PubMed Health⌕ Search

Biomedical subjects

L Benso

Publications and source records attributed to L Benso.

At least 19 recordsLinked to original sources
PubMed1995

Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, before and during puberty.

The objective of this study was to verify the GH-releasing activity of a synthetic hexapeptide, hexarelin (HEX), before and during puberty. Ninety-six children (54 boys and 42 girls, aged 4.1-17.4 yr) were studied. Fifty-two of the children were prepubertal, and the other 44 were in pubertal stage II-IV. The GH response to 2 micrograms/kg HEX, iv (n = 56), was higher (P < 0.001) than that induced by 1 microgram/kg GHRH, iv (n = 33). The iv dose of 2.0 micrograms/kg HEX induced a greater GH increase (P < 0.02) than the 1.0 microgram/kg dose. The GH-releasing effect of 10 mg HEX, orally, was greater (P < 0.03) than that of 1.0 microgram/kg GHRH, iv (n = 7). The iv dose of 2 micrograms/kg HEX elicited an increase in GH levels that was higher in pubertal children than in prepubertal children (77.5 +/- 8.5 vs. 39.4 +/- 4.4 micrograms/L; P < 0.001). Before puberty, there was no sex-dependent difference in the GH response to HEX. It increased during puberty (P < 0.05 and P < 0.002 for boys and girls, respectively), when it was higher (P < 0.05) in girls than in boys. In contrast, GH responses to GHRH were not related to sex differences and/or puberty. In conclusion, HEX is a potent and reproducible stimulus of GH secretion in children. The effect of HEX increases in puberty, with girls showing a more marked GH response.

Adolescent↗
PubMed1990

The effect of galanin on baseline and GHRH-induced growth hormone secretion in obese children.

We have evaluated the effect of the administration of galanin (Gal), a newly identified hypothalamic peptide, on baseline and GHRH-induced GH rise in five obese children and in seven controls. The GH response to GHRH (hpGRF(1-29), 1 microgram/kg i.v.), and to Gal (15 micrograms/kg/h for 1 h), evaluated both as the maximum GH peak and as integrated area under the curve (AUC), was significantly lower in the obese children than in the controls. Simultaneous administration of Gal plus GHRH significantly increased the GH response to GHRH in all the obese subjects, so that their mean peak GH levels and AUC after Gal plus GHRH were similar to those of the control children after GHRH. Also, in control children Gal caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean AUC after Gal plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Our data indicate that obese children have a blunted GH response to Gal, which, however, is able to enhance the GH response to GHRH. This observation strengthens the view that the mechanism of action of Gal involves modulation of endogenous somatostatin (SRIH) release. In addition, similarity between the effects of Gal and pyridostigmine on baseline and GHRH-stimulated GH release in obese children may indicate the existence of a cholinergic link in the action of Gal.

Child↗
PubMed1990

Evidence for involvement of endogenous somatostatin in the galanin-induced growth hormone secretion in children.

We have evaluated the effects of the combined administration of Galanin (Gal) plus growth hormone-releasing hormone (GHRH) and of pyridostigmine (PD), a cholinergic agonist, plus Gal on GH secretion in 15 children (12 males and three females, age 7.7-14.5 y) with short stature. Children were subdivided into two groups. In group 1 (n = 7) Gal (15 micrograms/kg h i.v.) plus GHRH (1 microgram/kg i.v.) administration induced a higher GH rise (peak = 73.1 +/- 10.2 ng/mL, mean +/- SD; area under the curve (AUC) = 531.9 +/- 78.7 ng.min.mL-1) than did GHRH alone (peak = 38.9 +/- 26.5 ng/mL, p less than 0.05; AUC = 256.9 +/- 165.6 ng/mL/min-1, p less than 0.005). Gal had a synergistic effect on the GHRH-induced GH response because the GHRH plus Gal AUC response was significantly higher (p less than 0.01) than the sum of the areas of response to GHRH and Gal alone. In group 2 (n = 8) PD administration (60 mg/kg p.o.) had no significant effects on the Gal-induced GH secretion (peak = 14.9 +/- 8.8 and 16.0 +/- 9.8 ng/mL after Gal and PD + Gal, respectively; AUC = 91.2 +/- 52.1 and 125.2 +/- 83.6 ng.mL.min-1 after Gal and PD + Gal, respectively). Our results confirm the ability of Gal to stimulate GH secretion in children, and strengthen the view that its mechanism of action involves modulation of endogenous somatostatin release.

Adolescent↗
PubMed1987

Enhancement of cholinergic tone by pyridostigmine promotes both basal and growth hormone (GH)-releasing hormone-induced GH secretion in children of short stature.

Increased cholinergic tone induced by pyridostigmine (PD) increases basal plasma GH levels and potentiates the GH response to GHRH in normal adults. In this study the effects of PD (60 mg, orally) on both basal and GHRH (1 microgram/kg)-induced GH secretion in seven children with familial short stature (FSS), six with GH deficiency (GHD) and 10 with constitutional growth delay (CGD) were studied and compared with results obtained by stimulation with insulin-induced hypoglycemia (IH) and GHRH alone. The mean peak plasma GH levels were variable, but individual values were frequently low in all groups after both IH [FSS, 9.7 +/- 1.3 (+/- SEM) ng/mL; GHD, 1.6 +/- 0.4 ng/mL; CGD, 7.0 +/- 0.8 ng/mL] and GHRH (FSS, 23.8 +/- 6.6 ng/mL; GHD, 11.1 +/- 5.8 ng/mL; CGD, 15.1 +/- 4.5 ng/mL) administration. PD induced GH responses (FSS, 14.5 +/- 1.6 ng/mL; GHD, 3.8 +/- 0.8 ng/mL; CGD, 18.3 +/- 3.2 ng/mL) that in many children in the FSS and CGD groups were higher than those after IH and GHRH treatment. PD clearly increased the GH response to GHRH in all children [FSS, 69.5 +/- 9.4 ng/mL (P less than 0.01 vs. other stimuli); GHD, 18.0 +/- 7.5 ng/mL; CGD, 50.0 +/- 8.5 ng/mL (P less than 0.01 vs. other stimuli)]. We conclude that in children with short stature, as in adults, enhancement of cholinergic tone increases both basal and GHRH-induced GH secretion, and that PD plus GHRH is the best provocative stimulus for evaluating the somatotroph response.

Adolescent↗
PubMed1986

Distinctive skeletal dysplasia in Cockayne syndrome.

Cockayne syndrome is a well-known autosomal recessive form of dwarfism with senile-like appearance. Skeletal changes such as flattening of vertebral bodies, ivory epiphyses and thickening of cranial vault, have been observed in some patients with this condition. We describe here a 5.5-year-old girl with the typical clinical signs of Cockayne syndrome and a distinctive form of bone dysplasia with major involvement of the spine.

Bone Diseases, Developmental↗