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  • 1
    Electronic Resource
    Electronic Resource
    Evidence for decreased sensitivity to glucose of isolated islets from spiny mice (Acomys cahirinus) (1974)
    Springer
    Diabetologia 10 (1974), S. 661-665 
    Details
    ISSN: 1432-0428
    Keywords: Spiny mice (Acomys cahirinus) ; isolated islets ; glucose ; theophylline ; arginine ; cytochalasin B ; vincristine ; insulin releasein vitro ; sensitivity to glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunoreactive insulin (IRI) release from collagenase isolated pancreatic islets of spiny mice (Acomys cahirinus) was examined in 15 min and 2 h incubations at glucose concentrations between 2.8 and 56 mM. The resultant glucose-insulin dose-response curves forAcomys islets were compared to those for similarly incubated rat islets. After 15 min incubations, IRI release fromAcomys islets was significantly lower than that from rat islets at all stimulating glucose concentrations. After 2 h incubations, however, maximal responses were similar forAcomys and rat islets, whereas thesensitivity ofAcomys islets to glucose was significantly less. Cyclic AMP 10 mM, theophylline 5 mM, arginine 10 mM, and cytochalasin B 10 Μg/ml, all enhanced IRI release in the presence of glucose 16.7 mM to a relatively greater extent fromAcomys than from rat islets. Vincristine 10−5M reduced IRI release from bothAcomys and rat islets, and this to a similar extent. The results suggest that defective IRI release fromAcomys islets may be the expression of decreased B-cell sensitivity to glucose, even though IRI release fromAcomys islets may improve in time with continued exposure to elevated glucose concentrations. The ability of B-cells ofAcomys to recognize other agents that enhance the action of glucose appeared unaltered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01222001
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanisms of glucose stimulated insulin secretion in health and in diabetes: Some re-evaluations and proposals (1975)
    Springer
    Diabetologia 11 (1975), S. 1-13 
    Details
    ISSN: 1432-0428
    Keywords: Glucose-induced insulin secretion ; initiation of release ; cyclic AMP ; cholera toxin ; phosphodiesterase inhibition ; glucoreceptor ; glucose utilization ; calcium ions ; potentiation of release ; adrenaline ; glucagon ; diabetes ; prediabetes ; Acomys ; isolated islets ; perifusion ; perfused pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422811
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  • 3
    Electronic Resource
    Electronic Resource
    Insulin antibodies: Description of specific serum protein localization in a patient with insulin resistant diabetes (1966)
    Springer
    Diabetologia 2 (1966), S. 45-51 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé 1. Un cas de diabète insulino-résistant est présenté en détail et l'attention attirée sur le rapport chronologique entre le début du diabète et une série de traitements antérieurs à l'insulino-choc. 2. Les anticorps anti-insuline ont été localisés dans les γ-globulines par l'emploi consécutif d'électrophorèse et de filtration sur Sephadex. La majorité des anticorps anti-insuline s'est révélée être des globulines γg, avec un débordement important sur la région des globulines γa. 3. La relation pathogénique possible entre la réaction immunologique de la malade et la manifestation du diabète est considérée.
    Abstract: Zusammenfassung 1. Ein Fall von insulinresistentem Diabetes mellitus bei einer Patientin wird ausführlich beschrieben. Das Verhältnis zwischen einer früheren Insulinbehandlung aus psychiatrischer Indikation und dem späterem Auftreten von manifestem Diabetes wird besonders berücksichtigt. 2. Die Lokalisierung der Insulinantikörper in der γg-Globulinfraktion mit Übergang auf die γa Fraktion wird beschrieben. 3. Der mögliche Zusammenhang zwischen der Immunisierung der Patientin und dem Manifestwerden der Krankheit wird diskutiert.
    Notes: Summary 1. A patient with insulin resistant diabetes mellitus has been described in detail with emphasis upon the time relationship between prior insulin therapy for mental illness and the subsequent development of overt diabetes. 2. The localization of the insulin antibodies in the γg-globulins with some extension into the region of γa has been delineated. 3. The possible relationship between the immunologic responsiveness of the patient and the eventual manifestation of the disease is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01106973
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  • 4
    Electronic Resource
    Electronic Resource
    Correction of diabetic pattern of insulin release from islets of the spiny mouse (Acomys cahirinus) by glucose priming in vitro (1985)
    Springer
    Diabetologia 28 (1985), S. 233-236 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; time-dependent potentiation ; non-insulin dependent-diabetes ; Acomys cahirinus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin release kinetics were studied in perifused islets of Langerhans, isolated from mildly hyperglycaemic and from normoglycaemic spiny mice (Acomys cahirinus), a rodent predisposed to develop spontaneously non-ketotic diabetes. In both groups, insulin response to glucose (16.7 mmol/l) was delayed in comparison with that of rat islets, the release kinetics being analogous to that of human Type 2 (non-insulin-dependent) diabetes. Thirty min priming of the isolated Acomys islets with glucose (16.7 mmol/l) resulted in potentiation of the insulin release to a second stimulation. The degree of potentiation decreased exponentially with the time interval between stimulations, showing a t 1/2 of 18 min. Induction of potentiation by glucose was time-dependent, giving a maximal effect after 20 min of priming. In addition to overall amplification of the insulin response, priming with glucose accelerated markedly the initial release rates, correcting the dynamics of the response. We conclude that: (1) decreased and delayed insulin secretion is found in Acomys cahirinus before the development of hyperglycaemia; (2) induction of time-dependent potentiation in the islet by priming with glucose corrects the diabetic-type dynamics of insulin release; (3) therefore the deficient insulin release of Acomys is of a functional nature, the mechanism of potentiation bypassing the defect; (4) since insulin release in Acomys resembles that in prediabetic and diabetic man, similar conclusions might apply to the islet dysfunction in Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00282239
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  • 5
    Electronic Resource
    Electronic Resource
    Decreased intravenous glucose tolerance and low plasma insulin response in spiny mice (Acomys cahirinus) (1974)
    Springer
    Diabetologia 10 (1974), S. 667-670 
    Details
    ISSN: 1432-0428
    Keywords: Spiny mouse (Acomys cahirinuis) ; intravenous glucose tolerance ; insulin in plasma ; obesity ; endocrine pancreas ; insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A technique was developed to permit estimation of intravenous glucose tolerance and the concomitant immunoreactive insulin (IRI) response in the Geneva colony of the semi-desert rodentAcomys cahirinus. Following intravenous injection of glucose 1.5 g/kg, youngAcomys (2–3 months, 25–35 g body weight) had a significantly lower glucose tolerance (p〈0.01) and a smaller 30 min integrated plasma IRI response (p〈0.001) than age and weight matched albino mice. With increasing age (8 and 21 months) and body weight (57 to 100 g) of theAcomys, glucose tolerance and plasma IRI response decreased further, and in the 21 month old group there were 2 overtly diabetic animals. There was a significant negative correlation between intravenous glucose tolerance and body weight in olderAcomys. The results suggest that pancreatic B-cell responsiveness to glucose is impaired inAcomys of all ages, and that this is associated with poor glucose tolerance which may be aggravated by obesity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01222002
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  • 6
    Electronic Resource
    Electronic Resource
    Time-dependent inhibition of insulin release: glucose-arginine interactions in the perfused rat pancreas (1984)
    Springer
    Diabetologia 26 (1984), S. 146-149 
    Details
    ISSN: 1432-0428
    Keywords: Perfused pancreas ; insulin secretion ; arginine ; synergism ; time-dependent inhibition ; time-dependent potentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The isolated perfused rat pancreas was stimulated sequentially with arginine or glucose to analyze the time-dependent modulation of insulin release. A 10-min perfusion with arginine (5.0 mmol/l) induced 75% inhibition of the insulin response to repeated arginine stimulation 10 min later. When glucose (8.3 mmol/l) was given as two pulses, inhibition of the second insulin response was less pronounced. The inhibitory effect generated by arginine also suppressed the insulin response to glucose (27.7 mmol/l), and this inhibitory effect persisted for over 80 min. Stimulation for 30 min with glucose (27.7 mmol/l) strongly potentiated the insulin responses to a pair of arginine stimuli given 20 min later. However, despite augmented secretion rates, the insulin response to the second arginine pulse was still inhibited by 75%. When insulin secretion was strongly amplified by two 10 min pulses of the synergistic mixture of arginine (5.0 mmol/l) and glucose (8.3 mmol/l), there was no inhibition of the second insulin response. If glucose (8.3 mmol/l) was present during the first arginine stimulation only, the response to the second arginine pulse was inhibited as in control experiments. However, when glucose was added to the second arginine pulse only, the inhibition generated by the first arginine pulse did not express itself, insulin release remaining similar to control. We conclude that: (1) short stimulations of the pancreas by arginine or glucose generate long-lasting inhibition of the insulin response to subsequent stimulations; (2) synergistic amplification of the insulin response by addition of glucose to arginine obliterates the inhibition; (3) glucose does not suppress the induction of inhibition, it blocks the expression of the inhibitory signal on insulin secretion; (4) these in vitro findings are in keeping with observations in normal and hyperglycaemic man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00281123
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of phentolamine and preperfusion with glucose on insulin release from the isolated perfused pancreas from fasted and fed rats (1975)
    Springer
    Diabetologia 11 (1975), S. 407-410 
    Details
    ISSN: 1432-0428
    Keywords: Insulin release ; perfused pancreas ; fasting ; phentolamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Starvation of rats for 24 hrs resulted in decreased insulin release from the isolated rat pancreas. The effect of fasting could not be counteracted by elevation of the glucose level in the equilibration medium from 0.8 to 1.5 mg/ml. The alpha-adrenergic blocking agent phentolamine (10 μg/ml) stimulated glucose induced insulin release to approximately the same extent in fasted as in fed rats. These findings illustrate the importance of endogenous catecholamines in the regulation of insulin secretion from the isolated pancreas. Our experiments suggest that the impairment of insulin secretion on fasting is due neither to the inhibitory effect of catecholamines nor to the lack of substrate in the pancreas at the initiation of the stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429908
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  • 8
    Electronic Resource
    Electronic Resource
    Somatostatin in the pancreas, stomach and hypothalamus of the diabetic Chinese hamster (1977)
    Springer
    Diabetologia 13 (1977), S. 463-466 
    Details
    ISSN: 1432-0428
    Keywords: Somatostatin ; diabetic Chinese hamsters ; islet cells ; A1-cells ; glucagon ; insulin ; hypothalamus ; stomach
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The inhibitory effects of somatostatin on the release of insulin and glucagon, as well as its localization to the A1-cells (D-cells) of the pancreatic islets, suggest a role of this peptide in carbohydrate metabolism. In the present study we have measured the percentage islet volume, the total weight of the A1-cells and the somatostatin concentration in the pancreas of normal and spontaneously diabetic Chinese hamsters. In addition, the concentration of somatostatin in the stomach and hypothalamus as well as the insulin and glucagon content of the pancreas were evaluated. The percentage islet volume in the normal hamsters was 0.66±0.12, which was in marked excess of that in the diabetic group, 0.38±0.04. Similarly, the total weight of the A1-cells in the controls, 0.17±0.02 mg, was significantly larger than that in the diabetic animals, 0.12±0.02 mg. In agreement with these findings there was also a decreased pancreatic concentration of insulin and somatostatin, whereas the glucagon concentration was in the normal range. Also the stomach of the diabetic hamsters showed a decreased concentration of somatostatin. In the hypothalamus the total content of somatostatin appeared similar in the two groups of animals, but when expressed per mg wet weight this value was also decreased in the diabetic hamsters. These observations strongly suggest that, in the diabetic Chinese hamster, apart from the well-known B-cell deficiency there exists also a decreased functional activity of the somatostatin-producing cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01234497
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  • 9
    Electronic Resource
    Electronic Resource
    Decreased cyclic AMP and Insulin responses to glucose in pancreatic islets of diabetic chinese hamsters (1976)
    Springer
    Diabetologia 12 (1976), S. 581-587 
    Details
    ISSN: 1432-0428
    Keywords: Insulin release ; diabetes ; Chinese hamster ; pancreatic islets ; adenosine-3′5′-monophosphate (cyclic AMP)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The dose as well as the time kinetics of insulin and adenosine-3′,5′-monophosphate (cyclic AMP) responses to glucose were compared in pancreatic islets isolated from normal and diabetic Chinese hamsters. The insulin content in diabetic islets was about one-half that in normal islets. Insulin release in diabetic islets incubated for 10 min with glucose 60–1000 mg/l00 ml was from one-third to one-half that in normal islets. Glucose 1000 mg/l00 ml stimulated three-fold increases in insulin release without increasing the accumulation of [3H] cyclic AMP in either normal or diabetic islets prelabelled with [3H] adenine. However, in the presence of 1.0 mM of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), glucose 150 mg/l00 ml elicited significant increases of insulin release (+ 134%) and [3H] cyclic AMP accumulation in islets (+ 44%) and incubation medium (+ 48%) of islets of normal but not diabetic hamsters. Also, in perifusion experiments with 0.1 mM IBMX, glucose 500 mg/l00 ml produced threefold greater increases in insulin release and two-fold greater increases in efflux of cyclic AMP in normal than diabetic islets. By contrast with the lesser effects of glucose in diabetic islets, 1.0 mM IBMX increased islet and medium cyclic AMP, as well as insulin release, similarly in normal and diabetic islets. It is suggested that the impairment of glucose induced insulin release in islets of the diabetic Chinese hamster may be due to a defective interaction of glucose with the adenylate cyclase-cyclic AMP system in the pancreatic B cell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01220634
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  • 10
    Electronic Resource
    Electronic Resource
    The metabolism of cyclic AMP and glucose in isolated islets from Acomys cahirinus (1979)
    Springer
    Diabetologia 16 (1979), S. 47-50 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; isolated islets ; spiny mouse (Acomys cahirinus) ; cyclic AMP ; glucose ; glibenclamide ; glucagon ; chloromercuribenzene-p-sulphonic acid ; glucose utilization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose-induced cyclic (3H) AMP accumulation, insulin secretory responses and the metabolism of glucose were studied in pancreatic islets from Acomys cahirinus. 27.7 mmol/l of glucose stimulated neither islet cyclic (3H) AMP accumulation nor insulin release during the first 5 min of incubation. Stimulation by glucose of cyclic (3H) AMP was observed after 15 min of incubation and insulin release was markedly stimulated between 15 and 30 min. The utilization of glucose, measured as the production of (3H)2O from (5-3H) glucose was stimulated by glucose after 10 min and proceeded at an apparently linear rate during a 20 min incubation period. In incubations of 5 min, glibenclamide, glucagon or chloromercuribenzene-p-sulphonic acid failed to stimulate islet cyclic (3H) AMP accumulation. 3-isobutyl-1-methylxanthine in a concentration of 1.0 mmol/l was the only agent tested that elevated rapidly (1 min) islet cyclic (3H) AMP. None of the agents tested elicited an insulin secretory response in 5 min incubations. It is concluded that 1) no gross defect is apparent in the utilization of glucose by Acomys islets, 2) the secretory derangement of the Acomys is associated with a delayed cyclic AMP response to glucose, 3) however a decreased level of cyclic AMP cannot be the sole explanation for the delayed insulin secretion in the Acomys.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00423150
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