AJP - Endocrinology and Metabolism, Vol 244, Issue 4 354-E360, Copyright © 1983 by American Physiological Society
Pentose phosphate shunt, pyridine nucleotides, glutathione, and insulin secretion of fetal islets
H. P. Ammon, G. Bumiller, H. Duppenbecker, E. Heinze, S. Lutz and E. J. Verspohl
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.
