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Silvia Grottoli, Mauro Maccario, Massimo Procopio, Salvatore Endrio Oleandri, Emanuela Arvat, Laura Gianotti, Romano Deghenghi, Franco Camanni, and Ezio Ghigo

Grottoli S, Maccario M, Procopio M, Oleandri SE, Arvat E, Gianotti L, Deghenghi R, Camanni F, Ghigo E. Somatotrope responsiveness to Hexarelin, a synthetic hexapeptide, is refractory to the inhibitory effect of glucose in obesity. Eur J Endocrinol 1996;135:678–82. ISSN 0804–4643

Both spontaneous and stimulated growth hormone (GH) secretion is reduced in obesity, in which state insensitivity to the inhibitory effect of hyperglycemiacemia also has been reported. To further investigate this point, in eight male obese (OB) patients (27–49 years old; body mass index = 39.5 ± 1.7 kg/m2) we studied the effect of oral glucose load (100 g) on the GH response to Hexarelin (HEX, 2 μg/kg iv), a synthetic hexapeptide belonging to the GH-releasing peptide family, which has been reported to be able to induce a marked GH rise even in obese patients. As a control group, six male age-matched normal subjects (NS) were studied (26–35 years old; body mass index = 22.3 ± 1.5 kg/m2). In all subjects the GH response to growth hormone-releasing hormone (GHRH, 1 μg/kg iv) was also studied. Basal GH and insulin-like growth factor I (IGF-I) levels in OB and NS were similar (0.3 ± 0.1 vs 0.5 ± 1.0 μg/l and 166.7 ± 12.3 vs 145.4 ± 6.9 μg/l, respectively). Hexarelin induced a clear GH rise in OB (peak: 20.0 ± 2.9 μg/l; AUC: 1193.0 ± 213.7 μg·l−1·120 min−1) but this response was clearly lower (p < 0.0002) than that observed in NS (62.6 ± 7.3 μg/l, 4587.5 ± 614.9 μg·l −1·120 min−1). The GHRH-induced GH rise was lower (p < 0.002) in OB (4.4 ± 1.2 μg/l, 331.0 ± 95.9 μg·l−1·120 min−1) than that in NS (20.2 ± 1.9 μg/l, 1281.0 ± 157.5 μg·l−1·120 min−1) and both were lower (p < 0.05) than those induced by HEX. In NS, glucose significantly blunted the GH response to HEX (38.4 ± 7.2 μg/l, 2236.5 ± 514.8 μg·l−1·120 min−1, p < 0.05) but failed to modify it in OB (19.4 ± 2.7 μg/l, 934.5 ± 151.3 μg·l−1·120 min−1). Plasma glucose peaks after oral glucose load in OB and NS were similar (164.5 ± 9.7 vs 145.8 ± 4.6 mg/dl). In conclusion, the present data demonstrate that, in contrast to normal subjects, in obese patients HEX has a reduced GH-releasing effect that is not inhibited by glucose. In OB patients as well as in normal subjects HEX releases more GH than GHRH. These findings strengthen the evidence that GH secretion in obesity is refractory either to stimulatory inputs or to the inhibitory effect of hyperglycemia.

E Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so A.M. Dogliotti 14, 10126 Torino, Italy

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Mauro Maccario, Silvia Grottoli, Paola Razzore, Massimo Procopio, Salvatore Endrio Oleandri, Enrica Ciccarelli, Franco Camanni, and Ezio Ghigo

Maccario M, Grottoli S, Razzore P, Procopio M, Oleandri SE, Ciccarelli E, Camanni F, Ghigo E. Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity. Eur J Endocrinol 1996;135:205–10. ISSN 0804–4643

In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18–46 years, body mass index = 21.8 ± 0.6 kg/m2, basal prolactin = 91.7 ± 16.5 μg/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23–48 years, body mass index = 38.3 ± 2.6 kg/m2) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26–32 years, body mass index = 20.6 ± 1.9 kg/m2) were studied as controls. The insulin response to glucose in HP (area under curve = 11460.8 ± 1407.5 mU·min·1−1) was not significantly different from NS (7743.7 ±882.9 mU·min·1−1) and OB (14 504.8 ± 1659.9 mU·min·1−1). The arginine-induced insulin release in HP and OB was similar (4219.4 ± 631.7 and 4107.3 ± 643.2 mU·min·1−1. respectively), both being higher (p < 0.02) than in NS (2178.1 ± 290.9 mU·min·1−1). Glucose and arginine had an additive effect on insulin release in HP and NS (19 769.1 ± 3249.6 and 10996.6 ± 1201.0 mU·min·1−1, respectively) and a synergistic effect in OB (28117.3± 5224.7 mU·min·1−1). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely.

Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

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Ezio Ghigo, Stefania Goffi, Enrico Mazza, Emanuela Arvat, Massimo Procopio, Jaele Bellone, Eugenio E. Müller, and Franco Camanni

Abstract. In normal adults, repeated GHRH administration leads to progressively decreasing somatotrope responses. To verify whether this GH secretory pattern also connotes normal growing children, we have studied the effects of two consecutive (every 120 min) 1 μg/kg iv GHRH boluses on GH release in normal adults (N = 7, age 23.2–30.6 years) children (N = 6, age 10.4–13.2 years). In the adults, the GH response to the second GHRH bolus (peak, mean ± sem: 2.9 ± 0.8 μg/l) was lower (P< 0.02) than that to the first bolus (15.9 ± 2.4 μg/l). Conversely, in children the GH response to the second GHRH bolus (25.6 ± 6.3 μg/l) overrode the first one (13.6 ± 6.5 μg/l), but this difference did not attain statistical significance. In adults cholinergic enhancement by pyridostigmine, a cholinesterase inhibitor, was previously shown to re-instate, even to potentiate somatotrope responsiveness to consecutive GHRH boluses. Thus, in 5 children GH response to repeated GHRH boluses was retested administering pyridostigmine (60 mg orally) 30 min before the second GHRH bolus. In these subjects, pyridostigmine failed significantly to potentiate the GH responsiveness to the second GHRH bolus (30.3 ± 4.6 vs 25.0 ± 7.6 μg/l). These data indicate that differently from in adults, in children repeated GHRH administration does not reduce somatotrope responsiveness and that cholinergic enhancement fails to potentiate GH responsiveness to the second GHRH bolus.

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Fabio Bioletto, Marco Barale, Mirko Parasiliti-Caprino, Nunzia Prencipe, Alessandro Maria Berton, Massimo Procopio, Desirée Deandreis, and Ezio Ghigo

Background. Primary hyperparathyroidism is characterized by an autonomous hypersecretion of parathyroid hormone by one or more parathyroid glands. Preoperative localization of the affected gland(s) is of key importance in order to allow minimally invasive surgery. At the moment, 11C-Methionine and 18F-Fluorocholine PET studies appear to be among the most promising second-line localization techniques; their comparative diagnostic performance, however, is still unknown.

Methods. PubMed/Medline and Embase databases were searched up to October 2020 for studies estimating the diagnostic accuracy of 11C-Methionine PET or 18F-Fluorocholine PET for parathyroid localization in patients with primary hyperparathyroidism. Pooled sensitivity and positive predictive value were calculated for each tracer on a “per-lesion” basis and then compared using a random-effect model subgroup analysis.

Results. Twenty-two studies were finally considered in the meta-analysis. Among these, 8 evaluated the diagnostic accuracy of 11C-Methionine and 14 that of 18F-Fluorocholine. No study directly comparing the two tracers was found. The pooled sensitivity of 18F-Fluorocholine was higher than that of 11C-Methionine (92% vs 80%, p < 0.01), while the positive predictive value was similar (95% vs 94%, p = 0.99). These findings were confirmed in multivariable meta-regression models, demonstrating their apparent independence from other possible predictors or confounders at a study level.

Conclusion. This was the first meta-analysis that specifically compared the diagnostic accuracy of 11C-Methionine and 18F-Fluorocholine PET for parathyroid localization in patients with primary hyperparathyroidism. Our results suggested a superior performance of 18F-Fluorocholine in terms of sensitivity, while the two tracers had comparable accuracy in terms of positive predictive value.

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Elisabetta Cecconi, Maurizio Gasperi, Maura Genovesi, Fausto Bogazzi, Lucia Grasso, Filomena Cetani, Massimo Procopio, Claudio Marcocci, Luigi Bartalena, and Enio Martino

Objective: To investigate, in a large group of postmenopausal primary hyperparathyroidism (PHP) women, whether the concomitance of GH deficiency (GHD) may contribute to the development of changes in bone mineral density (BMD).

Design: GH secretion, bone status and metabolism were investigated in 50 postmenopausal women with PHP and in a control group of 60 women with no evidence of PHP, matched for age, age at menopause and body mass index (BMI).

Methods: GH response to growth hormone-releasing hormone (GHRH)+arginine (Arg), femoral neck BMD (g/cm2) by dual energy X-ray absorptiometry, BMI, serum-ionized calcium, parathyroid hormone (PTH) and markers of bone remodelling were evaluated in all patients and controls.

Results: Among PHP patients, GH secretion was reduced (8.8 ± 4.2 μg/l, range 1.1–16.5 μg/l) in 34 patients and normal (28.7 ± 11.8 μg/l, range 17.9–55.7 μg/l) in the remaining 16 (P < 0.05), no women in the control group had GHD (peak GH 33.8 ± 10.9 μg/l, range 21.7 ± 63.2 μg/l). Osteoporosis (T-score < − 2.5) and osteopenia (T-score > −2.5 and < −1) were found in 73.5 and 17.6% of GHD patients, in 37.5 and 43.7% of patients with normal GH secretion and 3.1 and 27% of controls. T-score and BMD were not correlated with ionized calcium, age, age at menopause, BMI, GH peak and IGF-I but were correlated with serum PTH levels in both groups. T-score was correlated with serum levels of markers of bone remodelling only in PHP patients with GHD.

Conclusions: Concomitant impairment of GH secretion may play a pathogenetic role in the occurrence of changes in bone mass observed in PHP and contribute to make them more severe.