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Updated: Oct 3, 2026
An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
Published on: April 20, 2018
Comparative effects of chronic exposure to glucose or sodium butyrate on surfactant development in fetal rabbits
1Dalhousie University, Department of Obstetrics and Gyneccology, IWK Grace Health Center, Halifax, Nova Scotia, Canada. ttshiyombo@iwkgrace.ns.ca
Insights
Maternal diabetes can delay infant lung development. This study found that high glucose or sodium butyrate in pregnant rabbits did not impair fetal lung surfactant maturation, suggesting other factors cause delayed lung development in infants of diabetic mothers.
Area of Science:
- Perinatal medicine
- Developmental biology
- Endocrinology
Background:
- Infants of diabetic mothers (IDM) face increased risk of Respiratory Distress Syndrome (RDS) due to delayed lung development.
- Hyperglycemia and hyperinsulinemia are suspected causes, but mechanisms remain unclear.
- Sodium butyrate, elevated in IDM, may affect surfactant production.
Purpose of the Study:
- Investigate in vivo effects of glucose and sodium butyrate on maternal/fetal parameters.
- Assess impact on fetal lung surfactant maturation in rabbits.
Main Methods:
- Timed-pregnant rabbits received glucose, sodium butyrate, or placebo via pellets.
- Maternal and fetal blood samples collected for glucose and insulin.
- Fetal surfactant pools harvested and phospholipid profiles analyzed.
Main Results:
- Glucose and sodium butyrate increased fetal insulin and decreased fetal glucose.
- Neither treatment affected maternal glucose or insulin levels.
- No delay in fetal lung surfactant maturation parameters was observed.
Conclusions:
- Fetal hyperinsulinemia from elevated glucose or sodium butyrate does not cause delayed lung maturity.
- This challenges the hypothesis that these factors are primary drivers of lung immaturity in IDM.
Background:
Infants of diabetic mothers (IDM) often have delayed lung development and are thus at an increased risk of Respiratory Distress Syndrome (RDS). Both hyperglycemia and/or hyperinsulinemia have been implicated in this delay but the precise mechanism has not been clarified. Another metabolite, sodium butyrate, which is increased in IDM has been shown to decrease surfactant production in vitro but its effects on the development of the fetal lung surfactant system in vivo have not been studied.
Aim:
To investigate the in vivo effects of high glucose and sodium butyrate treatment on maternal and fetal glucose and insulin levels and on fetal lung surfactant maturation using timed-pregnant New Zealand White rabbits.
Methods:
On the 24th day of gestation the doe was implanted s.c. with time release pellets containing either glucose (300 mg), sodium butyrate (200 mg) or matching placebo. On the 27th or 30th day maternal (ear vein) and fetal (cardiac puncture) blood samples were drawn for glucose and insulin determinations. Fetal surfactant pools (both intra- and extracellular) were quantitatively harvested using differential and density gradient centrifugation and their phospholipid profiles determined. Data were statistically compared with ANOVA and Duncan's Multiple Range Test.
Results:
Neither glucose nor sodium butyrate affected maternal plasma glucose or insulin. Both metabolites significantly increased fetal plasma insulin, decreased fetal plasma glucose but did not delay any of the parameters of surfactant maturation examined.
Conclusions:
Fetal hyperinsulinemia, whether attained by prolonged exposure to elevated glucose or sodium butyrate in vivo does not appear to be the causative agent for delayed lung maturity which frequently occurs in infants of diabetic mothers.
