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Published on: February 2, 2024
Effects of postnatal growth restriction and subsequent catch-up growth on neurodevelopment and glucose homeostasis in
Erica E Alexeev1, Bo Lönnerdal2, Ian J Griffin3
1Department of Nutrition, University of California, Davis, CA, 95616, USA. eeebanks@ucdavis.edu.
Insights
Early postnatal growth restriction in rats impacts long-term development and insulin sensitivity. Severe restriction led to impaired learning and altered glucose tolerance, highlighting risks for preterm infants.
Area of Science:
- Developmental biology
- Neonatal research
- Metabolic studies
Background:
- Poor growth in preterm infants is linked to adverse long-term development.
- The effects of early postnatal growth restriction (PGR) are not fully understood.
- A rat model was used to investigate PGR consequences.
Purpose of the Study:
- To examine the consequences of different patterns of postnatal growth.
- To test the hypothesis that early growth failure impairs development and insulin resistance.
Main Methods:
- Rat pups were assigned to normal (N) or restricted intake (R) litters at birth.
- Restricted pups were re-randomized into varying litter sizes (R-6, R-10, R-16) at postnatal day 11.
- Development (T-maze test) and metabolic parameters (insulin and glucose tolerance tests) were assessed.
Main Results:
- By day 10, normal pups weighed 20% more than restricted pups.
- Catch-up growth varied by litter size: R-6 achieved normal weight, R-10 showed partial, and R-16 showed no catch-up.
- All restricted groups exhibited poorer T-maze performance; however, all showed altered glucose tolerance compared to controls.
Conclusions:
- Postnatal growth restriction patterns significantly alter developmental outcomes and insulin sensitivity in rats.
- These findings may help explain poor developmental outcomes observed in human preterm infants.
Background:
There is increasing evidence that poor growth of preterm infants is a risk factor for poor long-term development, while the effects of early postnatal growth restriction are not well known. We utilized a rat model to examine the consequences of different patterns of postnatal growth and hypothesized that early growth failure leads to impaired development and insulin resistance. Rat pups were separated at birth into normal (N, n = 10) or restricted intake (R, n = 16) litters. At d11, R pups were re-randomized into litters of 6 (R-6), 10 (R-10) or 16 (R-16) pups/dam. N pups remained in litters of 10 pups/dam (N-10). Memory and learning were examined through T-maze test. Insulin sensitivity was measured by i.p. insulin tolerance test and glucose tolerance test.
Results:
By d10, N pups weighed 20% more than R pups (p < 0.001). By d15, the R-6 group caught up to the N-10 group in weight, the R-10 group showed partial catch-up growth and the R-16 group showed no catch-up growth. All R groups showed poorer scores in developmental testing when compared with the N-10 group during T-Maze test (p < 0.05). Although R-16 were more insulin sensitive than R-6 and R-10, all R groups were more glucose tolerant than N-10.
Conclusion:
In rats, differences in postnatal growth restriction leads to changes in development and in insulin sensitivity. These results may contribute to better elucidating the causes of poor developmental outcomes in human preterm infants.
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