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  • 1
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 9 (1973), S. 287-293 
    ISSN: 1432-0428
    Keywords: Diabetes ; obesity ; modifying genes ; genetics ; hyperglycemia ; islet changes ; mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A new congenic strain of obese mice, C57BK/KsJ-ob, has been developed for comparison with the C57BL/6J-ob congenic strain. While obese mice of both strains are characterized by obesity, hyperphagia, and hyperglycemia, the C57BL/Ks obese mice have severe diabetes, marked hyperglycemia, temporarily elevated plasma insulin concentrations, and typical degenerative changes in the islets of Langerhans. In contrast, the C57BL/6J obese mice have mild hyperglycemia and marked hyperinsulinemia coupled with hypertrophy and hyperplasia of the islets of Langerhans. The severe diabetic condition produced by obese (ob) on the C57BL/KsJ background is similar, if not identical, to that produced by the diabetes (db) gene on the same background. The metabolic disorder produced by these mutations is associated with the capacity of the islets to respond to an increased demand for insulin. The islet response, whether atrophy or hypertrophy, appears to be due to the interaction of the obese and diabetes genes with modifiers in the genetic background rather than the specific consequences of the particular gene. The markedly different diabetic syndromes that result when the obese mutation is on different genetic backgrounds emphasize the importance of strict genetic control in studies with obese-hyperglycemic mutants.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 6 (1970), S. 263-267 
    ISSN: 1432-0428
    Keywords: Hereditary diabetes ; mouse ; lesions ; ventromedial nucleus ; satiety center ; hypothalamus ; gold thioglucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le noyau médioventral de la région hypothalamique de souris présentant un diabète génétique (db/db) et de souris normales (+/+) a été lésé par l'administration d'aurothioglucose ou par électrocautérisation. Les souris normales répondent de façon typique à l'un ou lautre de ces traitements en devenant hyperphagiques, obèses, et en montrant une élévation modérée de l'insulinémie tout en gardant des taux de glucose sanguins voisins de la normale. La destruction du noyau médioventral chez la souris diabétique empêche le développement d'une hyperglycémie sévère et a un effet thérapeutique chez les souris modérément hyperglycémiques. L'hyperphagie et l'accumulation rapide de tissu adipeux continuent à une cadence soutenue, comme prévu. La regranulation des cellulesβ du pancréas endocrine est accompagnée de taux de glucose sanguin normaux. L'amélioration prononcée des symptomes diabétiques dans ce syndrome chez la souris renforce l'hypothèse suivant laquelle le défaut primaire chez la souris diabétique implique une insuffisance hypothalamique, en particulier dans la région des centres de la satiété.
    Abstract: Zusammenfassung Bei hereditär diabetischen (db/db) und normalen (+/+) Mäusen wurde der ventromediale Kern des Hypothalamus entweder durch Goldthioglucose-injektion oder durch Elektrokauterisierung zerstört. Auf diese Behandlung reagierten normale Mäuse wie erwartet mit Hyperphagie, wurden fettsüchtig und zeigten bei normalen Blutzuckerkonzentrationen erhöhte Plasma-insulinkonzentrationen. Bei den diabetischen Tieren verhinderte der Eingriff den weitern Anstieg der Blutzuckerkonzentration und hatte bei mäßig hyperglykämischen Tieren eine Senkung des Blutzuckerspiegels zur Folge. Gleichzeitig blieb die für diedb/db Mäuse charakteristische Hyperphagie bestehen und führte wie bei unbehandeltendb/db Tieren zur Fettsucht. Im Pankreas wurde nach Setzen der hypothalamischen Läsionen eine Regranulation der B-Zellen beobachtet. Die deutliche Verbesserung der diabetischen Stoffwechsellage durch Zerstörung der ventromedialen Kerne des Hypothalamus läßt den Schluß zu, daß der primäre zur Entwicklung des Syndroms führende Defekt diese Strukturen des Zentralnervensystems betrifft.
    Notes: Summary Genetically diabetic (db/db) and normal (+/+) mice were lesioned in the ventromedial nucleus by either gold thioglucose or electrocauterization. The normal mice responded typically to either of these treatments by becoming hyperphagic, obese, and by exhibiting moderately elevated plasma insulin concentrations coupled with near normal blood sugar concentrations. In diabetic mice, destruction of the ventromedial nucleus prevented the development of severe hyperglycemia and had a therapeutic effect in those mice with established, but moderate, hyperglycemia. Hyperphagia and rapid accumulation of adipose tissue continued unabated as expected. Regranulation of theβ-cells of the endocrine pancreas was associated with the maintenance of blood sugar at normal concentrations. The marked improvement of the diabetic aspects of this syndrome in mice lends support to the hypothesis that the primary defect in diabetic mice may involve a defective hypothalamus, particularly in the regions of the satiety centers.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 80 (1941), S. 47-53 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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