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INFLUENCE OF SOMATOSTATIN ON PLASMA CYCLIC AMP AND METABOLIC SUBSTRATE RESPONSES TO I.V. ADRENALINE AND GLUCAGON IN HUMANS
Author(s) -
MADSEN S. NISTRUP,
CHRISTENSEN S. ENGKJÆR,
HANSEN AA. PRANGE,
THODE J.
Publication year - 1981
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1981.tb00685.x
Subject(s) - medicine , endocrinology , somatostatin , glucagon , substrate (aquarium) , chemistry , biology , hormone , ecology
SUMMARY The influence of somatostatin (a bolus injection of 250 μg i.v. followed by 6 μg/min for 40 min) on the plasma cyclic AMP, insulin, glucose and non‐esteri‐fied fatty acid (NEFA) responses to i.v. adrenaline (0·07 μg/kg body‐weight/min for 20 min) and the plasma cyclic AMP, insulin and glucose responses to a bolus injection of i.v. glucagon (0·01 mg/kg BW) were studied in normal subjects. Somatostatin suppressed the insulin response to glucagon and inhibited the insulin rebound observed on termination of adrenaline infusion. The plasma glucose response to glucagon was exaggerated by somatostatin, reflecting insulin deficiency. Neither the plasma glucose nor plasma non‐esterified fatty acid responses to adrenaline were influenced by somatostatin. Adrenaline produced a three‐fold and glucagon a twenty‐fold rise in plasma cyclic AMP after 15 min. This was not influenced by concurrent somatostatin infusion, indicating that somatostatin is not a universal inhibitor of hormone stimulated adenylate cyclase activity. This is supported by the failure of somatostatin to inhibit the metabolic actions of glucagon and adrenaline thought to be mediated by cyclic AMP.