Pentose phosphate shunt, pyridine nucleotides, glutathione, and insulin secretion of fetal islets.
In rat fetal islets it was tested whether their failure to respond to glucose with insulin secretion might be due to inadequate changes of the redox state of pyridine nucleotides and of glutathione. In islets of newborn (5 days) and adult (3 mo) rats elevation of glucose produced an increase in insulin secretion, pentose phosphate shunt (PPS) activity, and NADPH/NADP, NADH/NAD, and GSH/GSSG ratios. An increase in the NADH/NAD ratio was also observed in islets of fetal rats, but in contrast to islets of newborns and adults no increase in insulin release, PPS activity, and the GSH/GSSG ratio was observed. However, at all glucose concentrations tested islets of fetal rats exhibited a high NADPH/NADP ratio similar to the ratio of adult rats in the presence of 16.7 mM glucose. It is suggested that in fetal islets there exists a lack of hydrogen transfer from NADPH to GSSG. The high NADPH/NADP ratio may in turn suppress PPS activity. It is possible that the missing insulin release of fetal islets in response to glucose is at least in part due to the fact that the oxidation-reduction state of the GSH/GSSG system also does not respond to the elevation of the glucose concentration.
D000818:Animals; D005260:Female; D005333:Fetus; D005947:Glucose / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D009243:NAD / Q000378:metabolism*; D009249:NADP / Q000378:metabolism*; D010084:Oxidation-Reduction; D010428:Pentosephosphates / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D010428:Pentosephosphates; D009243:NAD; D009249:NADP; D005978:Glutathione; D005947:Glucose