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  • American Physiological Society  (2)
  • 1980-1984  (2)
Materialart
Verlag/Herausgeber
  • American Physiological Society  (2)
Sprache
Erscheinungszeitraum
  • 1980-1984  (2)
Jahr
Fachgebiete(RVK)
  • 1
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 1980
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 239, No. 6 ( 1980-12-01), p. E422-E429
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 239, No. 6 ( 1980-12-01), p. E422-E429
    Kurzfassung: The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.
    Materialart: Online-Ressource
    ISSN: 0193-1849 , 1522-1555
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1980
    ZDB Id: 1477331-4
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 1982
    In:  Journal of Applied Physiology Vol. 52, No. 3 ( 1982-03-01), p. 556-561
    In: Journal of Applied Physiology, American Physiological Society, Vol. 52, No. 3 ( 1982-03-01), p. 556-561
    Kurzfassung: Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1982
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Standort Signatur Einschränkungen Verfügbarkeit
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