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A thin phenotype is protective for impaired glucose tolerance and related to low birth weight in mice
Marcelino Hernandez-Valencia1, Mary-Elizabeth Patti
1Endocrine Research Unit, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico. mhernandezvalencia@prodigy.net.mx
Insights
Postnatal nutritional modification can prevent impaired glucose tolerance (IGT) in low-birth-weight mice. Restricting early postnatal weight gain protected offspring from developing IGT and diabetes later in life.
Area of Science:
- Metabolic health
- Developmental programming
- Nutritional science
Background:
- Low birth weight is a significant risk factor for impaired glucose tolerance (IGT) and type 2 diabetes in adulthood.
- This risk is observed in both preterm and term infants, highlighting the long-term consequences of early life conditions.
- Improved neonatal care increases survival rates of low-birth-weight infants, making preventative strategies crucial.
Purpose of the Study:
- To investigate the efficacy of postnatal nutritional modification in preventing low-birth-weight-associated glucose intolerance.
- To determine if preventing early postnatal weight gain can mitigate the risk of developing IGT and diabetes.
- To utilize a mouse model simulating maternal undernutrition during late pregnancy.
Main Methods:
- Three groups of mouse offspring were studied: controls (C), undernutrition with low birth weight (UN) fed ad libitum, and undernutrition with continued postnatal food restriction (UN-UN).
- Maternal undernutrition during the third week of pregnancy resulted in significantly reduced birth weights in UN and UN-UN groups compared to controls.
- Postnatal nutritional status was manipulated, with the UN group allowed to catch up on growth while the UN-UN group experienced continued caloric restriction.
Main Results:
- While initial birth weights were reduced, body weights were similar until 4 months. The UN-UN group showed reduced body weight at 6 months.
- Glucose tolerance, insulin tolerance, and glucose-stimulated insulin secretion were comparable among all groups at 2 months.
- By 6 months, UN mice developed IGT, whereas UN-UN mice were protected, showing glucose levels similar to controls, potentially due to improved insulin sensitivity.
Conclusions:
- Early postnatal nutritional interventions, specifically preventing rapid weight gain, are associated with the prevention of IGT in low-birth-weight individuals.
- Altering early nutrition can be a viable strategy to mitigate the long-term metabolic risks associated with low birth weight.
- These findings in a mouse model provide a basis for exploring similar interventions in human infants at risk.
Background:
Low birth weight is an independent risk factor for impaired glucose tolerance (IGT) and diabetes in adult life. This risk extends to both preterm and term infants, a particularly important finding given the increased survival of low-birth-weight infants with improvements in neonatal care. One potential strategy for prevention of low-birth-weight-associated glucose intolerance is postnatal nutritional modification and prevention of early postnatal weight gain. To determine the efficacy of this approach, we utilized our mouse model of low birth weight related to maternal undernutrition during the third week of pregnancy.
Methods:
We studied three experimental groups of offspring mice: controls (C), undernutrition with low birth weight (UN) fed ad lib postnatally, and undernutrition with food restriction continued in postnatal life (UN-UN). Mean birth weight was significantly reduced in both groups of undernutrition offspring in utero (C: 1.86 +/- 0.03 vs. UN: 1.37 +/- 0.04 and UN-UN: 1.32 +/- 0.06, p <0.001). As expected, and in accord with human data, differences in weight between C and UN mice disappeared by week 2 of life, indicating catch-up growth in the UN group.
Results:
Body weight was similar in all groups until 4 months of age, after which the UN-UN group had reduced body weight as compared with controls (p <0.05 at 6 months). Insulin tolerance test (1 U/kg), glucose tolerance test (2 g/kg) and glucose-stimulated insulin secretion test (3 g/kg) at 2 months of age were identical among C, UN, and UN-UN groups. By age 6 months, IGT had developed in the UN mice (p <0.05 vs. C). By contrast, UN offspring with caloric restriction postnatally (UN-UN) were protected from the development of glucose intolerance, with glucose levels identical to that of control mice. These differences appeared to be related to improved insulin sensitivity in the UN-UN mice as compared with UN mice, although data did not reach statistical significance.
Conclusions:
Our data suggest that alterations in early postnatal nutrition are associated with prevention of weight gain and the development of IGT in low-birth-weight mice.
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