized for obesity-related research.


2003 ◽  
Vol 11 (11) ◽  
pp. 1376-1383 ◽  
Author(s):  
Zoe A. Archer ◽  
D. Vernon Rayner ◽  
Jan Rozman ◽  
Martin Klingenspor ◽  
Julian G. Mercer

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