Recently,
somatostatin analogs have been introduced which can be used clinically in the treatment of tumorous or functional
hypoglycemia. In the present study we investigated in vitro the regulation, the degree of autonomy and the sensitivity to natural
somatostatin and its analog
SMS 201-995 of insulin secretion by monolayer cultures of human pancreatic cells obtained from patients with
insulinomas and from a newborn with
nesidioblastosis. All cultures released
insulin upon the addition of dibutyryl-cAMP and
calcium, demonstrating their intact viability. Insulin secretion from nontumorous pancreatic cells surrounding an
insulinoma was dose-dependently stimulated by
glucose. In contrast,
insulin release by B cells from a patient with
nesidioblastosis and from 2
insulinomas was not stimulated by the addition of
glucose. Native
somatostatin (SRIF) and the synthetic analog
SMS 201-995 inhibited insulin secretion from all cultures. The inhibitory effects of SRIF and SMS in the culture from the
nesidioblastosis tissue, could be reversed by the addition of 11.2 mmol
glucose/l, but not in one of the
insulinoma cultures. This demonstrates that some sensitivity to
glucose is present in B cells from the
nesidioblastosis tissue, despite the unresponsiveness to
glucose alone.
Insulin release by
insulinoma cells was blocked by
somatostatin, while it was inhibited to some extent only in the cultures of nontumor B cells and of cells from the
nesidioblastosis tissue. In conclusion, it was shown that
insulin release by the cultured B cells obtained from several pathological conditions differed with regard to the autonomy of
hormone release (
glucose sensitivity) and the sensitivity to
somatostatin and its analog.