Failure of glucose infusion to suppress the exaggerated GH response to GHRH in patients with anorexia nervosa

Rolla, M; Andreoni, A.; Belliti, D.; Ferdeghini, M; Ferrannini, Ele

doi:10.1016/0006-3223(90)90651-h

Cited by 19 publications

(7 citation statements)

References 21 publications

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“…In support of this proposition, in AN subjects two inhibitors of stimulated GH secretion that are reported to act via somatostatin, i.e. glucose load (Rolla et al 1990, Beck et al 1966) and pirenzepine, a cholinergic muscarinic antagonist (Rolla et al 1991), failed, or were less effective respectively, to blunt the GHRH-induced GH rise.…”

Section: Discussionmentioning

confidence: 81%

“…No significant difference in the response to CRH plus GHRH was found between AN subjects in the florid phase of the disease and NOS subjects, a fact that would assign a major role in dictating the response pattern to biological alterations shared by both diseases rather than to psychopathologic events. The enhanced GH secretion in subjects with eating disorders (Masuda et al 1988, Brambilla et al 1989, Rolla et al 1990), viewed in relation to the ability of CRH to blunt the GHRH-induced GH release, would suggest the existence of an endogenous GHRH hyperfunction not restrained at the pituitary level by CRH-driven somatostatinergic inputs. Brauman H & Grégoire F 1975 The growth homione response to insulin induced hypoglycaemia in anorexia nervosa and control underweight or normal subjects.…”

Section: Discussionmentioning

confidence: 96%

“…However, a major biological difference between the experimental model of starvation or undernutrition and subjects with eating disorders is that GH secretion is reduced in the former (Tannenbaum et al 1979) but very often increased in the latter (Masuda et al 1988, Brambilla et al 1989, Rolla et al 1990) and elevated titres of GH in the plasma, through a short-loop feedback, may regulate per se the synthesis and/or secretion of somatostatin (Berelowitz et al 1981a). Moreover, while fasting elicits a robust activation of the axis in humans (Vance & Thorner 1989) it is less effective in this context in rats (Brady et al 1990).…”

Section: Discussionmentioning

confidence: 98%

“…Thus an altered response of growth hormone (GH) to a variety of provocative stimuli (Brauman & Grégoire 1975, Macaron et al 1978, Kiriike et al 1987, Brambilla et al 1989, Rolla et al 1990) and an enhanced axis function (Kaye et al 1987), with increased levels of corticotrophin-releasing hormone (CRH) in the cerebrospinal fluid (Hotta et al 1986, Kaye et al 1987, have been reported in women with anorexia nervosa (AN).…”

Section: Introductionmentioning

confidence: 98%

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Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

Rolla

Andreoni²,

Bellitti³

et al. 1994

Journal of Endocrinology

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Previous studies have shown that corticotrophin-releasing hormone (CRH) inhibits GH secretion in response to GH-releasing hormone (GHRH) in normal women and men, and animal studies suggest that this effect is mediated by an increased release of somatostatin from the hypothalamus. It has been reported that there are abnormalities in the neuroendocrine regulation of the hypothalamo-pituitary-somatotrophic axis and the hypothalamo-pituitary-adrenocortical axis in patients with eating disorders. The present study therefore investigated the ability of CRH to inhibit the GH response to GHRH in eight young women with anorexia nervosa (AN) and in seven young women with eating disorders which were not otherwise specified (NOS). We also compared the effect of CRH in the patients with the response it caused in ten control women. In contrast to a previous report, combined i.v. administration of 50 micrograms human CRH (hCRH) and 50 micrograms GHRH(1-29) caused a GH response in control women which was higher, although not significantly so, than that induced by GHRH alone (area under the curve (AUC) 988.5 +/- 506.0 compared with 1568.4 +/- 795.6 (S.E.M.) ng/ml per 120 min for GHRH alone and GHRH plus hCRH respectively). Conversely, the administration of hCRH given together with GHRH markedly inhibited the GH response induced by the latter in both AN patients (AUC 2253.0 +/- 385.7 compared with 1224.4 +/- 265.7 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P < 0.005 and NOS patients (AUC 2827.4 +/- 281.1 compared with 308.5 +/- 183.4 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

Rolla

Andreoni²,

Bellitti³

et al. 1994

Journal of Endocrinology

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“…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. 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).…”

Section: Introductionmentioning

confidence: 99%

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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Growth Hormone Releasing Hormone: Behavioral Evidence for Direct Central Actions

Vaccarino¹,

Kennedy²

1996

Growth Hormone Secretagogues

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Failure of glucose infusion to suppress the exaggerated GH response to GHRH in patients with anorexia nervosa

Cited by 19 publications

References 21 publications

Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

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

Growth Hormone Releasing Hormone: Behavioral Evidence for Direct Central Actions

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