INHIBITORY EFFECT OF SOMATOSTATIN ON INSULIN SECRETION DURING α-ADRENERGIC BLOCKADE IN THREE DIFFERENT SPECIES

1979 ◽  
Vol 92 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Johannes Järhult ◽  
Bo Ahrén ◽  
Ingmar Lundquist
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Basal Plasma ◽  
Stimulation Of

ABSTRACT It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory α-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during α-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during α-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 μg/kg/min decreased basal plasma insulin concentration by 92 %. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85 %. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87 %, but its depressive effect during α-adrenergic blockade was comparatively less pronounced (68 %) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during α-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of α-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.

ADRENOCORTICOTROPHIN AND THE DEVELOPMENT OF INSULIN SECRETION IN THE RABBIT FOETUS

1975 ◽  
Vol 64 (1) ◽  
pp. 67-75 ◽  
Author(s):  
P. M. B. JACK ◽  
R. D. G. MILNER
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Cell Function ◽  
Pancreatic Tissue ◽  
High Rate ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Β Cell Function

SUMMARY Foetal rabbits were injected with adrenocorticotrophin (ACTH), decapitated, or decapitated and injected simultaneously with ACTH or cortisol in utero on day 24 of gestation. The foetuses were killed after Caesarian section on day 29, and blood was collected for measurement of plasma insulin concentration and pancreatic tissue was obtained for incubation in physiological buffer. Insulin release from the pancreatic tissue of decapitated foetuses was significantly greater than that from the pancreas of control litter-mates when incubated in media containing 3·3 mm-glucose, 16·5 mm-glucose or 16·5 mm-glucose plus 5 μg glucagon/ml, but was similar when the incubation medium contained 3·3 or 16·5 mm-glucose plus 1 mm-theophylline or 3·3 mm-glucose plus 60 mm-potassium. The pancreata of decapitated or intact foetuses injected with ACTH did not differ significantly from control foetuses in terms of insulin release in response to glucose in vitro. The plasma insulin concentration of decapitated foetuses and decapitated foetuses injected with ACTH was raised, whereas that of intact foetuses injected with ACTH was similar to that of the control foetuses. Cortisol injection at the time of decapitation resulted in a high rate of foetal mortality. The results indicate that foetal ACTH or foetal adrenocortical secretion influences the normal development of glucose-mediated insulin secretion in the rabbit and that exogenous ACTH corrects the effect of decapitation on β cell function in vitro but not on plasma insulin concentration.

Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

1988 ◽  
Vol 255 (5) ◽  
pp. E629-E635 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Plasma Insulin ◽  
Lactate Concentration ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Insulin Concentration ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration ◽  
Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

EFFECT OF DECAPITATION ON THE DEVELOPMENT OF INSULIN SECRETION IN THE FOETAL RABBIT

1973 ◽  
Vol 57 (1) ◽  
pp. 23-31 ◽  
Author(s):  
P. M. B. JACK ◽  
R. D. G. MILNER
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Β Cell ◽  
Plasma Insulin Concentration ◽  
Intrauterine Development ◽  
Foetal Head ◽  
Significant Difference ◽  
The Mean ◽  
Control Litter

SUMMARY One rabbit foetus in a litter was decapitated on day 24 of gestation. On day 29 the litter was killed and blood was collected from all foetuses for the measurement of plasma insulin concentration. The pancreas of the decapitated foetus and that of the control litter-mate with the nearest headless body weight were cut into pieces and incubated in a physiological buffer containing 0·6 or 3·0 mg glucose/ml. The pancreas of the decapitated foetus secreted significantly more insulin than that of the control foetus in either concentration of glucose in the medium. Higher insulin secretion from the decapitated foetus persisted for 4·5 h of incubation and was demonstrable in both the first 5 and subsequent 25 min of incubation when the pancreas was initially transferred to incubation medium containing 3·0 mg glucose/ml. The mean plasma insulin concentration of the foetuses decapitated on day 24 was higher on day 29 than that of the control foetuses but there was no significant difference between the concentration of insulin in the pancreas of the two groups of animals. The results indicate that removal of the foetal head influences the intrauterine development of the rabbit β-cell.

Effect of gestational hyperglycemia on insulin secretion in vivo and in vitro by fetal rat pancreas

1986 ◽  
Vol 251 (1) ◽  
pp. E86-E91 ◽  
Author(s):  
M. T. Bihoreau ◽  
A. Ktorza ◽  
A. Kervran ◽  
L. Picon
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Cell Function ◽  
Pregnant Rats ◽  
Fetal Rat ◽  
Gestational Hyperglycemia

The effects of gestational hyperglycemia on B-cell function were studied in near-term fetuses from unrestrained pregnant rats made slightly or highly hyperglycemic using continuous glucose infusion during the last week of pregnancy. Pancreatic and plasma insulin and insulin secretion in vitro were studied in the fetuses. Compared with controls, slightly hyperglycemic fetuses showed increased pancreatic and plasma insulin concentrations and similar insulin release in response to glucose in vitro. In highly hyperglycemic fetuses, pancreatic and plasma insulin concentrations were unchanged compared with controls, and insulin release in vitro was insensitive to glucose and to the mixture glucose plus theophylline. These results confirm that glucose is able to stimulate insulin secretion in normal or slightly hyperglycemic fetuses and suggest that severe hyperglycemia per se, without association of other metabolic disorders or toxic injuries, profoundly alters the stimulus-secretion coupling of the fetal rat B-cell.

Effects of hyperprolactinaemia on glucose tolerance and insulin release in male and female rats

1997 ◽  
Vol 153 (3) ◽  
pp. 423-428 ◽  
Author(s):  
F M Reis ◽  
A M Reis ◽  
C C Coimbra
Keyword(s):  
Glucose Tolerance ◽  
Insulin Release ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Female Rats ◽  
Insulin Concentration ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Male And Female ◽  
Male And Female Rats

Abstract It has been shown that prolactin (PRL) induces glucose intolerance, hyperinsulinaemia and insulin resistance in several animal species, including rats. However, the sex differences regarding glucose homeostasis and insulin release in hyperprolactinaemic subjects have not been assessed to date. In the present study, hyperprolactinaemic (pituitary-grafted) or control (sham-operated) male and female rats were submitted to an i.v. glucose tolerance test (30 mg/100 g body weight, 30% glucose). Grafted female rats had fasting plasma glucose concentrations 26% above control (P<0·01). After the glucose load there was a rapid and pronounced increase in plasma glucose levels in all animal groups, followed by a return to basal values within 30 min. However, the glucose concentrations in hyperprolactinaemic rats were significantly greater than those in controls at 5 min (males, P<0·05) and 30 min (females, P<0·05). The glucose disappearance rate was significantly increased in the grafted females compared with control (P<0·01) and slightly increased in the grafted males. Plasma insulin concentration increased just after glucose load and returned to basal values within 5 min in all groups except for the grafted females, which had recovered their basal insulin levels at 15 min. The grafted male rats had insulin concentrations higher than those of sham-operated controls at 2 min (28·9 ± 3·6 vs 17·3 ± 2·1 μU/ml, P<0·01), whereas females had plasma insulin concentrations greater than those in sham-operated controls 10 min after the glucose load (15·9 ± 1·9 vs 10·1 ± 1·4 μU/ml, P<0·05). The areas under the plasma insulin concentration–time curves were also significantly increased in the hyperprolactinaemic rats and were positively correlated with plasma PRL concentrations (r=0·613, P<0·01). These results demonstrate that moderate chronic hyperprolactinaemia is associated with increased glucose-induced insulin release, which was altered at different times after the glucose load in grafted male and female rats, whereas fasting hyperglycaemia was observed only in grafted females, indicating a sexual dimorphism in the diabetogenic effects of PRL in rats. Journal of Endocrinology (1997) 153, 423–428

Sensitivity of insulin secretion to feedback inhibition by hyperinsulinaemia

1981 ◽  
Vol 98 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Ralph A. DeFronzo ◽  
Christian Binder ◽  
John Wahren ◽  
Philip Felig ◽  
Eleuterio Ferrannini ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Feedback Inhibition ◽  
Normal Subjects ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
C Peptide ◽  
Endogenous Insulin ◽  
Arterial Plasma

Abstract. The ability of insulin to inhibit its own secretion was examined in 15 normal subjects given an intravenous infusion of insulin in a dose of 0.25, 0.50, 1.0, 5.0 or 10.0 mU/kg/min for two hours. Arterial plasma insulin concentration achieved during the infusion segregated into three levels of hyperinsulinaemia: 35 ± 1 (mean ± sem), 87 ± 15 and 828 ± 210 μU/ml. Plasma glucose concentration was kept constant at the basal level by a variable glucose infusion. Fasting C-peptide (0.29 ± 0.02 pmol/ml) fell significantly in all subjects during hyperinsulinaemia and reached a concentration of 0.19 ± 0.03 pmol/ml at 60 min and 0.14 ± 0.03 at 120 min after the start of the insulin infusion. The C-peptide response was not related to the infusion dose nor to the steady state plasma insulin concentration. It is concluded that (a) basal insulin secretion as evaluated from C-peptide measurements is inhibited by small (24 ± 3 μU/ml) physiological elevations in plasma insulin concentration independent of changes in plasma glucose, and (b) supraphysiological or even pharmacological elevations in plasma insulin do not result in a further decrease in endogenous insulin secretion above that achieved with mild hyperinsulinaemia.

Sodium-lithium countertransport and platelet cytosolic free calcium concentration in relation to peripheral insulin sensitivity in postmenopausal women

1992 ◽  
Vol 83 (3) ◽  
pp. 319-324 ◽  
Author(s):  
Ingrid Mattiasson ◽  
Kerstin Berntorp ◽  
Folke Lindgärde
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Normal Glucose Tolerance ◽  
Insulin Concentration ◽  
Glucose Disposal ◽  
Plasma Insulin Concentration ◽  
Normal Glucose ◽  
Basal Plasma

1. Peripheral glucose disposal (assessed by the euglycaemic-hyperinsulinaemic clamp technique), Na+-Li+ countertransport in erythrocytes and the cytosolic free Ca2+ concentration in platelets were determined in 41 women with impaired glucose tolerance and in 38 women with normal glucose tolerance. The groups were matched for body mass index (range 18–44 kg/m2) and diastolic blood pressure (range 58–109 mmHg). 2. Na+-Li+ countertransport was correlated significantly with body mass index, basal plasma insulin concentration and basal plasma glucose concentration, and was inversely correlated with peripheral glucose disposal rate. Stepwise regression analysis showed that Na+-Li+ countertransport was positively correlated with basal plasma insulin concentration (r2 = 8.7%). 3. Systolic blood pressure was correlated with fasting plasma insulin concentration (model r2 = 25%) and with Na+-Li+ countertransport (model r2 = 34%) in the group with impaired glucose tolerance. In the group with normal glucose tolerance there were no correlations between blood pressure and Na+-Li+ countertransport. 4. No correlation was found between platelet cytosolic free Ca2+ concentration and any of the variables measured. 5. It is concluded that Na+-Li+ countertransport is correlated with the degree of peripheral insulin sensitivity and with the plasma insulin concentration. Platelet cytosolic free Ca2+ concentration was not correlated with any of these variables, and there was no relationship between Na+-Li+ countertransport and the platelet cytosolic free Ca2+ concentration.

scholarly journals The effect of N-acylglucosamines on the biosynthesis and secretion of insulin in the rat

1976 ◽  
Vol 154 (3) ◽  
pp. 701-707 ◽  
Author(s):  
S J. H. Ashcroft ◽  
J R. Crossley ◽  
P C. Crossley
Keyword(s):  
Insulin Release ◽  
Plasma Insulin ◽  
Acyl Chain ◽  
Secretory Response ◽  
Insulin Concentration ◽  
Insulin Biosynthesis ◽  
Plasma Insulin Concentration ◽  
Rat Islets

The effects of N-acylglucosamines on insulin release have been studied. N-Acylglucosamines stimulated insulin release from rat islets in vitro only if a sub-stimulatory concentration of glucose was also present, and this secretory response was abolished by mannoheptulose. In perifused islets the rapidity of the secreotry response to N-acetyl-D-glucosamine was similar to that observed with D-glucose. Increasing acyl-chain length from N-acetyl- to N-hexanoyl-D-glucosamine impaired the secretory response; however, N-dichloroacetyl-D-glucosamine was a more potent stimulator of release than was N-acetyl-D-glucosamine. Polymers of N-acetyl-D-glucosamine containing two to six monomers linked α1-4 did not stimulate insulin release; glucosamine linked to dextran via a propionyl or hexanoyl spacer group was also without insulin-releasing ability. N-Acylglucosamines were also effective in eliciting insulin release in vivo when injected into conscious rats. At the dose used (86 mumol), N-acetylgucosamine elicited a rapid rise in plasma-insulin concentration; N-butyrylglucosamine was less effective, and there was little or no response to N-hexanoylglucosamine. The response to N-dichloroacetyl-glucosamine was greater than that to N-acetylglucosamine; an increase in plasma insulin concentration could be elicited by N-dichloroacetylglucosamine at a dose (17 mumol) at which neither glucose nor N-acetylglucosamine was effective. The secretory response to acetylglucosamine is not mediated by conversion into glucose. Rates of (pro)-insulin biosynthesis by rat islets have been measured (Pro)-insulin biosynthesis was stimulated by glucose, and this response was abolished by mannoheptulose. N-Acetylglucosamine also stimulated (pro)-insulin biosynthesis; this effect of N-acetylglucosamine did not require the presence of glucose, and was not abolished by mannoheptulose. It is concluded that there are differences in signal reception and/or transduction for the processes of insulin biosynthesis and release.

Sign in / Sign up

Export Citation Format

Share Document