The role of leptin and cortisol in hyperactivity in patients with acute and weight-recovered anorexia nervosa

Ehrlich, Stefan; Burghardt, Roland; Schneider, Nora; Broecker-Preuß, Martina; Weiss, Deike; Merle, Julia V.; Craciun, Eugenia Maria; Pfeiffer, E. F.; Mann, Klaus; Lehmkuhl, Ulrike; Hebebrand, Johannes

doi:10.1016/j.pnpbp.2009.03.007

Cited by 46 publications

(39 citation statements)

References 35 publications

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“…Withdrawal of leptin during weight loss reduces its counterregulation of insulin actions, increases the sensitivity of the brain reward substrates to locomotor, olfactory, and gustatory rewards and increases the efficiency of insulin actions leading to lipogenesis and recovery of depleted body energy reservoirs. Leptin administration to underweight humans and animals suppresses the motivation to eat [305] , insulin metabolic efficiency [203,204,305] , and motivation for spontaneous locomotion [306][307][308][309] . With body mass loss and declines in leptin and insulin concentration, increased parasympathetic activation and sensitivities of tissues to insulin and leptin action facilitate efficient energy storage.…”

Section: Body Mass Lossmentioning

confidence: 99%

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Borer¹

2014

WJD

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A re-examination of the mechanism controlling eating, locomotion, and metabolism prompts formulation of a new explanatory model containing five features: a coordinating joint role of the (1) autonomic nervous system (ANS); (2) the suprachiasmatic (SCN) master clock in counterbalancing parasympathetic digestive and absorptive functions and feeding with sympathetic locomotor and thermogenic energy expenditure within a circadian framework; (3) interaction of the ANS/SCN command with brain substrates of reward encompassing dopaminergic projections to ventral striatum and limbic and cortical forebrain. These drive the nonhomeostatic feeding and locomotor motivated behaviors in interaction with circulating ghrelin and lateral hypothalamic neurons signaling through melanin concentrating hormone and orexin-hypocretin peptides; (4) counterregulation of insulin by leptin of both gastric and adipose tissue origin through: potentiation by leptin of cholecystokinin-mediated satiation, inhibition of insulin secretion, suppression of insulin lipogenesis by leptin lipolysis, and modulation of peripheral tissue and brain sensitivity to insulin action. Thus weight-loss induced hypoleptimia raises insulin sensitivity and promotes its parasympathetic anabolic actions while obesity-induced hyperleptinemia supresses insulin lipogenic action; and (5) inhibition by leptin of bone mineral accrual suggesting that leptin may contribute to the maintenance of stability of skeletal, lean-body, as well as adipose tissue masses.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Insulin; Leptin; Weight regulation; Autonomic; Circadian Core tip: The novel proposal for the mechanism of body weight regulation deals with all three components of body mass: bone, lean tissue, and fat depots. It attributes the central control of counterbalancing energy expenditure and intake to an autonomic nervous systemcircadian clock command center that encompases brain reward substrates, lateral hypothalamic peptidergic circuits and areas of the cortex. The nonhomeostatic character of feeding and locomotion is driven and controlled by the reward circuits and modulated by shifts in insulin sensitivity induced by counterregulation by leptin of insulin as weight deviates between underweight and overweight and alters basal leptin concentrations.Borer KT. Counterregulation of insulin by leptin as key component of autonomic regulation of body weight. World J Diabetes 2014; 5(5): 606-629 Available from:

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Section: Body Mass Lossmentioning

confidence: 99%

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Borer¹

2014

WJD

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“…Bei Patientinnen mit Anorexia nervosa muss eine physiologisch (u. a. durch Veränderungen des Leptinspiegels) bedingte, nicht bewusst intendierte Bewegungsunruhe und Hyperaktivität von "zwanghaft-süchtiger" und von zielgerichteter körperlicher und sportlicher Aktivität zur Gewichtskontrolle unterschieden werden [ 16 , 17 ] . Erstere lässt bei positiver Energiebilanz wieder nach [ 18 ] . Es kann bei Anorexia nervosa dabei zu fl ießenden Übergängen zwischen Bewegungsunruhe, gesteigerter Alltagsaktivität zur Erhöhung des Kalorienverbrauchs (Treppenlaufen, schnelles Spazierengehen usw.)…”

Section: Ambulante Sporttherapie Für Patientinnen Mit Essstörungen: Eunclassified

Ambulante Sporttherapie für Patientinnen mit Essstörungen: Ein Pilotprojekt

Schlegel

Hafner

Hartmann

et al. 2012

Psychother Psych Med

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Many patients with Anorexia and Bulimia Nervosa (AN, BN) engage in sport and physical activity in an excessive and compulsive manner, mostly to influence weight and shape. Many of them experience guilt in case of not exercising. However, sport and physical exercise can also have a positive effect on mental illness by influencing mood, sense of self-esteem and body experience. Until now, only few programs for eating disorder patients exist which aim at changing physical activity behavior and use sport and exercise activities in a therapeutic way. We developed a sport-therapeutic program designed for outpatients with eating disorders. It supervises sport and physical exercise and helps patients to use sport and exercise in a healthy manner. This report presents the program's manual and first experiences based on half-standardized interviews.

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“…56 Results from studies in patients with AN have shown an association between excessive physical activity and low leptin levels, leading researchers to conclude that low leptin levels may directly or indirectly influence behaviors and cognitions that contribute to hyperactivity and motor restlessness. [57][58][59] Therefore, low leptin levels-as a consequence of weight loss due to starvation-may contribute to the maintenance of low body weight in patients with AN.…”

Section: Regulators Of Appetite and Body Weightmentioning

confidence: 99%

Laboratory Parameters and Appetite Regulators in Patients with Anorexia Nervosa

Himmerich

Schönknecht²,

Heitmann³

et al. 2010

Journal of Psychiatric Practice

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Anorexia nervosa (AN) has serious negative effects on multiple organs and systems of the human body. As patients often do not make their eating disorder the subject of discussion, the physician is forced to rely on the physical examination and laboratory parameters as diagnostic hints. Obvious signs of AN are a body mass index (BMI) below 17.5 kg/m, dry and scaly skin, lanugo, edema, acrocyanosis, petechias, dental problems, and low blood pressure. However, because the often complex laboratory alterations can be difficult for the general psychiatrist to interpret, this article presents some useful guidelines. The plasma of patients with AN often shows alterations in laboratory parameters and appetite regulators, including electrolytes, liver enzymes, leukocyte count, hemoglobin (Hb), leptin, neuropeptide Y (NPY), triiodothyronine (T3), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, ghrelin, pancreatic polypeptide (PP), tumor necrosis factor-alpha (TNF-alpha), and cortisol. Medical problems secondary to AN or due to the treatment itself may lead to further laboratory abnormalities. To date, despite these associated laboratory alterations, the diagnosis of anorexia is a clinical one, based on weight and specific psychopathology.

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The role of leptin and cortisol in hyperactivity in patients with acute and weight-recovered anorexia nervosa

Cited by 46 publications

References 35 publications

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Ambulante Sporttherapie für Patientinnen mit Essstörungen: Ein Pilotprojekt

Laboratory Parameters and Appetite Regulators in Patients with Anorexia Nervosa

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