Pirenzepine decreases basal and stimulated GH secretion in patients with type 2 (non-insulin-dependent) diabetes mellitus

V. Martina, A. E. Pontiroli, M. Tagliabue, A. Calderara, M. Maccario, M. Pacchioni, S. Bertaina, G. Bruno, G. Pozza, F. Camanni

Research output: Contribution to journalArticlepeer-review


Growth hormone (GH) hypersecretion has been described in diabetes mellitus and seems to be involved in the pathogenesis of diabetes complications. As pirenzepine (PZ), a cholinergic muscarinic antagonist, is able to inhibit GH hypersecretion in insulin-dependent diabetes mellitus (IDDM), we investigated whether PZ is also able to inhibit spontaneous and stimulated GH-release in non-insulin-dependent: diabetes mellitus (NIDDM). Ten non-obese well- controlled patients with NIDDM underwent in random order the following three double-blind one week treatments: placebo (PL), PZ at low dose (PL in the morning plus PZ 50 mg at 22 h) or high dose (PZ 50 mg at 8 h plus 100 mg at 22 h). Pirenzepine administration significantly (p <0.05) decreased nocturnal GH release after both low and high dose (AUC, PL vs PZ: 107.3±26.5 vs 48.3±10.5 and 57.6±9.6 μg/L/h, respectively). The GH response to arginine infusion was significantly inhibited by PZ at high dose (AUC, 147.1±48.8 vs 444.7±194.3 μg/L/h, p <0.01), but not at low dose. Glucose, insulin, glucagon and somatostatin responses to arginine infusion were not changed by pirenzepine treatment. In conclusion, the muscarinic blockade by PZ is able to inhibit the spontaneous and stimulated GH secretion also in NIDDM without affecting insulin secretion.

Original languageEnglish
Pages (from-to)148-151
Number of pages4
JournalHormone and Metabolic Research
Issue number3
Publication statusPublished - 1994


  • Growth Hormone
  • Insulin
  • Non-Insulin-Dependent-Diabetes Mellitus
  • Pirenzepine
  • Somatostatin

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology


Dive into the research topics of 'Pirenzepine decreases basal and stimulated GH secretion in patients with type 2 (non-insulin-dependent) diabetes mellitus'. Together they form a unique fingerprint.

Cite this