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Effects of - and β-Adrenergic Inhibition and Somatostatin on Plasma Glucose, Free Fatty Acids, Insulin, Glucagon, and Growth Hormone Responses to Prostaglandin E₁ in Man^*

Institute of Medical Pathology and Clinical Methodology, I Faculty of Medicine, University of Naples Naples, Italy

Address requests for reprints to: Dr. Dario Giugliano, Istituto di Patologia Speciale Medica, I Policlinico, Pzza L. Miraglia, 80100 Napoli, Italy.

It has been previously shown that prostaglandin E₁ (PGE₁) induced a significant increase in plasma glucose, FFA, glucagon, and GH levels when infused in normal man. In the present study, we evaluated the effects of - and β-adrenergic blockers and somatostatin on these metabolic and hormonal responses to PGE₁.

The pretreatment with propranolol (0.08 mg/min) reduced basal plasma glucagon from a mean value of 86 ± 6 to 70 ± 8 pg/ml (mean ± SEM; P < 0.05) and completely blunted glucagon and FFA responses to PGE₁ (0.2 µg/kg-min), but did not interfere with the rise in plasma glucose or GH levels. Phentolamine pretreatment (0.5 mg/min) caused a significant increase in basal glucagon and insulin (P < 0.05). Phentolamine had no effect on the responses of the various parameters to PGE₁. Plasma insulin levels remained essentially unchanged during the development of hyperglycemia during both and β blockade.

Somatostatin (250 µg/h) lowered basal plasma insulin and glucagon (P < 0.01) and prevented glucagon and GH increases by PGE₁. By contrast, plasma glucose rose from a mean basal value of 85 ± 4 to 135 ± 7 mg/100 ml (P < 0.001), and plasma FFA rose from a prestimulatory value of 600 ± 70 to 775 ± 76 µeq/liter (P < 0.05) after PGE₁. Plasma glucose and FFA levels were significantly higher during PGE₁ and somatostatin administration than when PGE₁ was given alone.

These results suggest that some (glucagon and FFA) but not all (glucose and GH) responses to PGE₁ are mediated by the β-adrenergic system, that PGE₁ inhibits insulin secretion not mediated by stimulation, and that somatostatin blocks the increases in glucagon and GH resulting from PGE₁ and also potentiates its hyperglycemic and lipolytic effects.

^* This work was presented in part at the 14th Annual Meeting of the European Association for the Study of Diabetes, Zagreb, September 27–30, 1978.

Received June 16, 1978.

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