Physiological Difference between Dietary Obesity-Susceptible and Obesity-Resistant Sprague Dawley Rats in Response to Moderate High Fat Diet.

Jang, In-Surk; Hwang, Dae-Yeon; Lee, JuEun; Chae, KabRyong; Kim, Yong Kyu; Kang, Tae-Seok; Kim, ChulKyu; Shin, Dong Hoon; Hwang, Jin-Hee; Huh, Youngbuhm; Cho, Jung-Sik

doi:10.1538/expanim.52.99

Cited by 24 publications

(23 citation statements)

References 30 publications

(29 reference statements)

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“…Obesity has been characterized by numerous comorbidities in addition to elevated weight and body fat, as mentioned above, including systemic insulin resistance, hyperinsulinaemia, hyperleptinaemia, hyperglycaemia, dyslipidaemia and elevated systolic arterial pressure (6,9,10,13,14). The increase in body weight and fat, due to the hypercaloric pellet-diet cycle used in this work, was associated with these co-morbidities.…”

Section: Discussionmentioning

confidence: 82%

“…Therefore, the aim of this study was to develop a more controlled diet consisting of a cycle of hypercaloric pellet-dietary formulations with a different palatability to induce experimental obesity in rats. Obesity is considered to be associated with numerous co-morbidities such as a systemic resistance to insulin, hyperglycaemia, dyslipidaemia, hyperleptinaemia, hyperinsulinaemia and systemic arterial hypertension (6,9,10,13,14) and these parameters were therefore investigated.…”

Section: Introductionmentioning

confidence: 99%

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A Hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats

Nascimento¹,

Sugizaki

Leopoldo

et al. 2008

Arq Bras Endocrinol Metab

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The present study was carried to develop and analyze the consequences of hypercaloric pellet-diet cycle that promotes obesity in rats. Male Wistar rats were randomly distributed into two groups that received either normal diet (ND; n =32; 3,5 Kcal/g) or a hypercaloric diet (HD; n =32; 4,6 Kcal/g). The ND group received commercial Labina rat feeding while the HD animals received a cycle of five hypercaloric diets over a 14-week period. The effects of the diets were analyzed in terms of body weight, body composition, hormone-metabolite levels, systolic arterial pressure and glucose tolerance at the 5% significance level. The hypercaloric pellet diet cycle promoted an increase in body weight and fat, systolic arterial pressure and a high serum level of glucose, triacylglycerol, insulin and leptin. The HD group also presented an impaired glucose tolerance. In conclusion, the results of this study show that the hypercaloric pellet-diet cycle promoted obesity in Wistar rats and displayed several characteristics that are commonly associated with human obesity, such as high arterial pressure, insulin resistance, hyperglycaemia, hyperinsulinaemia, hyperleptinaemia and dyslipidaemia.

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Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

A Hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats

Nascimento¹,

Sugizaki

Leopoldo

et al. 2008

Arq Bras Endocrinol Metab

View full text Add to dashboard Cite

show abstract

“…Interestingly, the differences in weight gain between these strains occurred within the first 4 wk of the dietary intervention, but beyond this time period both strains had similar weight gain patterns. Previous investigations comparing alternative animal models that are either prone or resistant to the development of obesity indicate much of these differences can be attributed to variable dietary consumption (30,32,44,45,55). In opposition to these findings, the differences in weight gain found between HCR and LCR rats cannot be explained by differences in energy intake, since both strains were consuming similar absolute amounts of energy.…”

Section: Discussionmentioning

confidence: 92%

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

Noland¹,

Thyfault²,

Henes³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

121

138

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Dohm GL, Cortright RN, Lust RM. Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance. Am J Physiol Endocrinol Metab 293: E31-E41, 2007. First published March 6, 2007; doi:10.1152/ajpendo.00500.2006.-Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)-and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance. fatty acid; lipid metabolism; liver; heart; skeletal muscle THE INCIDENCE OF METABOLIC DISEASES such as obesity and type II diabetes is increasing dramatically and is strongly linked to the rise in cardiovascular disease. In 2002, ϳ64% of the population in the United States was classified as overweight or obese (22), and health care costs attributable to these conditions exceeded $78 billion dollars (13). Although type II diabetes afflicts a substantially lower percentage (ϳ6.3%) of the population (9), this disease accounts for $132 billion in annual health care costs (24). With the increase in the incidence of such metabolic diseases reaching epidemic proportions and the threat of health care costs spiraling out of control, much research has been focused toward elucidating the mechanisms involved in the etiology of these conditions in hopes of ultimately discovering better treatments. Several therapies are currently used to alleviate symptoms of these diseases, but other than dietary modifications, endurance exercise is the only universally prescribed treatment.Enhanced aerobic capacity has long been associated with diminished morbidity and improvements in functional living, yet all the physiological mechanisms ...

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“…However, the high-fat-induced phenotype varies distinctly, even within a group of animals with the same genetic background,9 10 and it has recently been demonstrated that disctinct gut microbiota profiles are associated with different metabolic phenotypes 11. Gut microbiota of humans and mice are more than 95% made up of three phyla: Firmicutes, Bacteroidetes and Actinobacteria.…”

Section: Introductionmentioning

confidence: 99%

Intestinal microbiota determines development of non-alcoholic fatty liver disease in mice

Roy

Llopis

Lepage

et al. 2012

Gut

773

418

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Physiological Difference between Dietary Obesity-Susceptible and Obesity-Resistant Sprague Dawley Rats in Response to Moderate High Fat Diet.

Cited by 24 publications

References 30 publications

A Hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats

A Hypercaloric pellet-diet cycle induces obesity and co-morbidities in wistar rats

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

Intestinal microbiota determines development of non-alcoholic fatty liver disease in mice

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