PRESERVATION OF THE ANOMERIC SPECIFICITY OF GLUCOSE-INDUCED INSULIN RELEASE IN PARTIALLY PANCREATECTOMIZED RATS


LECLERCQMEYER V., MALAISSELAGAE F., COULIC V., AKKAN A. G. , MARCHAND J., MALAISSE W.

DIABETOLOGIA, vol.35, no.6, pp.505-509, 1992 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 35 Issue: 6
  • Publication Date: 1992
  • Doi Number: 10.1007/bf00400476
  • Title of Journal : DIABETOLOGIA
  • Page Numbers: pp.505-509

Abstract

Attenuation, suppression or even inversion of the normal preference of glucose-stimulated insulin release for the alpha-anomer of the hexose was recently proposed to represent a feature of Beta-cell glucotoxicity in Type 2 (non-insulin-dependent) diabetes mellitus. Since recent reports emphasize the possible significance of Beta-cell secretory hyperactivity as a determinant of such a glucotoxicity, the anomeric specificity of glucose-induced insulin release was examined in normoglycaemic partially pancreatectomized rats. About 80-85% of thc pancreas was removed, the animals then being given sucrose via their drinking water up to the time of killing. In these animals, alpha-D-glucose was more efficient than beta-D-glucose in stimulating insulin release from the perfused pancreas, the alpha/beta-ratio in insulin output not being significantly different from that found in control rats. It is concluded, therefore, that the anomeric malaise, taken as a manifestation of Beta-cell glucotoxicity, it attributable to hyperglycaemia rather than to Beta-cell secretory hyperactivity.