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. Corticotrophin-releasing hormone (CRH) is also a potent stimulator of TSH secretion ( Geris et al. 1996 , 2003 b ), whereas somatostatin (SRIH) was shown to inhibit TSH release at the level of the pituitary ( Geris et al. 2003 a , 2003 b ). The inhibition
Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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Physiology and Pharmacology and
Medicine, University of Western Ontario, Canada
Children’s Health Research Institute, London, Ontario, Canada
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, Vanderbilt University, Nashville, Tennessee, USA), rabbit anti-Glut-2 (1:500; Chemicon), rabbit anti-somatostatin (1:50; Chemicon) and rabbit anti-Mist1 (1:1000; Pin et al. 2001 ). In some cases, dual labeling was performed by co-incubating insulin
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islets and in long-term cultures enriched in nestin-positive cells. Low mRNA levels of insulin, glucagon and somatostatin were detected after prolonged subculturing in low serum medium without addition of differentiation-inducing factors. The attempt to
School of Applied and Engineering Physics, Cornell University, Ithaca, New York, USA
Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany
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Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany
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Laboratory for Nanoscale Cell Biology, Max-Planck-Institute for Biophysical Chemistry, Goettingen, Germany
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(NE), somatostatin, and several other agonists, prostaglandins inhibit the secretion of insulin by several mechanisms. These include (i) activation of K + channels to repolarize or hyperpolarize the cell ( Rorsman et al. 1991 , Sharp 1996
Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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Department of Medicine, University of Illinois at Chicago and Jesse Brown VA Medical Center, Research and Development, Chicago, Illinois 60612, USA
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-treated rat is more sensitive to the stimulatory actions of GHRH ( Sheppard et al. 1989 a , 1989 b ) and GH secretagogue (GHS) receptor (GHS-R) agonists (ipamorelin; Johansen et al. 2003 ) and less sensitive to the inhibitory actions of somatostatin
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ABSTRACT
The release of insulin, glucagon, somatostatin and pancreatic polypeptide (PP) by isolated mouse pancreatic islets was determined during 30-min incubations at 5.6 and 16.7 mmol glucose/l in the absence and presence of gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI) at concentrations of 1–1000 nmol/l. Insulin release was enhanced (>50%) by GIP (100–1000 nmol/l) and VIP (1 μmol/l) at 5.6 mmol glucose/l, but not at 16.7 mmol glucose/l. Glucagon release was increased by GIP (100–1000 nmol/l), and by VIP and PHI (1—1000 nmol/l) at both glucose concentrations in a dose-related manner (maximum increases > tenfold). Somatostatin release was similarly increased by GIP (10–1000 nmol/l) at both glucose concentrations. Only the highest concentration (1 μmol/l of PHI tested increased somatostatin release (twofold) at 5.6 mmol glucose/l, whereas PHI and VIP (1–1000 nmol/l reduced (>37%) somatostatin release at 16.7 mmol glucose/l. PP release was increased (49–58%) by 100–1000 nmol GIP/l, but was not significantly altered by VIP, and was reduced (39–56%) by PHI. The results indicate that GIP, VIP and PHI each stimulate glucagon release in a dose-related manner, but they exert discretely different effects on other islet hormones depending upon the dose and the prevailing glucose concentration.
Journal of Endocrinology (1990) 125, 375–379
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ABSTRACT
The effects of the islet cell hormones glucagon, somatostatin-28 and pancreatic polypeptide on insulin secretion from cultured cloned pancreatic B cells (HIT-T15 and RINm5F) have been investigated. Glucagon stimulates the secretion of insulin from HIT-T15 cells in the absence and presence of glucose and from RINm5F cells in the absence and presence of glyceraldehyde. HIT-T15 cells were more sensitive to the stimulatory effect of glucagon than RINm5F cells. Somatostatin-28 and pancreatic polypeptide, both alone and in combination, reduced glucose- and glucagon-stimulated insulin release from HIT-T15 cells and glyceraldehyde- and glucagon-stimulated insulin release from RINm5F cells. HIT-T15 cells were more sensitive to the inhibitory actions of somatostatin-28 and pancreatic polypeptide than RINm5F cells. This study supports the hypothesis that insulin release from normal B cells may be modified by the paracrine activity of islet hormones, glucagon, somatostatin and pancreatic polypeptide and probably occurs before any fine tuning imposed by subsequently released insulin.
Journal of Endocrinology (1989) 121, 479–485
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ABSTRACT
Injections and infusions of oxytocin into conscious dogs caused an increase in plasma concentrations of glucose, insulin and glucagon. When blood glucose was clamped at a raised level the injection of oxytocin still increased insulin and glucagon concentrations in plasma. Infusion of somatostatin suppressed plasma concentrations of glucagon and insulin but did not prevent oxytocin-induced increments in blood glucose. Injection of oxytocin still caused a marked release of glucagon, whereas the insulin response was greatly diminished. When endogenous insulin and glucagon secretion was suppressed by infusion of somatostatin and glucose levels were stabilized by concomitant infusions of glucagon and insulin, injections of oxytocin did not alter blood glucose concentrations. It is concluded that the increase in blood glucose following the administration of oxytocin is secondary to the release of glucagon and that oxytocin exerts a direct stimulatory effect on glucagon and possibly insulin secretion.
J. Endocr. (1986) 108, 293–298
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Somatostatin, the growth hormone release inhibitory hormone (Brazeau, Vale, Burgus, Ling, Butcher, Rivier & Guillemin, 1973), NH2-Ala-Gly-Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Thr-Ser-Cys-Co2H, is the first hypothalamic hormone shown unequivocally to exert a negative control over pituitary secretion. Its inhibition of growth hormone release has been confirmed in normal and diabetic men (Hansen, Ørskov, Seyer-Hansen & Lundbaek, 1973).
The present study was undertaken to determine whether somatostatin can also alter prolactin release. Cultures of secreting pituitary cells offer the least ambiguous model for such a question, because of the enormous population of viable secreting units, the expectation of direct interaction between receptor and hormone, and a level of basal secretion sufficiently high to show a range of changes by radioimmunoassay. Monolayer cultures of enzymically dispersed cells were prepared from whole pituitaries of normal Charles River CD male rats, using Eagle's minimal essential medium for growth (Grant, Clark & Rosanoff, 1973). After test
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ABSTRACT
Intraperitoneal injection of 5 μg cholecystokinin octapeptide (CCK-8) into male rats deprived of food for 48 h produced a transient (less than 15 min) increase in plasma levels of CCK-8 but suppressed food intake for an extended period (45 min). Plasma concentrations of CCK-8 after i.p. injection of CCK-8 were raised to levels which were fairly comparable to those after feeding. Intracerebroventricular (i.c.v.) injection of the CCK antagonist proglumide (100 μg) reversed the effect of CCK-8 on food intake, while i.p. injection of proglumide (100 μg) did not have this effect. Feeding increased the plasma concentrations of somatostatin and gastrin but not of oxytocin, and somatostatin and oxytocin but not gastrin were released in response to i.p. injection of CCK-8. However, neither somatostatin nor oxytocin affected food intake, and their release in response to CCK-8 was unaffected by i.c.v. injection of proglumide. These results support the suggestion that CCK-8 is a physiological 'satiety' peptide, which can affect food intake in rats by mechanisms involving both peripheral and central CCK receptors.
Journal of Endocrinology (1989) 121, 59–65
