GLUCOSE, INSULIN AND SOMATOSTATIN INFUSION FOR THE DETERMINATION OF INSULIN SENSITIVITY
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Abstract:
Glucose, insulin and somatostatin infusion over 2 hours effectively suppressed endogenous secretion of insulin, glucagon and growth hormones. Steady state plasma glucose level (SSPG) which should be inversely proportional to insulin sensitivity was obtained. In 6 adult-onset non-obese untreated diabetics, mean value of insulin sensitivity indices was significantly reduced compared with normal. In 5 insulin-treated diabetics and in 5 subjects with borderline glucose tolerance including 2 obese subjects, insulin sensitivity for glucose utilization was also significantly diminished.Keywords:
Insulin response
Insulin response
Carbohydrate Metabolism
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Insulin response
Bolus (digestion)
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The role of somatostatin for the suppression of insulin release in the early post-traumatic phase was investigated by measurement of somatostatin-like immunoreactivity in plasma during an intravenous glucose tolerance test. In accordance with previous findings the increase of insulin in response to glucose was significantly (p less than 0.001) reduced 2 hours after laparotomy as compared to control subjects. Simultaneously plasma somatostatin was decreased significantly (p less than 0.05). The present data with hormone determinations in peripheral blood does not support the hypothesis that somatostatin, a potent inhibitor of insulin release, mediates the insulin suppression in the early trauma phase.
Insulin response
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Insulin response
Glucose tolerance test
Glucose test
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Ketogenesis
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NON-SELECTIVE INHIBITION OF BASAL GLUCAGON RELEASE BY [d-CYS14]-ANALOGUES OF SOMATOSTATIN IN THE RAT
The effects of two [D-Cys14]-analogues of somatostatin on basal plasma levels of glucagon, insulin and glucose were determined in unanaesthetized rats to re-examine a glucagon-selective action of these peptides which has been claimed by others. Somatostatin, [D-Cys14]-somatostatin and [D-Trp8, D-Cys14]-somatostatin caused a short-lasting, dose-dependent decrease of plasma glucagon and insulin but they had no significant influence on plasma glucose. Glucagon and insulin reached the nadir 2 min after intravenous injection of the peptides (dose range 1--10 micrograms/kg) or 5 min after subcutaneous administration (30 and 300 micrograms/kg). At the nadir, insulin was decreased to a greater extent than glucagon and the effecer the nadir and at high doses, the time-course of some effects of the analogues on either glucagon or insulin differed from that of somatostatin. Thus, these [D-Cys14]-analogues may show partial kinetic dissociation of effects on glucagon and insulin but they are not truly selective inhibitors of glucagon release.
Basal (medicine)
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Glucose tolerance test
Glucose clamp technique
Blood sampling
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Somatostatin was infused for 6 h into seven normal subjects with and without a replacement dose of glucagon. The addition of glucagon to somatostatin resulted in a 30-40% rise in plasma glucagon, whereas plasma insulin declined by 40-50% in both treatment groups. Plasma glucose and glucose production initially increased 2-fold with glucagon replacement, and subsequently declined by 2-3 h to levels comparable to those observed with somatostatin alone. After 6 h plasma glucose and glucose kinetics were no different whether or not glucagon was present. The rise in blood ketones after somatostatin was not exaggerated by glucagon replacement. We conclude that glucagon lack is not a modifying factor in the late hyperglycemic and hyperketonemic response to prolonged infusions of somatostatin.
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