Masafumi Utsumi

Physiologic Role of Somatostatin Insulin Release from Rat Islets Treated by Somatostatin Antiserum

In order to clarify the physiologic role of somatostatin in insulin release, rat pancreatic islets treated by somatostatin antiserum were incubated in media containing various concentrations of glucose. Insulin release from antiserum-treated islets was significantly elevated above that from nontreated ones at 3.3 and 8.3 mM glucose, while the former was not different from the latter at 16.7 mM glucose. It is suggested that somatostatin plays an important role in the regulation of insulin release in the physiologic range of glucose concentration.

Determination of Immunoreactive Somatostatin in Rat Plasma and Responses to Arginine, Glucose and Glucagon Infusion

SummaryA method for the determination of immunoreactive somatostatin in rat plasma is described. Blood specimens were collected into aprotinin and EDTA. Plasma was separated, immediately diluted with acidified acetone and ultrasonicated. The resultant supernatant was lyophilised. The dilution curve of the material thus extracted was parallel to that of synthetic somatostatin. The material was eluted mainly in a similar position to that of synthetic somatostatin on Sephadex G-25 (f) column chromatography. The somatostatin immunoreactivity was degraded significantly from the pre-incubated value of 846±86 pg/ml (n=4, mean±SEM) to 102±16 pg/ml in the same manner as that of synthetic somatostatin when incubated with one ml of fresh rat plasma at 37 °C for 30 min. The mean recovery in quadruplicate of immunoreactive somatostatin at concentrations of 100, 200 and 400 pg/ml was 83±7, 95±4 and 76±4%, respectively. Using this method, plasma immunoreactive somatostatin responses to arginine, glucose and glucagon infusion were measured in pentobarbital anaesthetized rats. The mean basal plasma immunoreactive somatostatin concentration in the jugular vein was 35±3 pg/ml (n=7), while that in the hepatic portal vein was 120±17 pg/ml (n=7). Infusion of arginine, glucose and glucagon all resulted in 2–3 fold increases in portal plasma immunoreactive somatostatin concentration.

Somatostatin Concentration Responds to Arginine in Portal Plasma: Effects of Fasting, Streptozotocin Diabetes, and Insulin Administration in Diabetic Rats

Changes of somatostatin concentration in response to a single i.v. injection of arginine (400 mg/kg body weight) were examined in extracted portal plasma of normal and diabetic rats in the fully fed state and after 24 h of fasting, as well as in diabetic rats treated with insulin for one week. In both normal and diabetic animals fasted for 24 h, the basal level of somatostatin declined but the magnitude of the arginine-induced elevation of somatostatin was not affected, suggesting a physiologic role of the tetradecapeptide in nutrient homeostasis. When compared with intact rats, diabetic animals were shown to have increased levels of somatostatin before and after arginine administration, both of which were attenuated by insulin replacement therapy. These findings suggest that alterations of D cell function in streptozotocin diabetes may be related to either insulin deficiency or its metabolic consequences.

Monosodium glutamate (MSG) 投与による視床下部性肥満の膵-消化管ホルモンの動態

It has been reported that the neonatal administration of monosodium glutamate (MSG) in rodents produces lesions of the arcuate nucleus and the ventromedial nucleus of the hypothalamus and results in obesity in adulthood . Though there are a large number of reports using MSG-treated animals, most of them deal with neuronal and neuroendocrinological pathophysiology within the central nervous system. The present study, therefore, was designed to investigate the time-course of metabolic and hormonal changes in relation to the development of hypothalamic obesity induced by MSG in female Wister rats. In addition, responses of insulin and somatostatin to glucose loading were examined in rats with hypothalamic obesity . MSG, 2mg per g of body weight, was subcutaneously injected for 5 consecutive days after birth. Body weight, plasma glucose and immunoreactive insulin (IRI) were measured at oneto four-week intervals in rats aged from 6 days to 11 months. The Lee index, plasma triglyceride and immunoreactive glucagon (IRG) were measured at one-month intervals from one to 11 months. Immunoreactive somatostatin (IRS) and gastrin (IRGa) were determined at the 7th month or later. All parameters in plasma described above were assayed on samples drawn from the jugular vein. In addition, IRI and IRS in the pancreas were measured until 6 months. Further, responses of glucose, IRI and IRS to intragastric glucose loading (3g/kg body weight) were examined in portal plasma at the 11th month . All parameters in the MSG rats were compared with those in age-matched female controls which received the vehicle alone.