Preservation of the anomeric specificity of glucose-induced insulin release in partially pancreatectomized rats.
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.
Leclercq-Meyer
V
V
Laboratory of Experimental Medicine, Erasmus Medical School, Brussels Free University, Belgium.
Malaisse-Lagae
F
F
Coulic
V
V
Akkan
A G
AG
Marchand
J
J
Malaisse
W J
WJ
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D010180:Pancreatectomy; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D013237:Stereoisomerism; D013997:Time Factors
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose