Author(s): Volchegorski IA, Kostin IuK, Skobeleva NA, Lifshits RI
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Abstract Relationships between adrenergic exposure (stress, administration of adrenomimetics and adrenoblockers) and rat sensitivity to exogenic insulin were studied. The participation of beta-adrenoceptors in regulation of insulin sensitivity of the body was revealed. Drugs characterized by beta-adrenomimetic activity (adrenalin, novodrin, partusisten) enhanced insulin sensitivity upon prolonged (for 24 h) administration. One-hour immobilization stress also enhanced insulin sensitivity. The authors discuss beta-adrenoceptor desensitization phenomenon as a possible mechanism of the before events. Obsidan (a nonselective beta-adrenoblocker) also augmented insulin sensitivity. A single administration of partusisten (an adrenomimetic with a predominant affinity to beta 2-adrenoceptors) reduced insulin sensitivity. Augmentation of beta-adrenergic processes at the expense of beta-adrenoblockers (aminasin, haloperidol, butyroxan) effects also reduced insulin sensitivity. An inverse correlation between the capacity of adrenergic exposures to influence glycogen content in striated muscles and their effects on insulin coma latency (insulin sensitivity market) was detected. This relationship confirms the role of beta-adrenoceptors in insulin sensitivity regulation.
This article was published in Probl Endokrinol (Mosk)
and referenced in Journal of Diabetes & Metabolism