These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Preservation of the anomeric specificity of glucose-induced insulin release in partially pancreatectomized rats. Author: Leclercq-Meyer V, Malaisse-Lagae F, Coulic V, Akkan AG, Marchand J, Malaisse WJ. Journal: Diabetologia; 1992 Jun; 35(6):505-9. PubMed ID: 1612222. 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 the 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.[Abstract] [Full Text] [Related] [New Search]