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  • glucagon  (4)
  • [abr] PAI -; plasminogen activator inhibitor  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 176 (1991), S. 633-638 
    ISSN: 0006-291X
    Keywords: [abr] BME -; bovine microvascular endothelial ; [abr] PAI -; plasminogen activator inhibitor ; [abr] TGF-β -; transforming growth factor-β
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 176 (1991), S. 633-638 
    ISSN: 0006-291X
    Keywords: [abr] BME -; bovine microvascular endothelial ; [abr] PAI -; plasminogen activator inhibitor ; [abr] TGF-β -; transforming growth factor-β
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 23 (1981), S. 311-320 
    ISSN: 0303-7207
    Keywords: glucagon ; glucagon degradation ; glucagon intemalization ; isolated hepatocytes
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Pancreas ; islets of Langerhans ; insulin ; glucagon ; somatostatin ; pancreatic polypeptide ; immunohistochemistry ; embryology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Systematic sampling of human necropsy pancreases has revealed that pancreatic polypeptide (PP) cells are not distributed equally in the gland. PP-cells are the most abundant cell type in the posterior part of the pancreatic head while they are scarce or absent in the remainder of the gland. The PP-rich part of the head can be separated by blunt dissection from the pancreas as a discrete lobe. This lobe probably originates from the ventral pancreatic bud during embryogenesis. A quantitative study of the immunofluorescent endocrine cell types (insulin, glucagon, somatostatin and pancreatic polypeptide cells) in PP-rich and PP-poor regions of pancreases in 8 subjects with ages ranging from 33 fetal weeks to 80 years, showed that the proportions of the cell types were different in youngs and adults.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Chinese hamster ; spontaneous diabetes ; Cricetulus griseus ; pancreas ; islets of Langerhans ; A-cells ; lysosomes ; “α-granulolysis” ; glucagon ; glucagon and diabetes ; ultrastructure ; electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Les cellules A du pancréas endocrine de hamsters chinois atteints d'un diabète de degré et durée variables ont été examinées en microscopie électronique. Deux modifications prédominantes ont été observées: 1. La digestion lysosomiale des granules de sécrétion («granulolyse» ou «crinophagie») survient dans pratiquement toutes les cellules A d'animaux diabétiques. Par contre, elle n'est que rarement observée chez les animaux témoins non-diabétiques. Ce phénomène est interprêté comme étant une réponse des cellules A à l'arrêt de la libération du glucagon secondaire à l'hyperglycémic. 2. Dans les cellules A relativement dégranulées d'animaux présentant un diabète cétosique, une dilatation des cisternes du réticulum endoplasmique granulaire est observée avec accumulation d'un matériel pâle et flocconneux reflétant probablement une synthèse persistante ou augmentée du glucagon. En outre, de nombreux granules de sécrétion en état de formation ont été observées dans les cisternes du complexe de Golgi. Puisque ces deux phénomènes, apparemment contradictoires, peuvent se produire dans une même cellule, il se pourrait que la «granulolyse» résultela non seulement d'une libération diminuée de glucagon faisant suite à l'hyperglycémie, mais qu'il soit en outre nécessaire de faire intervenir des signaux indépendants de la synthèse du glucagon, de sa libération et de l'initiation de la «granulolyse».
    Abstract: Zusammenfassung Elektronenmikroskopische Untersuchungen der A-Zellen des Pankreas diabetischer chinesischer Hamster ließen vor allem zwei Veränderungen erkennen: 1. In praktisch allen A-Zellen diabetischer Tiere konnte der Abbau vonα-Granula in den von Lysosomen abgeleiteten Strukturen beobachtet werden („Granulolyse“, „Krinophagie“). Dieses Phaenomen wird als Reaktion der Zelle auf eine Verminderung der Glucagon-Sekretion angesichts anhaltender Hyperglykaemie aufgefaßt. 2. Eine Erweiterung der Cisternae des granulierten ergastoplastischen Reticulums durch eine Anhäufung flockigen, wenig dichten Materials war in A-Zellen ketotisch diabetischer Tiere zu sehen. Diese Beobachtung wird im Sinne einer anhaltenden oder gesteigerten Glucagonsynthese gedeutet. Da beide scheinbar gegensätzlichen Phänomene innerhalb der gleichen Zelle vorkommen, muß die Möglichkeit betrachtet werden, daß die Granulolyse nicht nur das Resultat einer durch Hyperglykaemie bedingten Verminderung der Glucagon-Sekretion zu sein braucht. Vielmehr ist es wahrscheinlich, daß verschiedene Regulationsmechanismen die Synthese des Glucagons, dessen Sekretion, sowie den Prozeß der „Granulolyse“ unabhängig voneinander zu beeinflussen vermögen. Dabei mag der Konzentration des zirkulierenden Glucagons besondere Bedeutung zukommen.
    Notes: Summary Pancreatic A-cells of chinese hamsters with diabetes of varying severity and duration were examined by electron microscopy. Two predominant changes were observed: 1. Lysosomal digestion of secretory granules (“granulolysis”, “crinophagy”) occurred in practically all A-cells of diabetic animals but was rarely observed in those of normoglycemic controls. This is considered a response of A-cells to the cessation of glucagon release secondary to hyperglycemia. 2. In relatively degranulated A-cells of ketotic diabetic animals, dilatation of the cisternae of the RER was seen together with accumulation of pale, flocculent material, possibly reflecting persisting or enhanced glucagon synthesis. In addition, numerous maturing secretory granules were seen in the cisternae of the Golgi complex. Since these apparently contradictory phenomena may be seen in the same cell, it is suggested that “granulolysis” may not only result from decreased hormone release secondary to hyperglycemia but that different and independent stimulatory signals may exist for glucagon synthesis, for glucagon release, and for the initiation of “granulolysis”.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Alpha cells ; glucagon ; anti-insulin serum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine the effect of neutralization of endogenous insulin upon the glucagon response to a rise and fall of glucose concentration, pancreata isolated from normal rats were perfused with either a potent anti-pork insulin guinea pig serum or a nonimmune guinea pig serum for 30 min. During this period glucose concentration was changed from 100 mg/dl to either 130, 180 or 80 mg/dl for 10 min. Antiserum perfusion at 100 mg/dl caused an approximately two-fold increase in glucagon which was not suppressed by an increase in glucose concentration to either 130 or 180 mg/dl, although glucagon secretion was significantly suppressed in the control experiments in which nonimmune serum was perfused. However, the 0.38±0.21 ng/min rise in glucagon secretion in response to a reduction in glucose concentration to 80 mg/dl in the control experiments was not abolished by antiserum perfusion but, instead, was enhanced (2.66±0.60 ng/min). These findings suggest that insulin may be required for glucose-mediated suppression of glucagon in the isolated pancreas of normal rats but not for stimulation of glucagon secretion by mild glucopenia. Alternatively, neutralization of insulin-mediated release-inhibition of glucagon secretion may simply have altered alpha cell responsiveness in a direction that desensitized it nonspecifically to suppression and sensitized it to stimulation.
    Type of Medium: Electronic Resource
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