Effect of a modulation of somatostatin release on TSH secretion in healthy volunteers

N. Bouali; B. Corvilain; F. Devuyst

Objectives: In normal subjects, inhibitory effect of a glucose load (OGTT) on GH secretion is probably mediated by an increase in hypothalamic release of somatostatin whereas the stimulatory effect of arginine on GH secretion is probably mediated by a decrease in somatostatin release. In humans and animals, somatostatin infusion inhibits basal and TRH-stimulated TSH secretion but little is known on the role of endogenous somatostatin in the regulation of TSH secretion. The aim of this study was to evaluate TSH response to situations known to modulate somatostatin release in vivo (OGTT and arginine infusion).

Methods: OGTT (75 g) or arginine infusion (30 g in 30 min) were performed in seven healthy male volunteers. In five subjects results were also obtained after TRH injection. Isotonic saline infusion was used as control. Tests were begun 60 min after a catheter has been inserted (T=0 min). Blood samples were taken every 15 min from −60 to 240 min for glucose, TSH, PRL, GH measurements. Basal level for TSH and PRL was chosen as the mean of the value at T −15 and 0 min. Results were expressed as % of basal value (mean±S.E.M.). GH values were expressed in ng/ml.

Results: Statistical analysis was performed employing one-way ANOVA followed by Bonferroni’s multiple comparison tests. OGTT exerted a typical inhibitory effect on GH secretion (Nadir GH <0.25 ng/ml) and arginine a stimulatory effect (peak GH: 11±3.64 and 7.46±1.51 ng/ml when combined with TRH; P<0.01).

As expected, PRL secretion was stimulated by arginine and TSH by TRH. Effects of a glucose load and of arginine on TSH secretion were less clear. TSH nadir observed during OGTT was statistically different from basal values but not from the nadir obtained with saline. The stimulatory effect of Arginine on TSH secretion was not significant when compared to basal value but statistically significant when compared to he value obtained during saline perfusion. No changes were observed on TSH stimulated values.

Conclusions: cccc

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

**Table 1** Modulation of somatostatin release *in vivo* by a glucose load or arginine infusion plays a minor role in basal or TRH-stimulated TSH secretion.
	Nacl 0.9%	OGTT	Arginine	Nacl 0.9%+TRH	OGTT+TRH	Arginine+TRH
TSH (% of basal value)	85.2±3.9	79.0±5.1*^,^a	117.0±8.3^†	828±115*	663±63*	731±86*
PRL (% of basal value)	75.7±5.9	76.5±3.5	339.5±4.5*	720±82*	853±129*	988±146*
*P<0.01 vs basal values; ^†P<0.01 vs saline values.
^aNS vs saline.

Endocrine Abstracts

P1441