Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of agricultural and food chemistry 12 (1964), S. 390-392 
    ISSN: 1520-5118
    Source: ACS Legacy Archives
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of agricultural and food chemistry 12 (1964), S. 537-538 
    ISSN: 1520-5118
    Source: ACS Legacy Archives
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 23 (1982), S. 119-123 
    ISSN: 1432-0428
    Keywords: Pancreas ; mice ; gold thioglucose ; islet metabolism ; insulin synthesis and release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood insulin, blood glucose and the biosynthesis and release of insulin have been studied in mice made obese with a single injection of gold thioglucose. In such mice, blood glucose levels were normal, though serum insulin rose in parallel with the development of obesity. When compared with controls, insulin secretion and synthesis were increased in isolated islets of Langerhans from obese mice, over a wide range of glucose concentrations. However, in obese animals, insulin biosynthesis was augmented above control levels at 2 mmol/l glucose, whilst the increase in insulin secretion accompanying obesity only became evident at glucose concentrations 〉 5 mmol/l. After 2 min incubation, cyclic AMP rose more in islets from obese mice than in controls, though cyclic AMP levels did not significantly differ in either group after 10 min incubation with glucose. Glucose oxidation was also increased in islets of Langerhans from obese mice. It seems possible that changes in glucose oxidation, as well as in cyclic AMP levels, contribute to the alteration in the B cell response in this type of obesity.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1432-0428
    Keywords: Diabetes ; EMC virus ; DBA2 mice ; islets of Langerhans ; ultrastructure ; insulin ; glucagon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Infection of DBA2 mice with the M strain of EMC virus was used to study the effects of virusinduced diabetes on the A and B cells of the islets of Langerhans. A transient hypoglycaemia was seen in 48% of mice 2–3 days after infection and probably resulted from increased serum insulin concentrations together with inhibition of glucagon secretion at that time. Islets from hypoglycaemic mice showed no significant alterations from control level in basal or fluoride-stimulated adenylate cyclase activity. Overall, 70% of infected mice became hyperglycaemic with a maximum incidence 6 days after infection. Hyperglycaemia was accompanied by a dramatic reduction in the total pancreatic insulin content and in insulin secretory responses to glucose and theophylline, while A-cell structure and function appeared relatively unaffected in diabetic animals. Basal adenylate cyclase activity was increased in hyperglycaemic mice at 7 days after infection, while fluoride-stimulated adenylate cyclase activity was normal throughout the course of infection. Ultrastructural alterations were observed in a small proportion of B cells from two days after infection and included abnormalities of mitochondrial structure and increased electron opacity of the cytoplasm of affected cells, which subsequently led to complete necrosis. The results suggest that EMC virus specifically affects the B cells of the islets and that disturbances of A cell function may be secondary to B cell damage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 18 (1980), S. 323-328 
    ISSN: 1432-0428
    Keywords: Insulin release ; insulin synthesis ; protein synthesis ; adenylate cyclase ; pancreatic islets ; tissue culture ; growth hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of rat growth hormone (1 μg/ ml) on the synthesis and release of insulin by isolated rat islets of Langerhans were studied. There was no effect of growth hormone on the release of insulin from freshly isolated islets during 30 min incubation periods. By contrast, islets previously cultured for 16h with growth hormone exhibited a 40% increase in the release of insulin in response to glucose or to glucose and theophylline. These islets also showed specific increases in basal and glucose-stimulated insulin synthesis of 16% and 21% respectively, together with a 22% increase in the basal rate of total protein synthesis. The total insulin content of islets was not affected by culture with growth hormone. The adenylate cyclase activity of islet homogenates was unaffected by the presence of growth hormone during 30 min incubations. When homogenates from islets previously cultured with growth hormone were studied, basal adenylate cyclase activity was unchanged, while fluoride-stimulated adenylate cyclase activity was increased by 37%. It is concluded that growth hormone can directly affect the synthesis and release of insulin in islets of Langerhans, without relation to its metabolic activities in other target organs.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 10 (1974), S. 755-759 
    ISSN: 1432-0428
    Keywords: Virus-induced diabetes ; Coxsackie B4 virus ; Coxsackie B3 virus ; islet cell damage ; CD1 mice ; pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetes was induced in 20–30% of adult CD1 mice 15–20 days after infection by a tissue culture propagated strain of Coxsackie B4 virus. Serum insulin and insulin release from isolated islets indicated a relative insulin deficiency in diabetic animals. In some animals diabetes appeared to be permanent whilst in many it was of a temporary nature. Histology showed only slight damage in both islet and acinar tissue. Infection with pancreas and heart adapted strains of Coxsackie B3 virus failed to produce diabetes in mice and, in contrast to the effects of Coxsackie B4, severe acinar cell damage was seen.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 8 (1972), S. 236-243 
    ISSN: 1432-0428
    Keywords: Islets ; metabolic changes ; diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 36 (1993), S. 687-695 
    ISSN: 1432-0428
    Keywords: Beta cell ; Coxsackievirus ; diabetes ; insulin-dependent diabetes mellitus ; islet ; picornavirus ; virus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Many different viruses belonging to several genera have the potential to damage beta cells. The mechanisms they employ are varied, and infection may result in either a direct destruction of islets and rapid insulin deficiency, or in a more gradual loss of functioning islets with the onset of diabetes many years later. Several case histories involving extensive cytolysis of beta cells can be directly linked to viral infection, whilst an example of diabetes occurring many years after viral infection is found in individuals who had a congenital infection with rubella virus. Here, the virus induces an autoimmune reaction against beta cells. Autoimmune phenomena have also been observed in islets following infections with viruses other than rubella, and thus activation of autoimmune mechanisms leading to beta-cell destruction may be a relatively frequent occurrence. Recent evidence shows that picornaviruses are not exclusively lytic, and can induce more subtle, long-term changes in beta cells, which may be important in the aetiology of diabetes. The exact mechanisms involved are not known, but it is clear that several viruses can directly inhibit insulin synthesis and induce the expression of other proteins such as interferons, and the HLA antigens. Strain differences in viruses are important since not all variants are tropic for the beta cells. Several laboratories are in the process of identifying the genetic determinants of tropism and diabetogenicity, especially amongst the Coxsackie B (CB) virus group. The sequence of one such diabetogenic CB4 strain virus has been determined. It is clear therefore that there are many viruses with the potential to induce diabetes, and a viral involvement in the pathogenesis of diabetes has been established in some instances. Further research work at both a fundamental and epidemiological level is now urgently needed to define the nature of the interaction of such viruses with the beta cell.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    ISSN: 1432-0428
    Keywords: Beta cells ; Coxsackie B4 virus ; insulin release ; islets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Infections with Coxsackie viruses (especially Coxsackie B4) are thought to be involved in the pathogenesis of diabetes. Many interdependent variables determine the outcome of an infection with a Coxsackie virus, one of them being the tropism of the virus for a specific tissue. The extent to which Beta cell tropic variants of Coxsackie B4 virus occur naturally was assessed. Human isolates of this virus were tested in an in vitro system in which elevated insulin release from infected islets incubated at a non-stimulatory (2 mmol/l) glucose concentration appears to be related to viral attack. Using this technique, 8/24 isolates tested, impaired secretory function in mouse islets. Some strains of Coxsackie B4 virus, therefore, will directly infect mouse islets in vitro leading to changes in islet cell function. In conclusion, these findings confirm that variants of Coxsackie B4 virus with the potential to damage Beta cells occur quite frequently in the natural population. In certain circumstances the damage they inflict on Beta cells may cause destruction of these cells, or precipitate overt diabetes.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    ISSN: 1432-0428
    Keywords: Isolated islets of Langerhans ; A2-cells ; B-cells ; glucose oxidation ; fatty acid oxidation ; glucagon.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé L'oxydation du glucose et des acides gras a été mesurée dans les îlots normaux de Langerhans chez le cobaye, ainsi que dans les îlots riches en cellules A2 du cobaye traité à la streptozotocine. Le taux d'oxydation de ces composés dans les cellules A2 et les cellules B du cobaye a été estimé. Dans les cellules B, l'oxydation du glucose et de l'acide octanoique a fortement répondu à des changements dans les taux extra-cellulaires de ces substrats. L'acide palmitique ne semble pas avoir été oxydé par les cellules B. Au contraire, l'oxydation de l'acide octanoique et de l'acide palmitique dans les cellules A2 était très sensible aux changements dans la concentration des acides gras extra-cellulaires. La sensibilité de l'oxydation du glucose envers les changements dans la concentration du glucose était comparativement faible. Le taux élevé de l'oxydation des acides gras dans les cellules A2 corrobore l'hypothèse que le degré du métabolisme des acides gras dans ces cellules joue un rôle important dans la régulation de la sécrétion du glucagon.
    Abstract: Zusammenfassung An normalen Langerhansschen Inseln vom Meerschweinchen und an mit A2-Zellen angereicherten Inseln von streptozotozin-behandelten Meerschweinchen wurde die Oxidation von Glucose und Fettsäuren gemessen und die Oxidationsrate in A2-Zellen und B-Zellen des Meerschweinchens bestimmt. In den B-Zellen hing die Oxidation von Glucose und Octansäure stark von den Änderungen der extracellulären Konzentrationen dieser Substanzen ab. Palmitinsäure schien in den B-Zellen nicht oxidiert zu werden. Dagegen war die Oxidation von Oktansäure und Palmitinsäure in den A2-Zellen sehr von den Schwankungen der extracellulären Fettsäurekonzentration abhängig. Die Änderung der Glucoseoxidation bei Schwankungen der Glucosekonzentration war im Verhältnis dazu gering. Die hohe Oxidationsrate der Fettsäuren in den A2-Zellen unterstützt die Theorie, daß der Fettsäuremetabolismus dieser Zellen eine wesentliche Rolle in der Regulierung der Glucose-sekretion spielt.
    Notes: Summary Glucose and fatty acid oxidation has been measured in normal guinea-pig islets of Langerhans, and in A2-cell rich islets from streptozotocin-treated guinea-pigs. The rate of oxidation of these compounds in guinea-pig A2-cells and B-cells has been estimated. In the B-cells, the oxidation of glucose and octanoic acid responded markedly to changes in the extracellular levels of these substrates. Palmitic acid did not appear to be oxidized by the B-cells. In contrast, the oxidation of octanoic acid and palmitic acid in the A2-cells was very sensitive to changes in the extracellular fatty acid concentration. The sensitivity of glucose oxidation to changes in the glucose concentration was small by comparison. The high rate of oxidation of fatty acids in the A2-cells supports the view that the rate of fatty acid metabolism in these cells plays an important role in the regulation of glucagon release.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...