Inhibition of proinsulin biosynthesis and conversion by a putative insulin mediator.
The phospho-oligosaccharide (POS), presumed to act at the postreceptor level as the insulin second messenger, was recently reported to inhibit glucose-stimulated insulin release from rat pancreatic islets. In the present study, POS was also found to inhibit glucose-stimulated proinsulin biosynthesis and conversion in rat islets. By comparison with prior findings on the effects of both exogenous insulin and anti-insulin serum upon proinsulin synthesis, these results argue against the view that insulin would normally exert a negative feedback control upon the biosynthetic and secretory activities of islet B-cells.
Camara
J
J
Fundacion Jimenez Diaz and Consejo Superior de Investigaciones Cientificas, Madrid, Spain.
Albor
A
A
Mato
J M
JM
Malaisse
W J
WJ
Valverde
I
I
D000818:Animals; D005947:Glucose / Q000494:pharmacology; D007295:Inositol Phosphates; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism; D009844:Oligosaccharides / Q000494:pharmacology*; D011134:Polysaccharides; D011384:Proinsulin / Q000096:biosynthesis*; D051381:Rats; D015290:Second Messenger Systems
D007295:Inositol Phosphates; D007328:Insulin; D009844:Oligosaccharides; D011134:Polysaccharides; C028039:inositol phosphate glycan; D011384:Proinsulin; D005947:Glucose