AgRP(83–132) and SHU9119 differently affect activity-based anorexia

Hillebrand, J.J.G.; Kas, Martien; Scheurink, Antonius; Dijk, Gertjan van; Adan, Roger A.H.

doi:10.1016/j.euroneuro.2005.11.004

Cited by 40 publications

(36 citation statements)

References 65 publications

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“…24 Furthermore, increased body temperature has been reported in some treatments that increase survival in ABA, such as olanzapine 35 and the Agouti-related protein, AgRP, an endogenous antagonist of the MC system. 16,17 Interestingly, leptin also prevented hypothermia in rats but its additional food intake suppression aggravated weight loss and survival was impossible. 15 Because of the integrated, nonlinear nature of energy homeostasis neurocircuitry, the most up-todate efforts to find a single peptide or hormone for ABA recovery have been fruitless.…”

Section: Resultsmentioning

confidence: 97%

“…12,13 This animal model has advanced our understanding of the interaction between starvation and hyperactivity, and some pharmacological interventions have been moderately successful in partially preventing the development of the ABA outcome. These studies have focused on well characterized neuroendocrine systems involved in energy homeostasis, either on peripheral signaling to the hypothalamus, as in the case of the hormone leptin secreted by adipocytes, 14,15 or on central systems such as the melanocortin (MC), 16,17 and serotoninergic (5-HT) [18][19][20] systems. However, research using the ABA model has yet to identify a pharmacological agent that will aid rats to recover once running escalates and weight loss exceeds 20% of baseline body weight.…”

Section: Introductionmentioning

confidence: 99%

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Heat reversal of activity‐based anorexia: Implications for the treatment of anorexia nervosa

Gutiérrez

Cerrato

Carrera

et al. 2008

Intl J Eating Disorders

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Section: Resultsmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Heat reversal of activity‐based anorexia: Implications for the treatment of anorexia nervosa

Gutiérrez

Cerrato

Carrera

et al. 2008

Intl J Eating Disorders

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“…raISH procedure has been described previously (Hillebrand et al, 2006). Expression of AgRP, NPY, and POMC in the arcuate nucleus and expression of MCH and prepro-orexin in the LH were quantified using Image J software (National Institutes of Health, Bethesda, MD).…”

Section: Methodsmentioning

confidence: 99%

Differential Effects of Recombinant Adeno-Associated Virus-Mediated Neuropeptide Y Overexpression in the Hypothalamic Paraventricular Nucleus and Lateral Hypothalamus on Feeding Behavior

Tiesjema¹,

Adan²,

Luijendijk³

et al. 2007

J. Neurosci.

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It is well known that neuropeptide Y (NPY) increases food intake. The hypothalamic paraventricular nucleus (PVN) and the lateral hypothalamus (LH) are both involved in the acute, hyperphagic effects of NPY. Although it is obvious that increased energy intake may lead to obesity, it is less understood which aspects of feeding behavior are affected and whether one or multiple neural sites mediate the effects of long-term increased NPY signaling. By long-term overexpressing NPY in either the PVN or the LH, we uncovered brain site-specific effects of NPY on meal frequency, meal size, and diurnal feeding patterns. In rats injected with adeno-associated virus-NPY in the PVN, increased food intake resulted from an increase in the amount of meals consumed, whereas in rats injected in the LH, increased food intake was attributable to increased meal size. Interestingly, food intake and body weight gain were only temporarily increased in PVN-injected rats, whereas in LH-injected rats hyperphagia and body weight gain remained for the entire 50 d. Moreover, in LH-NPY rats, but not in PVN-NPY rats, diurnal rhythmicity with regard to food intake and body core temperature was lost. These data clearly show that the NPY system differentially regulates energy intake and energy expenditure in the PVN and LH, which together adjust energy balance.

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“…Another study of the same group likewise revealed no significant effect of centrally infused AgRP on running wheel activity. 107 Nevertheless, it has been suggested that a hyperactive melanocortinergic system underlies the SIH phenotype. 104,105,107 Other possible effectors downstream of the leptin receptor that might be implicated in SIH are the serotonergic and/or dopaminergic system as well as the hypothalamic-pituitary adrenal axis.…”

Section: Hyperactivitymentioning

confidence: 99%

The role of leptin in anorexia nervosa: clinical implications

et al. 2006

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Leptin is a hormone with pleiotropic functions affecting several tissues. Because leptin has a crucial role in the adaptation of an organism to semi-starvation, anorexia nervosa (AN) serves as a model disorder to elucidate the functional implications of hypoleptinaemia; vice versa, several symptoms in patients with this eating disorder are related to the low leptin levels, which are characteristic of acute AN. Weight gain in AN patients can induce relative hyperleptinaemia in comparison to controls matched for body mass index; circulating leptin concentrations in AN patients thus transverse from subnormal to supranormal levels within a few weeks. We review findings on leptin secretion in AN and focus on implications, particularly for the hypothalamus-pituitary-gonadal axis, bone mineral density and physical hyperactivity. Undoubtedly, the elucidation of leptin's function as a trigger of diverse neuroendocrine adaptations to a restricted energy intake has substantially advanced our knowledge of the pathogenesis of distinct symptoms of AN, including amenorrhoea that represents one of the four diagnostic criteria. The fact that hypoleptinaemia can induce hyperactivity in a rat model for AN has led to a series of studies in AN patients, which support the notion that application of leptin to severely hyperactive patients might prove beneficial.

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AgRP(83–132) and SHU9119 differently affect activity-based anorexia

Cited by 40 publications

References 65 publications

Heat reversal of activity‐based anorexia: Implications for the treatment of anorexia nervosa

Heat reversal of activity‐based anorexia: Implications for the treatment of anorexia nervosa

Differential Effects of Recombinant Adeno-Associated Virus-Mediated Neuropeptide Y Overexpression in the Hypothalamic Paraventricular Nucleus and Lateral Hypothalamus on Feeding Behavior

The role of leptin in anorexia nervosa: clinical implications

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