Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for  Obesity Intervention

Roth, Christian

doi:10.3390/jcm4091774

Cited by 66 publications

(55 citation statements)

References 181 publications

(274 reference statements)

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“…Damage to the arcuate nucleus, resulting in leptin resistance and hyperinsulinaemia, is thought to result in hyperphagia; leptin supplementation is not a therapeutic option for these patients, but recent trials have included strategies to reduce insulin secretion (see below and Table ). There are multiple reasons for reduced energy expenditure in CP, including visual and neurological disability, somnolence, reduced sympathetic tone, and deconditioning from obesity, the identification of which may provide a therapeutic target . Excessive energy storage mediated by hyperinsulinism may be targeted with pharmaceutical interventions or with metabolic surgery .…”

Section: Obesitymentioning

confidence: 99%

“…The impact of radiotherapy on long‐term weight gain must also be considered; one study has shown a detrimental effect of radiotherapy on physical activity . Weight gain is particularly rapid in the first year after surgery . A description of the function of hypothalamic nuclei in energy balance, which may be damaged by tumour bulk or surgical insult, is provided in Table with a cartoon description in Figure and is reviewed in detail by Roth …”

Section: Obesitymentioning

confidence: 99%

“…Weight gain is particularly rapid in the first year after surgery . A description of the function of hypothalamic nuclei in energy balance, which may be damaged by tumour bulk or surgical insult, is provided in Table with a cartoon description in Figure and is reviewed in detail by Roth …”

Section: Obesitymentioning

confidence: 99%

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Management of hypothalamic disease in patients with craniopharyngioma

Thompson

Costello

Crowley

2019

Clinical Endocrinology

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Patients with craniopharyngioma experience excess morbidity and mortality when compared with the background population and with other hypopituitary patients.Large, suprasellar tumours which form micropapillae into surrounding structures can cause hypothalamic damage before any therapeutic intervention; attempted gross total resection can lead to hypothalamic obesity, sleep disorders, thirst disorders and dysregulation of temperature as well as panhypopituitarism. The management of tumour bulk and the pathophysiology of hypothalamic complications have been reviewed extensively. We present a practical, clinical approach to management of hypothalamic disease in a patient with craniopharyngioma and highlight potential targets for future pharmacological or surgical intervention. K E Y W O R D Scraniopharyngioma, hypopituitarism, hypothalamus, obesity, sleep disorders, thirst

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Section: Obesitymentioning

confidence: 99%

Section: Obesitymentioning

confidence: 99%

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Management of hypothalamic disease in patients with craniopharyngioma

Thompson

Costello

Crowley

2019

Clinical Endocrinology

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“…Although 12–19% of affected patients are already obese at diagnosis, the most rapid, uncontrollable weight gain usually occurs during the first 6–12 months following neurosurgical intervention [6]. Adding to the well-established characteristics of hypothalamic obesity, extremely obese craniopharyngioma patients typically suffer from panhypopituitarism and demonstrate significant hyperleptinemia due to anatomic leptin resistance, inadequate hyperinsulinemia for their degree of obesity, impaired incretin response, and reduced levels of blood catecholamines and urinary metabolites, and α-MSH [5, 7, 8]. …”

Section: Introductionmentioning

confidence: 99%

Treatment of Hypothalamic Obesity with Dextroamphetamine: A Case Series

Denzer¹,

Denzer²,

Lennerz³

et al. 2019

Obes Facts

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Background: A limited number of published case reports suggest a positive effect of dextroamphetamine, an adrenergic agonist affecting both the central nervous system (CNS) and peripheral nervous system, on physical activity and weight in patients with hypothalamic obesity (intractable obesity following CNS insult). Here, we present our clinical experience with dextroamphetamine treatment for hypothalamic obesity. Methods: The clinical course of all patients started on dextroamphetamine treatment for severe hypothalamic obesity at our institution between 2010 and 2013 is reported. Dextroamphetamine administration was initiated at a single dose of 5 mg per day and titrated to effect up to a dose of 20 mg/day. BMI z-score velocity was calculated as change in BMI z-score over standardized intervals of 12 months. Parameters of treatment success and adverse events were assessed in a standardized fashion. Results: Seven patients (2 males; mean age 17.6 years [range 12.9–24.5]) underwent individual treatment attempts with dextroamphetamine between 2010 and 2013. The primary diagnoses were craniopharyngioma (n = 4), ganglioglioma WHO I (n = 1), astrocytoma (n = 1), and neonatal meningitis (n = 1). Time from initial CNS insult to initiation of dextroamphetamine treatment averaged 5.2 years (range 2.4 months to 16.5 years). All patients demonstrated a steady increase in BMI z-score from the time of initial diagnosis until initiation of dextroamphetamine treatment. Mean baseline BMI z-score was +3.17 ± 0.93 (+1.9 to +4.4). Mean BMI z-score velocity decelerated to –0.18 ± 0.12 per year during the first year of treatment and stabilized at +0.05 ± 0.32 per year during the second year of treatment. No significant adverse events were reported. Conclusion: Dextroamphetamine treatment led to stabilization or reduction of BMI z-score in a cohort of 7 patients with hypothalamic obesity, with no adverse effects. Considering the projected increase in BMI z-score according to the natural course of the disease, these findings are promising and warrant further study.

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“…The hypothalamus regulates glucose metabolism through parasympathetic activity. Hypothalamic damage, mainly due to brain tumour, may result in upregulation of parasympathetic activity resulting in hyperinsulinemia [199]. Often, obesity is associated with hyperinsulinemia, both under fasting conditions and post-prandially.…”

Section: Somatostatin and Obesitymentioning

confidence: 99%

Role of Somatostatin in the Regulation of Central and Peripheral Factors of Satiety and Obesity

Kumar

Singh

2020

IJMS

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Obesity is one of the major social and health problems globally and often associated with various other pathological conditions. In addition to unregulated eating behaviour, circulating peptide-mediated hormonal secretion and signaling pathways play a critical role in food intake induced obesity. Amongst the many peptides involved in the regulation of food-seeking behaviour, somatostatin (SST) is the one which plays a determinant role in the complex process of appetite. SST is involved in the regulation of release and secretion of other peptides, neuronal integrity, and hormonal regulation. Based on past and recent studies, SST might serve as a bridge between central and peripheral tissues with a significant impact on obesity-associated with food intake behaviour and energy expenditure. Here, we present a comprehensive review describing the role of SST in the modulation of multiple central and peripheral signaling molecules. In addition, we highlight recent progress and contribution of SST and its receptors in food-seeking behaviour, obesity (orexigenic), and satiety (anorexigenic) associated pathways and mechanism.Contrary to obesity, satiety is a sense of fullness due to ephemeral lack of interest in further ingestion of food, which eventually leads to the suppression of appetite. Fullness is supposed to have a vital role in weight management because it will impact the frequency and amount of food and drink consumed later [53]. The feeling of satiety is a well-organized and biologically oriented process [54,55]. Satiety is a well-articulated process which reduces gastric distension and cholecystokinin (CCK) release in gut post ingestion of nutrients and importantly has been associated with signals from periphery via vagal afferent fibers that terminate in nucleus of the tractus solitaries (NTS) in the brain stem [56]. Besides, leptin, a hormone secreted by adipocytes, is also associated with satiety signals and studies further indicate that satiety response to CCK that was blocked in leptin receptor-deficient rat was regained following restoration of the leptin receptor in arcuate nucleus (ARC) [57][58][59]. Studies also support the role of NTS vagus afferent in response to leptin [60,61]. Feeling satiated will, in the long run, smother the inclination for cravings and lead to lesser consumption of food in the next meal. Satiety is not a response; it involves a complex mechanism for its operation, which includes the crucial role of the hypothalamus and peripheral hormones and determines energy expenditure [62]. Measurement of satiation can be done either directly by assessing food intake or indirectly by subjectively rating the urge for appetite [63]. Schwartz et al. demonstrated that hypothalamus is the central brain region responsible for adiposity signal; however, it is not an active participant in satiety [64]. It is interesting to note that most satiety associated information is relayed to NTS afferent fibers from the vagus nerve and afferent from GIT through the spinal cord. Mechanical or chemical stimula...

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Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Cited by 66 publications

References 181 publications

Management of hypothalamic disease in patients with craniopharyngioma

Management of hypothalamic disease in patients with craniopharyngioma

Treatment of Hypothalamic Obesity with Dextroamphetamine: A Case Series

Role of Somatostatin in the Regulation of Central and Peripheral Factors of Satiety and Obesity

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