Expanding the definition of hypothalamic obesity

Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of hypothalamic tumours. However, polyphagia and weight gain complicate other disorders related to the hypothalamus, including those that cause...

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Published inObesity reviews Vol. 11; no. 10; pp. 709 - 721
Main Authors Hochberg, I, Hochberg, Z
Format Journal Article
LanguageEnglish
Published Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.10.2010
Blackwell Publishing Ltd
Subjects
animal injuries
Eating - physiology
Energy Metabolism - physiology
Homeostasis - physiology
Humans
hypothalamic obesity
Hypothalamus - physiology
Hypothalamus - physiopathology
Obesity - chemically induced
Obesity - etiology
Obesity - genetics
Obesity - therapy
Prader-Willi syndrome
Prader-Willi Syndrome - genetics
Prader-Willi Syndrome - physiopathology
Psychotropic Drugs - adverse effects
trauma
Weight Gain
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Abstract Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of hypothalamic tumours. However, polyphagia and weight gain complicate other disorders related to the hypothalamus, including those that cause structural damage to the hypothalamus like tumours, trauma, radiotherapy; genetic disorders such as Prader-Willi syndrome; side effects of psychotropic drugs; and mutations in several genes involved in hypothalamic satiety signalling. Moreover, 'simple' obesity is associated with polymorphisms in several genes involved in hypothalamic weight-regulating pathways. Thus, understanding HyOb may enhance our understanding of 'simple' obesity. This review will claim that HyOb is a far wider phenomenon than hitherto understood by the narrow definition of post-surgical weight gain. It will emphasize the similarity in clinical characteristics and therapeutic approaches for HyOb, as well as its mechanisms. HyOb, regardless of its aetiology, is a result of impairment in hypothalamic regulatory centres of body weight and energy expenditure. The pathophysiology includes loss of sensitivity to afferent peripheral humoral signals, such as, leptin on the one hand and dysfunctional afferent signals, on the other hand. The most important afferent signals deranged are energy regulation by the sympathetic nervous system and regulation of insulin secretion. Dys-regulation of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity and melatonin may also have a role in the development of HyOb. The complexity of the syndrome requires simultaneous targeting of several mechanisms that are deranged in the HyOb patient. We review the studies evaluating possible treatment strategies, including sympathomimetics, somatostatin analogues, triiodothyronine, sibutramine, and surgery.
AbstractList SummaryHypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of hypothalamic tumours. However, polyphagia and weight gain complicate other disorders related to the hypothalamus, including those that cause structural damage to the hypothalamus like tumours, trauma, radiotherapy; genetic disorders such as Prader-Willi syndrome; side effects of psychotropic drugs; and mutations in several genes involved in hypothalamic satiety signalling. Moreover, 'simple' obesity is associated with polymorphisms in several genes involved in hypothalamic weight-regulating pathways. Thus, understanding HyOb may enhance our understanding of 'simple' obesity. This review will claim that HyOb is a far wider phenomenon than hitherto understood by the narrow definition of post-surgical weight gain. It will emphasize the similarity in clinical characteristics and therapeutic approaches for HyOb, as well as its mechanisms. HyOb, regardless of its aetiology, is a result of impairment in hypothalamic regulatory centres of body weight and energy expenditure. The pathophysiology includes loss of sensitivity to afferent peripheral humoral signals, such as, leptin on the one hand and dysfunctional afferent signals, on the other hand. The most important afferent signals deranged are energy regulation by the sympathetic nervous system and regulation of insulin secretion. Dys-regulation of 11b-hydroxysteroid dehydrogenase 1 (11b-HSD1) activity and melatonin may also have a role in the development of HyOb. The complexity of the syndrome requires simultaneous targeting of several mechanisms that are deranged in the HyOb patient. We review the studies evaluating possible treatment strategies, including sympathomimetics, somatostatin analogues, triiodothyronine, sibutramine, and surgery.
Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of hypothalamic tumours. However, polyphagia and weight gain complicate other disorders related to the hypothalamus, including those that cause structural damage to the hypothalamus like tumours, trauma, radiotherapy; genetic disorders such as Prader-Willi syndrome; side effects of psychotropic drugs; and mutations in several genes involved in hypothalamic satiety signalling. Moreover, 'simple' obesity is associated with polymorphisms in several genes involved in hypothalamic weight-regulating pathways. Thus, understanding HyOb may enhance our understanding of 'simple' obesity. This review will claim that HyOb is a far wider phenomenon than hitherto understood by the narrow definition of post-surgical weight gain. It will emphasize the similarity in clinical characteristics and therapeutic approaches for HyOb, as well as its mechanisms. HyOb, regardless of its aetiology, is a result of impairment in hypothalamic regulatory centres of body weight and energy expenditure. The pathophysiology includes loss of sensitivity to afferent peripheral humoral signals, such as, leptin on the one hand and dysfunctional afferent signals, on the other hand. The most important afferent signals deranged are energy regulation by the sympathetic nervous system and regulation of insulin secretion. Dys-regulation of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity and melatonin may also have a role in the development of HyOb. The complexity of the syndrome requires simultaneous targeting of several mechanisms that are deranged in the HyOb patient. We review the studies evaluating possible treatment strategies, including sympathomimetics, somatostatin analogues, triiodothyronine, sibutramine, and surgery.
Summary Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of hypothalamic tumours. However, polyphagia and weight gain complicate other disorders related to the hypothalamus, including those that cause structural damage to the hypothalamus like tumours, trauma, radiotherapy; genetic disorders such as Prader–Willi syndrome; side effects of psychotropic drugs; and mutations in several genes involved in hypothalamic satiety signalling. Moreover, ‘simple’ obesity is associated with polymorphisms in several genes involved in hypothalamic weight‐regulating pathways. Thus, understanding HyOb may enhance our understanding of ‘simple’ obesity. This review will claim that HyOb is a far wider phenomenon than hitherto understood by the narrow definition of post‐surgical weight gain. It will emphasize the similarity in clinical characteristics and therapeutic approaches for HyOb, as well as its mechanisms. HyOb, regardless of its aetiology, is a result of impairment in hypothalamic regulatory centres of body weight and energy expenditure. The pathophysiology includes loss of sensitivity to afferent peripheral humoral signals, such as, leptin on the one hand and dysfunctional afferent signals, on the other hand. The most important afferent signals deranged are energy regulation by the sympathetic nervous system and regulation of insulin secretion. Dys‐regulation of 11β‐hydroxysteroid dehydrogenase 1 (11β‐HSD1) activity and melatonin may also have a role in the development of HyOb. The complexity of the syndrome requires simultaneous targeting of several mechanisms that are deranged in the HyOb patient. We review the studies evaluating possible treatment strategies, including sympathomimetics, somatostatin analogues, triiodothyronine, sibutramine, and surgery.
Author Hochberg, Z.
Hochberg, I.
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– name: Blackwell Publishing Ltd
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SecondaryResourceType review_article
Snippet Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for excision of...
Summary Hypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for...
SummaryHypothalamic obesity (HyOb) was first defined as the significant polyphagia and weight gain that occurs after extensive suprasellar operations for...
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SubjectTerms animal injuries
Eating - physiology
Energy Metabolism - physiology
Homeostasis - physiology
Humans
hypothalamic obesity
Hypothalamus - physiology
Hypothalamus - physiopathology
Obesity - chemically induced
Obesity - etiology
Obesity - genetics
Obesity - therapy
Prader-Willi syndrome
Prader-Willi Syndrome - genetics
Prader-Willi Syndrome - physiopathology
Psychotropic Drugs - adverse effects
trauma
Weight Gain
Title Expanding the definition of hypothalamic obesity
URI https://api.istex.fr/ark:/67375/WNG-R92V1BQK-Q/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1467-789X.2010.00727.x
https://www.ncbi.nlm.nih.gov/pubmed/20233310
https://search.proquest.com/docview/755174217
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Volume 11
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