<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Diabetes during pregnancy results in congenital malformations
and long-term postnatal diseases. Experimental
models are still needed to investigate the mechanism
responsible for these alterations. Thus, by the administration
of different doses of streptozotocin (STZ) (0, 25,
30, or 35 mg/kg body weight, intravenous) at the onset
of pregnancy in rats, the present study sought an appropriate
animal model for this pathology. At day 6 of pregnancy,
plasma glucose was progressively higher with an increasing
STZ dose, and in rats receiving the 35-mg dose,
2 subgroups were detected: some animals had plasma glucose
levels above controls but below 200 mg/dL (mildly diabetic,
MD), whereas others had levels above 400 mg/dL
(severely diabetic, SD). At day 20 of pregnancy, the MD
rats had normal glycemia, but after an oral glucose load
(2 g/kg body weight), plasma glucose increased more and
insulin increased less than in controls. The SD rats maintained
their hyperglycemia and had a greatly impaired
oral glucose tolerance. At day 20, fetuses of SD dams were
fewer, weighed less, and had enhanced plasma glucose and
triglycerides and decreased insulin, whereas those from
MD dams did not differ from controls. At birth, newborns
from MD dams had higher body weight, plasma insulin,
and liver triglycerides as well as total body lipid concentrations
than controls, and on day 21, remained macrosomic and showed higher plasma glucose and liver triglyceride
concentrations. At 70 days of age, offspring of MD dams had
impaired oral glucose tolerance but normal plasma insulin
change in the case of females, whereas plasma insulin increased
less in males. These alterations were manifest more
in those offspring from dams that had &gt; 50% macrosomic
newborns than in those from dams that had &lt; 50% macrosomic
newborns. In conclusion, whereas our MD rats mimic
the changes taking place in gestational diabetic women and
show the long-term risk of macrosomia, the SD rats are
more similar to uncontrolled diabetics. Thus these two rat
models, obtained with moderate amounts of STZ, could be
used to study the pathophysiological consequences of these
different diabetic conditions.</p>
[]
Exp Diabesity Res. 2003; 4(2):107-118