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Effect of different iodine nutrition on cerebellum Pcp-2 in rat offspring during lactation
Lu Zhang1, Yi Na Sun, Yong Mei Li
1Institute of Endocrinology, Tianjin Medical University, Key Lab of Hormones and Development, Ministry of Health, 22, Qi-Xiang-Tai Road, 300070, Tianjin, China.
Insights
Severe iodine deficiency in lactating mothers impairs offspring cerebellum development, indicated by reduced Purkinje cell protein-2. Mild deficiency or excess iodine allows for compensatory mechanisms, maintaining normal development.
Area of Science:
- Endocrinology
- Neuroscience
- Developmental Biology
Background:
- Maternal iodine status is crucial for infant thyroid function and central nervous system development.
- Purkinje cell protein-2 (PCP-2) is a specific marker for cerebellar Purkinje cells, reflecting postnatal cerebellar development.
Purpose of the Study:
- To investigate the impact of varying maternal iodine nutritional levels on offspring cerebellum growth during lactation.
- To assess the relationship between maternal and neonatal thyroid function and cerebellar development markers.
Main Methods:
- Measurement of Purkinje cell protein-2 mRNA and protein levels in rat cerebellum at postnatal days 14 and 28.
- Assessment of maternal and neonatal thyroid hormone (T4) levels under conditions of severe iodine deficiency, mild iodine deficiency, and iodine excess.
- Analysis of Purkinje cell protein-2 mRNA and protein levels in offspring rats.
Main Results:
- Severe iodine deficiency led to maternal and neonatal thyroid dysfunction and significantly reduced Purkinje cell protein-2 mRNA and protein levels in offspring.
- Mild iodine deficiency and excessive iodine intake maintained normal thyroid function and normal Purkinje cell protein-2 levels.
- These findings suggest that the mother's and offspring's compensatory mechanisms, particularly in mammary glands, protect cerebellum development from mild iodine variations.
Conclusions:
- Severe iodine deficiency retards cerebellum development by reducing Purkinje cell protein-2 expression.
- Mild iodine deficiency and iodine excess do not significantly impair cerebellum development due to compensatory mechanisms.
- Maternal mammary glands play a key role in compensating for mild iodine imbalances during lactation.
Abstract:
The thyroid functions of breastfed infants, as well as (indirectly) the development of their central nervous system, are dependent on the iodine status of the lactating mother. Purkinje cell protein-2 is a cell-specific marker of the cerebellum Purkinje cell and is a suitable indicator for observing the postnatal development of the cerebellum after birth. We measured the Purkinje cell protein-2 mRNA and protein levels in the rat cerebellum in the critical postnatal (14 days after birth) and maturation periods (28 days after birth) to determine the effect of different nutritional iodine levels on cerebellum growth in the offspring during lactation. We found that severe iodine deficiency resulted in thyroid dysfunction in lactating rats and their offspring on both 14 and 28 days, showing maternal total T(4) 16.7 ± 12.0 vs 36.4 ± 15.0, P < 0.05 (14 days) and 22.6 ± 18.7 vs 53.4 ± 9.4, P < 0.01 (28 days), and neonatal total T(4) 10.6 ± 2.3 vs 16.4 ± 4.7, P < 0.01(14 days) and 12.8 ± 2.9 vs 16.7 ± 3.4, P < 0.05 (28 days), respectively. The Purkinje cell protein-2 mRNA and its protein levels in offspring rats were significantly reduced that showed Purkinje cell protein-2 mRNA 1.12 ± 0.04 vs 2.25 ± 0.53, P < 0.05 (14 days) and 1.74 ± 0.94 vs 8.69 ± 2.71, P < 0.01 (28 days). However, mild iodine deficiency and excessive iodine maintained almost normal thyroid function in maternal and neonatal rats and normal Purkinje cell protein-2 mRNA and protein levels in offspring's cerebellum. We conclude that severe iodine deficiency could significantly reduce Purkinje cell protein-2 mRNA and its protein levels, indicating that the cerebellum development was retarded, but mild iodine deficiency and excessive iodine could maintain them at an approximately normal level by the mother's and offspring's compensations, especially by the mother's mammary glands.
