Leptin levels in patients with anorexia nervosa are reduced in the acute stage and elevated upon short-term weight restoration

Hebebrand, Johannes; Blum, Werner; Barth, Nikolaus; Coners, H; Englaro, Piera; Juul, Anders; Ziegler, Andreas; Warnke, Andreas; Rascher, Wolfgang; Remschmidt, Helmut

doi:10.1038/sj.mp.4000282

Cited by 216 publications

(148 citation statements)

References 2 publications

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“…Basal body temperature of ad libitum-fed rats was not altered following chronic olanzapine treatment, which is in contrast with another study reporting dose-dependent hypothermia following acute olanzapine treatment in ad libitum-fed rats (Oerther and Ahlenius 2000). It has previously been shown that peripheral leptin treatment reduced hyperactivity of rats exposed to the semistarvation-induced hyperactivity model (Exner et al 2000), and it was proposed that decreases in leptin signaling might trigger hyperactivity in rats, as well as in AN patients (Hebebrand et al 1997). In our study, plasma leptin levels were undetectable in both vehicle-and olanzapine-treated ABA rats.…”

Section: Discussionsupporting

confidence: 46%

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Hillebrand

Elburg

Kas

et al. 2005

Biological Psychiatry

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Section: Discussionsupporting

confidence: 46%

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Hillebrand

Elburg

Kas

et al. 2005

Biological Psychiatry

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“…In this model, administration of L-tryptophan and serotonin agonists and antagonists reduced physical activity (Pirke et al 1993) and tyrosine supplementation improved appetite and cognitive function and delayed the onset of fatigue in mice . Just as activity levels and restlessness in AN are sustained by a negative energy balance and low plasma leptin concentrations (van Elburg et al 2007), hypoleptinemia (Hebebrand et al 1997) and low glucose levels increase wheel running in rats (Takeda et al 2003).…”

Section: Animal Models Of Anmentioning

confidence: 99%

Relevance of animal models to human eating disorders and obesity

2008

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Background and rationale This review addresses the role animal models play in contributing to our knowledge about the eating disorders anorexia nervosa (AN) and bulimia nervosa (BN) and obesity. Objectives Explore the usefulness of animal models in complex biobehavioral familial conditions, such as AN, BN, and obesity, that involve interactions among genetic, physiologic, psychological, and cultural factors. Results and conclusionsThe most promising animal model to mimic AN is the activity-based anorexia rodent model leading to pathological weight loss. The paradigm incorporates reward elements of the drive for activity in the presence of an appetite and allows the use of genetically modified animals. For BN, the sham-feeding preparation in rodents equipped with a gastric fistula appears to be best suited to reproduce the postprandial emesis and the defects in satiety. Animal models that incorporate genes linked to behavior and mood may clarify biobehavioral processes underlying AN and BN. By contrast, a relative abundance of animal models has contributed to our understanding of human obesity. Both environmental and genetic determinants of obesity have been modeled in rodents. Here, we consider single gene mutant obesity models, along with models of obesigenic environmental conditions. The contributions of animal models to obesity research are illustrated by their utility for identifying genes linked to human obesity, for elucidating the pathways that regulate body weight and for the identification of potential therapeutic targets. The utility of these models may be further improved by exploring the impact of experimental manipulations on the behavioral determinants of energy balance.

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“…Os autores postulam que a recuperação precipitada da leptina plasmática pode explicar a resistência a ganho de peso observada em pacientes em tratamento, em particular, nas fases em que os pacientes estão próximos ao peso alvo. Um outro grupo independente também observou que a elevação dos níveis da leptina ocorreu antes da recuperação integral do peso em pacientes com anorexia em fase de tratamento (74). Do ponto de vista reprodutivo, a leptina de jejum em pacientes com anorexia nervosa é um fator preditivo da volta da menstruação melhor do que IMC, massa de tecido gorduroso ou porcentagem da gordura corporal (75).…”

Section: Transtornos Alimentaresunclassified

Leptina: o diálogo entre adipócitos e neurônios

Negrão¹,

Licinio

2000

Arq Bras Endocrinol Metab

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The discovery of leptin led to a renewed interest in the study of enegy homeostasis. It is now recognized that white adipose tissue is the major site of leptin synthesis. After it is secreted into the bloodstream leptin binds itself to specific receptors in the brain, providing the central nervous system with a satiety signal that reflects the amount of energy stored as fat. Acting through receptors that transduce a signal by the JAK/STAT pathway, leptin modifies the expression and activity of hypothalamic peptides that regulate appetite and energy expenditure. In addition, leptin signals nutritional status to other physiological systems and modulates the function of several target glands. More recently, recombinant leptin was successfully given to an obese patient with leptin deficiency due to a mutation in the ob gene. On the other hand, the effects of recombinant leptin in the only study with obese patients and increased levels of circulating leptin were less impressive.Here we review the complexity of leptin actions with a focus on its integrative role as a signal of nutritional status for the organism.

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Leptin levels in patients with anorexia nervosa are reduced in the acute stage and elevated upon short-term weight restoration

Cited by 216 publications

References 2 publications

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Relevance of animal models to human eating disorders and obesity

Leptina: o diálogo entre adipócitos e neurônios

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