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  • 1
    Electronic Resource
    Electronic Resource
    Inhibition of insulin and glucagon release from the perfused rat pancreas by cyproheptadine (Periactinol®, Nuran®) (1976)
    Springer
    Diabetologia 12 (1976), S. 201-206 
    Details
    ISSN: 1432-0428
    Keywords: Insulin release ; glucagon release ; cyproheptadine ; tolbutamide ; arginine ; theophylline ; calcium ; perfused rat pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The tricyclic compound cyproheptadine (Periactinol®, Nuran®) inhibited glucose-induced insulin release from the perfused rat pancreas. Tolbutamide-stimulated insulin release was significantly reduced in the presence and completely suppressed in the absence of a substimulatory glucose concentration (5 mM). Arginine produced a slow rise of insulin release, which was completely abolished by cyproheptadine. Furthermore the biphasic glucagon release due to the stimulus was inhibited. Oxidation of 14C-glucose in isolated islets was unaltered in the presence of cyproheptadine, and pyruvate added to the perfusion medium failed to reverse the inhibitory effect on glucose induced insulin release, indicating that impaired glucose metabolism is not responsible for the inhibition. In addition, the inhibition remained unchanged when phentolamine was present, suggesting that the effect is not mediated by inhibitory adrenergic alpha receptors. Theophylline, in contrast, partly overcame the inhibition. When the calcium concentration of the medium was enhanced, the inhibitory effect of cyproheptadine was still visible, although the relative inhibition had become smaller. The results suggest that cyproheptadine blocks insulin release by affecting a fundamental step of the stimulus-secretion coupling common to peptide hormones. A participation of a calcium-antagonizing effect in the inhibition is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422086
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  • 2
    Electronic Resource
    Electronic Resource
    The inhibition of insulin secretion from the perfused rat pancreas after thyroxine treatment (1976)
    Springer
    Diabetologia 12 (1976), S. 495-500 
    Details
    ISSN: 1432-0428
    Keywords: Rat pancreas perfusion ; insulin secretion ; thyroxine treatment ; D-glucose ; D-glyceraldehyde ; D-mannose ; tolbutamide ; L-glucose ; D-fructose ; dihydroxyacetone ; DL-glyceric acid ; pyruvate ; L-lactate ; propionic acid ; α-ketobutyrate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thyroxine treatment did not significantly affect the immediate insulin secretory response of the perfused rat pancreas, but it inhibited the late phase of D-glucose-induced insulin secretion. Thyroxine treatment did not inhibit D-glyceraldehyde-, D-mannose-, and tolbutamide-induced insulin release from the perfused pancreas. An increase in the D-glucose concentration of the perfusion medium as well as feeding of the rats did not restore insulin secretion after thyroxine treatment. The inhibition of D-glucose-induced insulin release in response to thyroxine treatment was reversed after addition of either D-glyceraldehyde, dihydroxyacetone, DL-glyceric acid, pyruvate, or α-ketobutyrate to the perfusion medium. Tolbutamide, L-glucose, D-fructose, D-mannose, L-lactate, and propionic acid were not able to overcome the inhibition of D-glucose-induced insulin secretion. Except for α-ketobutyrate all substances which were effective in reversing the inhibition of D-glucose-induced insulin release were glycolytic intermediates. Comparing the glycolytic α-ketoacid pyruvate and the non-glycolytic ketoacid α-ketobutyrate, the only part common to both substances was the ketoacid moiety. It is concluded from these findings that the ketoacid moiety of the α-ketoacids plays an important role in reversing the effect of thyroxine on D-glucose-induced insulin release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219514
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  • 3
    Electronic Resource
    Electronic Resource
    Comparison of the effects of insulin, PDGF, interleukin-6, and interferon-g on glucose transport in 3T3-L1 cells: lack of cross-talk between tyrosine kinase receptors and JAK/STAT pathways (1996)
    Springer
    Diabetologia 39 (1996), S. 1432-1439 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin ; glucose transport ; tyrosine kinase ; 3T3-L1 cells ; PDGF receptor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of insulin, insulin-like growth factor (IGF)-I, platelet-derived growth factor (PDGF), interleukin (IL)-6 and interferon-γ on 2-deoxyglucose uptake and insulin receptor substrate (IRS)-1 phosphorylation were compared in 3T3-L1 cells at confluence and after differentiation to the adipocyte-like phenotype. Insulin and IGF-I produced the expected stimulation of glucose transport and tyrosine phosphorylation of IRS-1 in both confluent and differentiated cells. In contrast, IL-6 and interferon-γ failed to stimulate glucose transport or IRS-1 phosphorylation, although a marked stimulation of the JAK/STAT pathways as shown by acute-phase response factor (APRF)/Stat3 or Stat1 activation was observed in fibroblasts (IL-6, interferon-γ) and adipocytes (IL-6). PDGF-AA and PDGF-BB stimulated glucose transport in confluent, undifferentiated cells to the same extent as insulin (approximately six-fold stimulation), but produced only a small portion of the effect of insulin in differentiated cells. Similarly, mRNA levels and autophosphorylation of PDGF receptors were much lower in differentiated cells than in confluent fibroblasts. In contrast to insulin and IGF-I, PDGF failed to stimulate tyrosine phosphorylation of IRS-1. All effects of insulin, IGF-I, and PDGF on glucose transport were inhibited by Wortmannin; the half-maximally inhibiting concentration (IC50) of Wortmannin was increased by insulin. These data demonstrate distinct signalling potentials of the investigated receptors, and indicate that the IL-6 and interferon-γ controlled JAK/STAT pathways lack the potential to stimulate glucose transport. IRS-1 does not appear to be involved in the PDGF receptor-mediated effects, whereas activation of phosphatidylinositol (PI) 3-kinase is a crucial event in all pathways leading to stimulation of glucose transport. [Diabetologia (1996) 39: 1432–1439]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050595
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  • 4
    Electronic Resource
    Electronic Resource
    Long-term and rapid regulation of ob mRNA levels in adipose tissue from normal (Sprague Dawley rats) and obese (db/db mice, fa/fa rats) rodents (1996)
    Springer
    Diabetologia 39 (1996), S. 758-765 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Leptin ; ob gene ; gene expression ; insulin resistance ; obesity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Increased levels of mRNA transcribed from the ob gene in adipose tissue of obese/hyperinsulinaemic Zucker (fa/fa) rats were detectable as early as 3 weeks after birth and continued to rise there after in parallel with body weight and serum insulin. mRNA levels of two other fat-specific genes (ARL4, FST44) were unaltered. In C57BL/KsJ db/db mice, ob mRNA levels also increased in parallel with body weight and serum insulin, and remained elevated in older animals when insulin levels decreased. In heterozygous control animals (db/ + ; fa/Fa), mRNA levels were comparable with those in the homozygous controls. In normal Sprague Dawley rats, the ob mRNA increased continuously, but more slowly than in Zucker rats, in parallel with body weight and insulin levels, and reached 15 times higher levels in the heaviest rats (400 g) studied. In Sprague Dawley rats made diabetic by an injection of streptozotocin, ob mRNA levels were reduced by approximately 50 % after 24 h. A 24-h fasting period reduced the ob mRNA by 50 % in lean Sprague Dawley and Fa/Fa, but not in obese Zucker fa/fa rats, although insulin levels were reduced in both groups. These data indicate that ob mRNA levels increase in both normal and obese rodents in parallel with age, body weight and serum insulin, reflecting an early (Zucker rats, db-mice) or slowly developing (Sprague Dawley rats) resistance to leptin and insulin. This increase does not appear to be mediated by the recently described rapid regulation of ob mRNA by insulin, but seems to be due to a different, long-term control mechanism which signals the size of the fat depots. [Diabetologia (1996) 39: 758–765]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050508
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  • 5
    Electronic Resource
    Electronic Resource
    The regulation of glucose transport in insulin-sensitive cells (1989)
    Springer
    Diabetologia 32 (1989), S. 831-838 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00297447
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  • 6
    Electronic Resource
    Electronic Resource
    Quantitative trait loci for obesity and insulin resistance (Nob1, Nob2) and their interaction with the leptin receptor allele (LeprA720T/T1044I) in New Zealand obese mice (2000)
    Springer
    Diabetologia 43 (2000), S. 1565-1572 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Obesity ; insulin resistance ; New Zealand obese mouse ; quantitative trait locus ; leptin receptor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To locate genes responsible for obesity and insulin resistance, a backcross model of New Zealand obese (NZO) mice with the lean Swiss/Jackson Laboratory (SJL) strain was stablished. Results. In female NZO x F1 backcross mice, two major quantitative trait loci for variables of obesity (body weight, body mass index, total body fat) and insulin resistance (hyperinsulinaemia) were identified on chromosomes 5 (Nob1) and 19 (Nob2) close to the markers D5Mit392 and D19Mit91. The aberrant alleles have presumably contributed by the NZO genome. Whereas Nob1 contributed mainly to higher body weight, Nob2 seemed to mainly aggravate insulin resistance independent of obesity. The leptin receptor variant of NZO (Lepr A720T/T1044I) failed to alter any of the variables of obesity. It seemed, however, to enhance the effect of Nob1 on body weight and that of Nob2 on serum insulin concentration. When expressed in COS-7 cells, Lepr A720T/T1044I produced a normal basal and maximum activation with a minor increase in the EC50 of leptin. Conclusions/interpretation. The data identify two new quantitative trait loci that are responsible for a major part of obesity and hyperinsulinaemia as produced by recessive genes in NZO mice. Lepr A720T/T1044I alone cannot produce obesity, but may enhance the effects of other obesity/insulin resistance genes in this mouse model. [Diabetologia (2000) 43: 1565–1572]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051570
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  • 7
    Electronic Resource
    Electronic Resource
    Physiology Does gut hormone PYY 3–36 decrease food intake in rodents? (2004)
    [s.l.] : Nature Publishing Group
    Nature 430 (2004), S. 0 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Arising from: R. L. Batterham et al. Nature 418, 650–654 (2002); Batterham et al. replyBatterham et al. report that the gut peptide hormone PYY3–36 decreases food intake and body-weight gain in rodents, ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature02665
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  • 8
    Electronic Resource
    Electronic Resource
    Insulinresistenz und metabolisches Syndrom (2000)
    Springer
    Zeitschrift für Kardiologie 89 (2000), S. 377-382 
    Details
    ISSN: 1435-1285
    Keywords: Key words Diabetes – hypertension – obesity – insulin resistance ; Schlüsselwörter Diabetes –¶Hypertonie – Adipositas –¶Insulinresistenz
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das metabolische Syndrom ist ein heterogener Symptomenkomplex mit Adipositas, Insulinresistenz, Dyslipoproteinämie, Hypertonie und Typ-2-Diabetes. Diese Komponenten sind zum Teil genetisch determiniert und stehen miteinander in enger pathophysiologischer Beziehung. Adipositas entsteht durch eine polygene Konstellation und löst obligatorisch Insulinresistenz, Hypertonie und Dyslipidämie aus. Zusätzlich können Defekte in der Signaltransduktion des Insulins die Insulinresistenz unabhängig von der Adipositas verstärken. Diabetes mellitus wird durch eine dritte genetische Komponente verursacht und tritt im Verlauf des metabolischen Syndroms erst dann auf, wenn die pankreatischen β-Zellen versagen und die Insulinresistenz nicht mehr kompensieren können. Da Auftreten und Verlauf des Diabetes von Insulinresistenz und Adipositas abhängig sind, liegt hier der aussichtsreichste Ansatzpunkt für präventive und therapeutische Interventionen.
    Notes: Summary The metabolic syndrome represents a complex combination of the symptoms obesity, insulin resistance, dyslipoproteinemia, hypertension, and type 2 diabetes. These components have a heterogenous genetic basis and appear to be closely linked. Obesity is determined by a polygenic constellation and produces insulin resistance, hypertension and dyslipidemia. In addition, defects in the signal transduction of insulin appear to aggravate the insulin resistance independent of obesity. Type 2 diabetes is produced by a third genetic predisposition and is precipitated by the failure of pancreatic β-cell to compensate insulin resistance. Because prevalence and course of the diabetes markedly depend on the extent of obesity and insulin resistance, these symptoms of the metabolic syndrome represent crucial targets for preventive and therapeutic strategies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003920050501
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  • 9
    Electronic Resource
    Electronic Resource
    Subcellular B cell calcium and insulin secretion in vitro (1978)
    Springer
    Virchows Archiv 379 (1978), S. 203-217 
    Details
    ISSN: 1432-2307
    Keywords: B cell calcium in vitro ; Calcium ultracytochemistry ; Biphasic insulin secretion ; Glucose stimulation ; Cyproheptadine inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using the ultracytochemical pyroantimonate technique different patterns of calcium containing precipitates were found in the B cells of the isolated perfused rat pancreas under conditions of stimulated and inhibited insulin secretion. The calcium specificity of the ultracytochemical method was assessed by perfusion with a EGTA containing calcium-free medium, which markedly reduced the extent of precipitation. Perfusion with 20 mM D-glucose over a period of 30 min resulted in calcium distribution patterns which could be related to the biphasic insulin release. The calcium patterns differed significantly in their quality and quantitative morphometry from those after 5 mM D-glucose or cyproheptadine (CPH) perfusion (20 mM D-glucose plus 0.1 mM CPH). After 3–5 min of 20 mM glucose perfusion there was an increased calcium precipitation along the inner side of the B cell membranes. After 20–30 min an additional increase in precipitation was found in the cytoplasmic matrix and in the secretory granules. B cells in a CPH-inhibited state of secretion and also after perfusion with 5 mM glucose lacked these findings. The data suggest that an increase in the membrane associated calcium may induce the first phase of insulin secretion by triggering the exocytosis of peripheral granules, while the cytoplasmic calcium may be involved in long term regulation of insulin release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432636
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  • 10
    Electronic Resource
    Electronic Resource
    Modulation of glucose transport in hamster adipocytes by insulin and byβ- andα 2-adrenoceptor agonists (1986)
    Springer
    Diabetologia 29 (1986), S. 371-377 
    Details
    ISSN: 1432-0428
    Keywords: Adipose tissue ; hamsters ; glucose ; insulin ; adrenoceptor agonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose transport in hamster adipocytes and its modulation by insulin and isoprenaline was characterized with the aid of the non-metabolizable hexose 3-0-methylglucose. Insulin stimulated the initial uptake rates by an increase in Vmax of the transport without any detectable change in Km. The hormone concentration producing half maximal stimulation was identical to that required in rat adipocytes. However, hamster adipocytes were much less responsive to insulin (3-fold stimulation as compared to a 12-fold stimulation in rat fat cells), and maximal transport rates were 10-fold lower than that observed in rat adipocytes. Accordingly, the number of glucose transporters, as assessed by glucose-inhibitable cytochalasin-B binding, was considerably lower in plasma membranes of hamster adipocytes. Moreover, no transporters were detected in the low-density microsomes which in insulin-sensitive cell types represent the intracellular pool of recruitable glucose transporters. The relative insulin resistance of the hamster fat cells may therefore be due to a depleted pool of intracellular glucose transporters. In the presence of adenosine, theβ-adrenoceptor agonist isoprenaline produced a moderate stimulation of the basal transport rate which was antagonized by theα 2-agonist clonidine. If adenosine deaminase was added in order to remove endogenous adenosine, isoprenaline inhibited the insulin-stimulated transport by 50%. In contrast to the stimulatory effects of insulin and isoproterenol, the inhibitory effect of the catecholamine was reversed by cooling the cells to 22°. Glucagon produced a comparable inhibition, suggesting that the inhibitory effect was mediated by adenylate cyclase or its regulatory subunits. Theα 2-adrenoceptor agonist clonidine fully antagonized the inhibitory effect of isoproterenol. The effect of glucagon was reversed by adrenaline, if propranolol was added in order to unmask the α2-agonist action of the catecholamine. The data demonstrate thatα 2-adrenoceptors participate in the regulation of glucose transport by antagonizing both theβ-receptor mediated stimulation and inhibition produced by catecholamines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00903347
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