Related Experiment Videos
Insulin-receptor development in normal and diabetic pregnancies. Role of membrane fluidity
Insights
Diabetic pregnancy in rats leads to increased insulin receptors in fetal offspring, despite normal fetal insulin levels. This suggests altered insulin sensitivity may contribute to developmental changes in offspring.
Area of Science:
- Reproductive biology
- Endocrinology
- Developmental biology
Background:
- Maternal diabetes can cause macrosomia and hypoglycemia in offspring.
- These conditions are often attributed to increased insulin sensitivity in the fetus.
Purpose of the Study:
- To investigate changes in insulin receptor development in fetuses from a rat model of diabetic pregnancy.
- To understand the impact of maternal diabetes on fetal insulin signaling.
Main Methods:
- Used streptozocin to induce diabetes in pregnant Sprague-Dawley rats.
- Assayed maternal and fetal blood for glucose and insulin levels.
- Analyzed fetal liver membranes for insulin binding, lipid composition, and membrane fluidity using 125I-insulin and DPH probe.
Main Results:
- Maternal and fetal glucose levels were elevated in diabetic rats.
- Fetal insulin levels were not significantly different between groups.
- Fetal offspring of diabetic rats showed increased insulin binding to liver membranes due to more high- and low-affinity receptors.
- Membranes from fetuses of diabetic mothers exhibited altered fluidity.
Conclusions:
- Maternal diabetes alters fetal insulin receptor development.
- Increased insulin receptor numbers in fetal offspring may play a role in altered insulin sensitivity.
- These findings contribute to understanding the developmental consequences of diabetic pregnancy.
Abstract:
In the hyperinsulinemic offspring of the diabetic mother, both significant macrosomia and postnatal hypoglycemia are thought to be due to increased insulin sensitivity. The purpose of this study is to characterize changes in insulin-receptor development in fetal offspring of an experimental model of diabetic pregnancy. Two groups of Sprague-Dawley female rats were studied after timed mating. Both groups received injections of either vehicle (controls) or streptozocin (diabetic), 40 mg/100 g body wt, on day 7 of pregnancy and were killed at either 17, 20, or 21 days of gestation. Maternal and fetal blood were assayed for glucose and insulin, and fetal liver membranes were prepared for 125I-labeled insulin binding, lipid composition, and fluorescence polarization studies with the probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Maternal and pooled fetal glucose levels were elevated in streptozocin-treated rats; however, pooled fetal insulin values were not elevated in the offspring of diabetic animals compared with controls (33 +/- 1 vs. 50 +/- 5 microU/ml). 125I-insulin binding was greater in fetal offspring of diabetic (FD) rat membranes at each gestational age studied [P less than .001 by analysis of variance (ANOVA)] due to significantly greater numbers of both high- and low-affinity receptors. The highest insulin-binding capacity was seen on membranes obtained from FD rats at day 21 (9.92 M X L-1 X 100 micrograms membranes-1 vs. 6.38 M X L-1 X 100 micrograms protein-1 in fetal control (FC) rats. At each gestational age, membranes from FDs had lower values for fluorescence polarization (using the probe DPH) than did gestational-age--matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)