Acute hyperglycaemia and mast-cell-dependent mitogenesis in rat.
Hyperglycaemia is considered to be of possible aetiological significance for proliferative lesions in diabetes. We recently found that mast-cell-mediated proliferation in mesentery and skin is augmented in hyperglycaemic rats with longstanding diabetes. We now report a study to examine whether acute hyperglycaemia affects the proliferative response of fibroblasts and mesothelial cells that follows local mast-cell secretion in healthy rats. Hyperglycaemia was achieved by continuous intravenous infusion of glucose over a period of 2.5 h preceding and 9.5 h following administration of the mast-cell secretagogue compound 48/80. The 48/80 was given intraperitoneally which causes rapid mast-cell secretion and prompt subsequent mesenteric mitogenic stimulation. Hyperglycaemia thus persisted throughout the prereplicative period, during which stimulated cells are recruited into the cell cycle from a quiescent state. Because the ensuing mesenteric mitogenic response, estimated by specific DNA activity and mitosis counting, was unaffected by glucose infusion, acute hyperglycaemia itself appears to be of no aetiological significance for the accelerated mast-cell-dependent mesenteric mitogenesis in the diabetic rat.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology; D006943:Hyperglycemia / Q000473:pathology* / Q000503:physiopathology; D007263:Infusions, Parenteral; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000473:pathology*; D008938:Mitosis / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D003189:p-Methoxy-N-methylphenethylamine / Q000494:pharmacology
D001786:Blood Glucose; D003189:p-Methoxy-N-methylphenethylamine; D005947:Glucose