Feeding and temperature responses to intravenous leptin infusion are differential predictors of obesity in rats

Ruffin, Marie-Pierre; Adage, Tiziana; Kuipers, Folkert; Strubbe, J.H.; Scheurink, Antonius; Dijk, Gertjan van

doi:10.1152/ajpregu.00508.2002

Cited by 10 publications

(12 citation statements)

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“…There was, in fact, a slight decrease in the intake of chow (12% suppression relative to basal intake). This is consistent with one of our previous studies using the same paradigm, which finally led to an 82% increase in body weight relative to a group of rats that were left on chow (19). During the last week of HED exposure, rats were subjected to IVGTTs.…”

Section: Assessment Of Sensitivity To Mtii and Leptin And Their Relatsupporting

confidence: 91%

“…This diet consisted of a 10% sucrose solution in which corn oil was emulsified. This diet was based on the work of Lucas and Sclafani (17) and Smith et al (18) and causes DIO in rats (19). The concentration of corn oil was doubled every 2 wk starting with 4% and finally ending up at 32% corn oil over the last weeks.…”

Section: Experimental Designmentioning

confidence: 99%

“…The concentration of corn oil was doubled every 2 wk starting with 4% and finally ending up at 32% corn oil over the last weeks. The diet was freshly made each day, and specifics for preparation can be found elsewhere (19). Food intake (chow and HED) and body weight of rats were assessed on the final day of each dietary step.…”

Section: Experimental Designmentioning

confidence: 99%

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Reduced Anorexigenic Efficacy of Leptin, But Not of the Melanocortin Receptor Agonist Melanotan-II, Predicts Diet-Induced Obesity in Rats

Dijk¹,

Vries²,

Nyakas³

et al. 2005

Endocrinology

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Leptin gains access to the central nervous system where it influences activity of neuronal networks involved in ingestive behavior, neuroendocrine activity, and metabolism. In particular, the brain melanocortin (MC) system is important in leptin signaling and maintenance of energy balance. Although leptin or MC receptor insensitivity has been proposed to be associated with obesity, the present study compared central leptin and MC receptor stimulation on some of the above-mentioned parameters and investigated whether these treatments predict proneness to diet-induced obesity (DIO) in outbred Wistar rats. Third-cerebroventricular administration of equi-anorexigenic doses of leptin and of the MC agonist melanotan-II caused comparable increases in plasma ACTH and corticosterone levels and c-Fos-labeling in approximately 70% of paraventricular hypothalamic (PVN) neuronal cell bodies containing CRH. This reinforces involvement of paraventricular CRH neurons in the short-term neuroendocrine and ingestive effects of leptin and melanocortins. In the DIO prediction study, anorexigenic efficacy of melanotan-II was not correlated with any parameter linked to DIO but was highly correlated with MC in situ binding (with labeled [Nle(4),D-Phe(7)]alpha-MSH) as well as CRH immunoreactivity in the PVN of DIO rats. This suggests intricate relationships among MC signaling, the CRH system, and ingestive behavior unrelated to DIO. In the same animals, leptin's anorexigenic efficacy was not correlated with PVN MC in situ binding or CRH immunoreactivity but correlated inversely to post-DIO plasma leptin, liver weight, and abdominal adiposity, the latter being correlated to insulin resistance. Thus, differences in leptin but not MC signaling might underlie DIO, visceral obesity, and insulin resistance.

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Section: Assessment Of Sensitivity To Mtii and Leptin And Their Relatsupporting

confidence: 91%

Section: Experimental Designmentioning

confidence: 99%

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Reduced Anorexigenic Efficacy of Leptin, But Not of the Melanocortin Receptor Agonist Melanotan-II, Predicts Diet-Induced Obesity in Rats

Dijk¹,

Vries²,

Nyakas³

et al. 2005

Endocrinology

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“…35 Rats that were relatively insensitive to leptin's anorexigenic effect were more prone to obesity when fed a high-fat diet. 36 Because leptin-sensitive neurons are also present in areas important for reward mechanisms, 31,32,37 it would be interesting to study whether the leptin sensitivity and the motivation to press for sucrose that both predict future obesity are related.…”

Section: Discussionmentioning

confidence: 99%

A reciprocal interaction between food-motivated behavior and diet-induced obesity

et al. 2007

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Objectives: One of the main causes of obesity is overconsumption of diets high in fat and sugar. We studied the metabolic changes and food-motivated behavior when rats were subjected to a choice diet with chow, lard and a 30% sucrose solution (high fat high sugar (HFHS)-choice diet). Because rats showed considerable variations in the feeding response to HFHS-choice diet and in food-motivated behavior, we investigated whether the motivation to obtain a sucrose reward correlated with the development of obesity when rats were subsequently subjected to HFHS-choice diet. Method: We first studied feeding, locomotor activity and body temperature, fat weights and hormonal concentrations when male Wistar rats were subjected to HFHS-choice diet for 1 week. Second, we studied sucrose-motivated behavior, using a progressive ratio (PR) schedule of reinforcement in rats that were subjected to the HFHS-choice diet for at least 2 weeks, compared to control rats on a chow diet. Third, we measured motivation for sucrose under a PR schedule of reinforcement in rats that were subsequently subjected to HFHS-choice diet or a chow diet for 4 weeks. Fat weights were measured and correlated with the motivation to obtain sucrose pellets. Results: One week on the HFHS-choice diet increased plasma concentrations of glucose and leptin, increased fat stores, but did not alter body temperature or locomotor activity. Moreover, consuming the HFHS-choice diet for several weeks increased the motivation to work for sucrose pellets. Furthermore, the motivation to obtain sucrose pellets correlated positively with abdominal fat stores in rats subsequently subjected to the HFHS-choice diet, whereas this correlation was not found in rats fed on a chow diet. Conclusion: Our data suggest that the motivation to respond for palatable food correlates with obesity due to an obesogenic environment. Conversely, the HFHS-choice diet, which results in obesity, also increased the motivation to work for sucrose. Thus, being motivated to work for sucrose results in obesity, which, in turn, increases food-motivated behavior, resulting in a vicious circle of food motivation and obesity. IntroductionObesity is one of the fastest growing medical problems in modern society. It contributes to the development of chronic disorders such as cardiovascular disease, type 2 diabetes, hypertension and some cancers. 1 For healthy body weight regulation, it is important to balance energy intake and energy expenditure. Modern society, however, is characterized by a sedentary lifestyle and a calorie intake, which is not adjusted for that. Although regulatory mechanisms that balance intake and expenditure are known , 2,3 it still remains unclear why this fails in obese individuals. It has been postulated that the ability to overconsume high-energy dense foods (in the face of plentiful food availability) was selected during evolution. Thus, under conditions when food availability is uncertain and scarce, consuming highenergy dense foods is an adequate adaptation (for a review see Uli...

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“…Selective breeding has shown that the DIO phenotype is not simply the result of a primary hyperphagia (45). Outbred DIO rats demonstrate reduced anorectic sensitivity to leptin (62,65) and to insulin (15). Studies with selectively bred DIO rats confirm the reduced leptin sensitivity (45) and suggest that this is a preexisting defect and not related to the reduction of leptin transport that occurs upon development of obesity.…”

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confidence: 96%

Physiological regulation of food intake

Cupples¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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3 other HighWire-hosted articles: This article has been cited by http://ajpregu.physiology.org/content/288/6/R1438#cited-by including high resolution figures, can be found at: Updated information and services http://ajpregu.physiology.org/content/288/6/R1438.full can be found at: and Comparative Physiology American Journal of Physiology -Regulatory, Integrative about Additional material and information http://www.the-aps.org/publications/ajpregu This information is current as of April 15, 2013.

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Feeding and temperature responses to intravenous leptin infusion are differential predictors of obesity in rats

Cited by 10 publications

References 40 publications

Reduced Anorexigenic Efficacy of Leptin, But Not of the Melanocortin Receptor Agonist Melanotan-II, Predicts Diet-Induced Obesity in Rats

Reduced Anorexigenic Efficacy of Leptin, But Not of the Melanocortin Receptor Agonist Melanotan-II, Predicts Diet-Induced Obesity in Rats

A reciprocal interaction between food-motivated behavior and diet-induced obesity

Physiological regulation of food intake

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