N. Moller et al., SOMATOSTATIN ENHANCES INSULIN-STIMULATED GLUCOSE-UPTAKE IN THE PERFUSED HUMAN FOREARM, The Journal of clinical endocrinology and metabolism, 80(6), 1995, pp. 1789-1793
Somatostatin is widely used in experimental metabolic studies to contr
ol hormone actions. It has also been suggested that, in addition to it
s well known suppressive effects, somatostatin per se may increase ins
ulin sensitivity. In order to examine this suggestion, we gave six hea
lthy male volunteers (age 33 +/- 1 yr, mean +/- SEM; body mass index,
24.1 +/- 0.6 kg/m(2)) either a local intraarterial (brachial artery) o
r a systemic venous infusion of 25 mu g/h somatostatin twice. The stud
y consisted of a 1-h basal period and a 2-h systemic hyperinsulinemic
(0.4 mU/ kg . min) euglycemie clamp. Compared with the systemic contro
l infusion, local forearm perfusion with somatostatin caused a 55% inc
rease in insulin-stimulated forearm glucose uptake (0.74 +/- 0.18 vs.
0.47 +/- 0.19 mmol/L, P < 0.05). Intraarterial somatostatin perfusion
did not alter basal forearm glucose uptake (0.14 +/- 0.07 us. 0.17 +/-
0.12 mmol/L), the amount of glucose administered during the clamp (M-
value, 3.2 +/- 0.5 vs. 3.0 +/- 0.6 mg/kg . min), or the levels of insu
lin, C-peptide, glucagon, or GH. Intermediary metabolite exchange acro
ss the forearm, total forearm blood flow, and oxygen saturations also
remained stable. Glucose concentrations were slightly higher (0.06 +/-
0.01 mmol/L) in arterial than in arterialized blood, whereas lactate
concentrations were comparatively decreased (108 +/- 51 mu mol/L) in a
rterial blood. Our data suggest that somatostatin increases insulin-st
imulated muscle utilization of glucose through local mechanisms. Altho
ugh the nature of this increase remains to be established, it should b
e taken into consideration in metabolic studies using somatostatin.