Growth Hormone Neuroregulation and Its Alterations in Disease States

Diéguez, Carlos; Page, M. D.; Scanlon, M. F.

doi:10.1111/j.1365-2265.1988.tb01209.x

Cited by 228 publications

(65 citation statements)

References 239 publications

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“…The existence of a robust somatotroph responsiveness to GHRH in A-AN is widely acknowledged (5,7,8,26), although few exceptions have also been reported (45). In the present study, the GHRH-induced GH response in A-AN overrode the one recorded in NW, whereas it was within normal limits in R-AN.…”

Section: Discussionmentioning

confidence: 32%

“…GH secretion in AN has also been shown to be particularly refractory to the inhibitory effect of muscarinic cholinergic antagonists (7,8), as well as to the stimulatory effect of cholinergic agonists or b-adrenergic antagonists (25,26), or acute glucorticoid administration (27). As central cholinergic and b-adrenergic functions and glucorticoids would influence GH secretion via modulation of hypothalamic SS release (28), the existence of an impaired SS activity in AN has also been suggested (5,6,8,25,26). Along this line also are the low cerebrospinal fluid (CSF) concentrations of SS detected in anorectic patients (29).…”

Section: Introductionmentioning

confidence: 99%

“…Alternatively, in AN, a primary alteration in the neural control of somatotroph function involving GH-releasing hormone (GHRH) (5,6) may underlie GH hypersecretion. In fact, so far, low or absent GH response to insulin-induced hypoglycemia (17) or dopaminergic agonists (18), exaggerated GH responses to GHRH (7,8,19,20), paradoxical GH rises after glucose load (21,22), thyrotropin-releasing hormone (23), or gonadotropin-releasing hormone (GnRH) (24) have been reported.…”

Section: Introductionmentioning

confidence: 99%

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Somatostatin infusion withdrawal: studies in the acute and recovery phase of anorexia nervosa, and in obesity

Pincelli¹,

Rigamonti²,

Scacchi³

et al. 2003

European Journal of Endocrinology

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Objective: Changes in GH/IGF-I axis activity occur in both anorexia nervosa (AN) and obesity (OB). A GH hypersecretory state with very low plasma IGF-I levels is present in AN, whereas in morbid OB, GH secretion is dull and plasma IGF-I levels are generally preserved. Endogenous GHRH activity in AN and OB has never been directly studied, although indirect evidence would indicate that GHRH function is altered in either condition, possibly enhanced and reduced respectively. Somatostatin (SS) infusion withdrawal (SSIW) is followed by a rebound rise of plasma GH in animals and humans, an event which, allegedly, is mediated by endogenous GHRH release. Methods: In the present study, 28 young women, eight with active AN (A-AN), six with AN in the recovery phase (R-AN), eight with morbid OB, and six healthy age-matched normal weight subjects (NW), were studied. All subjects underwent, on different occasions, the following two tests: (i) acute GHRH injection (1 mg/kg, i.v.); (ii) infusion of SS (9 mg/kg per h i.v. over 60 min), with blood samples drawn prior to and at different intervals after drug injections. Plasma GH levels were measured at each time interval in all sessions, and, in addition, baseline plasma estradiol, free triiodothyronine, TSH, IGF-I and insulin were measured at 2 30 min. Results: Baseline plasma GH concentrations were significantly higher in A-AN than in NW ð4:7^0:7 vs 2:1^0:6 mg=l; P , 0:01Þ: Baseline GH levels in R-AN were also higher than in NW, but the difference did not reach statistical significance (5:6^1:7 mg=l; not significant (NS)). Baseline plasma GH concentrations were significantly lower in OB than in NW ð0:3^0:1 mg=l; P , 0:01Þ: GHRH-stimulated GH release was significantly higher in A-AN than in NW (mean change in area under the curve (DAUC) 1904:9^626:1 vs 613:9^75:9 mg=l per min, P , 0:01), whereas no statistically significant difference was present between R-AN and NW (mean DAUC 638:2^293:0 mg=l per min, NS); in OB, GHRH failed to evoke a plasma GH rise (mean DAUC 239:8^89:9 mg=l per min vs A-AN, R-AN, and NW, P , 0:01). SS infusion markedly reduced plasma GH concentrations in both A-AN and R-AN and, to a lesser extent, in NW, but failed to do so in OB. In A-AN, SSIW was followed by a plasma GH rise markedly higher than that present in NW (mean DAUC 193:0^42:3 vs 60:1^11:4 mg=l per min, P , 0:01), whereas in R-AN the GH response after SSIW was nearly superimposable on that registered in NW (mean DAUC 72:9^22:8 mg=l per min, NS). There were no changes in plasma GH levels after SSIW in OB (mean DAUC 22:8^9:7 mg=l per min). In all groups, DAUCs of the GH response to GHRH and after SSIW were highly positively correlated ðr ¼ 0:7; P , 0:01Þ: Conclusions: These data support the view that a high endogenous GHRH tone, which subsides in the recovery phase of the disease, is present in AN, whereas GHRH hypofunction, possibly associated with pituitary impairment, might indicate OB.

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Section: Discussionmentioning

confidence: 32%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Somatostatin infusion withdrawal: studies in the acute and recovery phase of anorexia nervosa, and in obesity

Pincelli¹,

Rigamonti²,

Scacchi³

et al. 2003

European Journal of Endocrinology

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“…Büyüme hormonu (GH) salınımı streste büyüme hormonu salgılatıcı hormonun (GhRH) salınmasının azalması yoluyla baskılanır. [74] Bununla birlikte bu durumun mekanizması henüz tam olarak açıklığa kavuş-mamıştır. Ruhsal gerilim altında artan NPY düzeyleri stres yanıtında rol alır.…”

Section: Büyüme Ve Ergenlik (Puberte)unclassified

Neuropeptide Y and Stress

Gülsün¹,

Tamam²

2012

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychia

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ÖZETStres ve bireysel baş etme yetilerinin nörobiyolojik yönü birçok araştırmacının ilgi odağı olmuştur. Bir dizi çalışmada genetik değişkenler ile strese tepki düzeyleri ve yaşam olayları arasında bir ilişki olduğu gösterilmiştir. Nöropeptid Y stres esnekliğini düzenleyen sistemlerden biridir. Uzun süreli ya da tekrarlayan stres durumlarında nöropeptid Y beynin anahtar bölgelerinden salınır. Bu sistem stresle ilgili bozukluklara yatkınlığı farklı kişilerde farklı esneklikte işleyiş gösterir. Gen-çevre etkileşimleri için özellikle ilgi çekici olan strese duyarlı sinyal moleküllerini kodlayan genlerin değişimidir. Bu durum strese yatkınlığa ya da esnekliğe katkıda bulunabilir. Nöropeptid Y sistemi de strese davranışsal uyumda anahtar rol oynamaktadır. Nöropeptid Y düzeyinin azalmış olması tedaviye dirençli depresyonda ve travma sonrası stres bozukluğunda da gözlenmiştir. Düşük nöropeptid Y ekspresyonunun ya da strese yanıt olarak nöropeptid Y sisteminin yeterince işlevsel olmaması ve sonucunda ortaya çıkan stres esnekliğinin az olması stresle ilişkili bozukluklara yatkınlığı arttırabilmektedir. Anahtar Sözcükler: Nöropeptid Y, stres, stres esnekliği ABSTRACTThe neurobiological aspects of stress and coping skills has been the focus of interest for many researchers. Some of the studies has shown that there is a significant relationship among genetically variables, stress response and life events. Neuropeptide Y is one of the systems regulating the stress response. Under the prolonged or repeated trauma neuropeptide Y is released from the brain's key areas. This system shows different levels of functioning in individuals with different levels of resilience. There is particular interest in the variations of genes that encode stress-sensitive signaling molecules during geneenvironment interaction. This condition may contribute to susceptibility of stress or stress resilience. Neuropeptide Y system plays a key role in the adaptation to behavioral stress. The reduced levels of neuropeptide Y have also been observed in treatment-resistant depression and posttraumatic stress disorder. Lower level of neuropeptide Y expression and dysfunctional neuro-

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“…Prolonged activation of the HPA axis leads to suppression of growth hormone (GH) secretion and inhibition of somatomedin C and other growth factor effects on target tissues by glucocorticoids, [76][77][78][79][80][81] the latter presumably occurring through inhibition of the c-jun/c-fos heterodimer by the ligand-bound glucocorticoid receptor. Acute elevations of GH concentration in plasma may occur at the onset of the stress response, however, or after acute administration of glucocorticoids, presumably through stimulation of the GH gene by glucocorticoids through glucocorticoid-responsive elements in its promoter region.…”

Section: Growth Axismentioning

confidence: 99%

Organization and Integration of the Endocrine System: The Arousal and Sleep Perspective

Chrousos

2007

Sleep Medicine Clinics

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Growth Hormone Neuroregulation and Its Alterations in Disease States

Cited by 228 publications

References 239 publications

Somatostatin infusion withdrawal: studies in the acute and recovery phase of anorexia nervosa, and in obesity

Somatostatin infusion withdrawal: studies in the acute and recovery phase of anorexia nervosa, and in obesity

Neuropeptide Y and Stress

Organization and Integration of the Endocrine System: The Arousal and Sleep Perspective

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