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Increased Pancreatic Islet Blood Flow in 48-Hour Glucose-Infused Rats: Involvement of Central and Autonomic Nervous Systems¹

Laboratoire de Physiopathologie de la Nutrition, CNRS URA 307, Université Paris VII (N.A., M.-C.L., J.-M.N., A.K., L.P.), Paris; and Laboratoire de Neurobiologie, Plasticité Tissulaire et Métabolisme Energétique, UPRESA 5018 Université Paul Sabatier-CNRS, IFR Louis Bugnard, CHU Rangueil (L.P.), Toulouse, France; and Laboratoire des Régulations Physiologiques, Faculté des Sciences Ibn Tofail (N.A., N.M.), Kenitra, Maroc

Address all correspondence and requests for reprints: Dr. L. Pénicaud, Laboratoire de Neurobiologie, Plasticité Tissulaire et Métabolisme Energétique, UPRESA 5018 Université Paul Sabatier-CNRS, 1 avenue Jean Poulhés 31054 Toulouse Cedex, France. E-mail: penicaud{at}rangueil.inserm.fr

The pancreatic islet blood flow of rats 24 h after a prolonged (48-h) glucose infusion was investigated using a nonradioactive microsphere technique. In the basal state, islet blood flow was significantly increased in previously hyperglycemic rats (HG) compared to that in controls (C). During an iv glucose challenge, both plasma insulin and islet blood flow were increased in the two groups, but these increases were significantly higher in HG than in C rats. Although less pronounced, the results were similar when glucose was injected into the carotid artery toward the brain at a dose that did not modify the peripheral glucose level. The effect of this intracarotid injection was abolished after bilateral subdiaphragmatic vagotomy in both C and HG rats. Furthermore, in the latter group, both plasma insulin concentration and islet blood flow returned to values similar to those observed in the basal state in C rats. After pretreatment with the ₂-adrenoceptor agonist clonidine, the insulin response to the intracarotid glucose load was totally blunted in the two groups of rats. By contrast, whereas such a pretreatment lowered the glucose-induced increase in islet blood flow in C rats, it was without effect in HG rats. These data suggest that a period of hyperglycemia and/or hyperinsulinemia is sufficient to induce a perturbation of pancreatic islet blood flow, which appears to be mainly due to an increased parasympathetic activity, whereas the decrease in sympathetic tone does not play a role. These modifications in autonomic nervous system activity could be due to alterations in some brain areas involved in "glucose sensing."

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