RELEASE OF IMMUNOREACTIVE AND RADIOACTIVELY PRELABELLED ENDOGENOUS (PRO-)INSULIN FROM ISOLATED ISLETS OF RAT PANCREAS IN THE PRESENCE OF EXOGENOUS INSULIN

1977 ◽  
Vol 74 (2) ◽  
pp. 243-249 ◽  
Author(s):  
H. SCHATZ ◽  
E. F. PFEIFFER

To study the influence of insulin on its own secretion, collagenase-isolated islets of rat pancreas were prelabelled with [3H]leucine for 2 h. After washing the islets, (pro-)insulin release was stimulated by glucose in the presence or absence of exogenous insulin (up to 2·5 mu./ml). Hormone release was unchanged by the presence of exogenous insulin as judged by determination of both immunoreactive insulin and radioactivity incorporated into the proinsulin and insulin fractions of the medium. No direct feedback mechanism for insulin secretion was apparent from this study.

1994 ◽  
Vol 131 (2) ◽  
pp. 201-204 ◽  
Author(s):  
Claes-Göran Östenson ◽  
Bo Ahrén ◽  
Sven Karlsson ◽  
Jens Knudsen ◽  
Suad Efendic

Östenson C-G, Ahrén B, Karlsson S, Knudsen J, Efendic S. Inhibition by rat diazepam-binding inhibitor/ acyl-CoA-binding protein of glucose-induced insulin secretion in the rat. Eur J Endocrinol 1994;131:201–4. ISSN 0804–4643 Diazepam-binding inhibitor (DBI) has been localized immunohistochemically in many organs. In porcine and rat pancreas, DBI is present in non-B-cells of the pancreatic islets. Porcine peptide also has been shown to suppress insulin secretion from rat pancreas in vitro. Recently, acyl-CoA-binding protein (ACBP) was isolated from rat liver and shown to be identical structurally to DBI isolated from rat brain. Using this rat DBI/ACBP, we have studied its effects on glucose-stimulated insulin secretion in the rat, both in vivo and in isolated pancreatic islets. Infusion iv of rDBI/ACBP (25 pmol/min) during glucose stimulation induced a moderate and transient reduction of plasma insulin levels. Moreover, rDBI/ACBP suppressed insulin release from batch-incubated isolated islets, stimulated by 16.7 mmol/l glucose, by 24% at 10 nmol/l (p < 0.05) and by 40% at 100 nmol/l (p < 0.01). The peptide (100 nmol/l) also inhibited the insulin response to glucose (16.7 mmol/l) from perifused rat islets by 31% (p < 0.05), mainly by affecting the acute-phase response. Finally, incubation of isolated islets in the presence of rDBI/ACBP antiserum (diluted 1:100 and 1:300) augmented the insulin response to 16.7 mmol/l glucose (p < 0.05 or even less). We conclude that rDBI/ACBP, administered iv or added to the incubation media, suppresses insulin secretion in the rat but that the effect is moderate despite the high concentration used. It is therefore unlikely that the peptide modulates islet hormone release, acting as a classical hormone via the circulation. However, the occurrence of DBI/ACBP in the islets and the enhancing effect by the rDBI/ACBP antibodies on glucose-stimulated insulin release suggest that the peptide is a local modulator of insulin secretion. C-G Östenson, Department of Endocrinology, Karolinska Hospital, S-171 76 Stockholm, Sweden


1976 ◽  
Vol 23 (5) ◽  
pp. 407-412 ◽  
Author(s):  
SEIJI SUZUKI ◽  
HIROSHI OKA ◽  
HIROKO YASUDA ◽  
TOSHIO KANEKO ◽  
KAMEJIRO YAMASHITA ◽  
...  

1984 ◽  
Vol 105 (3) ◽  
pp. 398-406 ◽  
Author(s):  
Francois Rey ◽  
Charlotte Mauron ◽  
Elisabetta Bobbioni ◽  
Bernard Jeanrenaud ◽  
Viktor Mutt ◽  
...  

Abstract. A crude mixture of thermostable peptides extracted from porcine duodenum was fractionated by electrofocusing. A neutral fraction, different from the basic fractions of GIP, VIP, PHI and CCK was found to promote insulin secretion when injected in vivo to normal rats. This neutral fraction, extracted from the crude mixture by chromatography, stimulated insulin output from an isolated rat pancreas and enhanced glucoseinduced insulin release. The insulinotrophic effect of this partially purified duodeno-jejunal material disappeared following digestion with trypsin. The insulin-releasing activity was found to correspond to a compound of molecular weight higher than that of insulin (i.e. higher than 6000). No GIP-like immunoreactivity was found in this neutral fraction indicating that the active peptide(s) are not GIP related compounds. These observations suggest that porcine duodenum contains and incretin activity different from that of the insulinotrophic factors already reported.


1977 ◽  
Vol 168 (3) ◽  
pp. 591-593 ◽  
Author(s):  
I L Campbell ◽  
K W Taylor

Inosine is a potent simulant of insulin release from rat but not from rabbit islets of Langerhans. Further investigation showed that nucleoside phosphorylase activity is exceptionally low in rabbit islets. The ability of inosine to promote insulin release seems to be related to islet nucleoside phosphorylase activity, which can display marked species differences.


1987 ◽  
Vol 114 (2) ◽  
pp. 185-189 ◽  
Author(s):  
O. Berglund

ABSTRACT Perfusion of the mouse or rat pancreas with 20 mmol d-glucose/l caused a biphasic release of insulin. The second phase was nearly constant in the mouse but rose in the rat. Repeated pulses of 8, 20 or 30 mmol d-glucose/l did not potentiate subsequent insulin responses in the mouse, whereas repeated pulses of 20 mmol/l did in the rat. When 20 mmol d-glucose/l was introduced through the mesenteric artery or aorta of the mouse, the pattern of insulin release was the same as when it was introduced through the coeliac artery. Thus, insulin secretion in mice differs from that in rats both in not showing an increasing second phase in response to continuous stimulation with glucose and also in not showing successive enhancement in the insulin response to repeated pulses of glucose. J. Endocr. (1987) 114, 185–189


1975 ◽  
Vol 78 (3) ◽  
pp. 510-515 ◽  
Author(s):  
S. Efendić ◽  
R. Luft

ABSTRACT Somatostatin, the recently discovered growth hormone release-inhibiting hormone in the hypothalamus, also inhibited glucose induced insulin release from the isolated perfused rat pancreas. The lowest effective dose of somatostatin was 1 ng/ml of perfusate. By increasing the dose to 100 ng/ml an almost complete inhibition of basal as well as stimulated insulin release was obtained. The inhibition of glucose stimulated insulin release mediated by somatostatin might be of competitive nature since somatostatin seemed to dislocate the glucose-insulin dose-response curve to the right.


1994 ◽  
Vol 40 (3) ◽  
pp. 39-41 ◽  
Author(s):  
A. V. Sitozhevsky ◽  
I. V. Dusta ◽  
A. V. Trofimov ◽  
V. V. Ivanov ◽  
O. A. Karpenko

Rates of basal and glucose-stimulated insulin and glutathione secretion were studied in experiments with isolated rat pancreas, as were prooxidant effects on these values. The rate of oxidized and recovered glutathione release was found increased at glucose concentration increase to 16.7 mmoles in perfusion solution. Addition of prooxidants (tret- butyl hydroperoxide and Fe2+) in concentrations 10~4 mole did not change basal insulin secretion but resulted in reduction of glucose-stimulated hormone release. Under such conditions a reduction of the rate of oxidized and recovered glutathione release by the pancreas was observed which was adequate to changed GSH/GSSG ratio in isolated Langerhans islets. It may be supposed that lipid peroxidation results in changed thiol-disulfide ratio in Langerhans islets В cells and in reduction of their sensitivity to secretogen effect.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Faradianna E. Lokman ◽  
Harvest F. Gu ◽  
Wan Nazaimoon Wan Mohamud ◽  
Mashitah M. Yusoff ◽  
Keh Leong Chia ◽  
...  

Aims. To evaluate the antidiabetic properties of borapetol B known as compound 1 (C1) isolated fromTinospora crispain normoglycemic control Wistar (W) and spontaneously type 2 diabetic Goto-Kakizaki (GK) rats.Methods. The effect of C1 on blood glucose and plasma insulin was assessed by an oral glucose tolerance test. The effect of C1 on insulin secretion was assessed by batch incubation and perifusion experiments using isolated pancreatic islets.Results. An acute oral administration of C1 improved blood glucose levels in treated versus placebo groups with areas under glucose curves 0–120 min being72±17versus344±10 mmol/L (P<0.001) and492±63versus862±55 mmol/L (P<0.01) in W and GK rats, respectively. Plasma insulin levels were increased by 2-fold in treated W and GK rats versus placebo group at 30 min (P<0.05). C1 dose-dependently increased insulin secretion from W and GK isolated islets at 3.3 mM and 16.7 mM glucose. The perifusions of isolated islets indicated that C1 did not cause leakage of insulin by damaging islet beta cells (P<0.001).Conclusion. This study provides evidence that borapetol B (C1) has antidiabetic properties mainly due to its stimulation of insulin release.


1985 ◽  
Vol 107 (1) ◽  
pp. 1-8 ◽  
Author(s):  
C.S.T. Hii ◽  
S.L. Howell

ABSTRACT The effects of some flavonoids, a group of naturally occurring pigments one of which has been claimed to possess antidiabetic activities, on insulin release and 45Ca2+ handling have been studied in isolated rat islets of Langerhans. Insulin release was enhanced by approximately 44–70% when islets were exposed to either (−)epicatechin (0·8 mmol/l) or quercetin (0·01–0·1 mmol/l); others such as naringenin (0·1 mmol/l) and chrysin (0·08 mmol/l) inhibited hormone release by approximately 40–60%. These effects were observed only in the presence of 20 mmol glucose/l. Quercetin (0·01 mmol/l) and (−)epicatechin (0·8 mmol/l) both inhibited 45Ca2+ efflux in the presence and absence of extracellular Ca2+. In the presence of 20 mmol glucose/l both the short-term (5 min) and steady-state (30 min) uptake of 45Ca2+ were significantly increased by either quercetin or (−)epicatechin. These results suggest that the stimulatory compounds such as quercetin and (−)epicatechin may, at least in part, exert their effects on insulin release via changes in Ca2+ metabolism. J. Endocr. (1985) 107, 1–8


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