| Iodine is an essential component for the synthesis of thyroid hormones. Iodine deficiency and iodine excess both lead to thyroid changes in morphology and function, causing various disorders. In the critical brain development period (ie, prenatal and early postnatal periods), thyroid hypofunction caused by iodine deficiency will lead to irreversible damage in brain development. Iodine nutrition of fetal and infants (breastfed) can only come from mother, therefore the iodine nutrition of pregnant and lactating women is essential for the offspring's physical growth and development, in particular brain development. Because infant's neural development is still in progress in early postnatal period (ie, breast-feeding), as well as a strong proponent of breast-feeding in current, the iodine status of lactating women can not be ignored. According to this, our study has done a great deal of research work, to explore whether breast-feeding mothers and their mammary gland have the compensatory ability to iodine deficiency or iodine excess (that is, the protection of infants and young children) in different aspects, providing experimental basis for iodine deficiency and iodine excess prevention of breast-feeding women.In our study, we successfully established Wistar rat model of iodine deficiency and iodine excess in different degrees, and on the based of that, we studied the iodine metabolism, thyroid function and morphology changes of the mother and child in lactation, measured the growth and development status and cerebellum-specific gene and protein of child rat, and explored the compensatory mechanisms of the lactating mammary gland with different iodine supply, to explain the compensatory regulation mechanism of lactating mammary gland and its protection to child. The present experimental methods, findings and conclusions are summarized as follows:Methods:4-6 weeks healthy Wistar female rats were randomly divided into severe iodine deficiency (SID), mild iodine deficiency (MiID), normal iodine (NI) and excessive iodine (ExI) groups by body weight. All female rats were fed on an iodine deficient food and drinking water with different doses of KI for 8 weeks until to mating.The male rats were fed as NI. Lactating mother and their young rats on 14 and 28 days after birth were empirical studied. Iodine level in urine, blood and milk were detected in lactating mother and their young rats by As-Ce catalytic spectrophotometry. TSH and thyroid hormones (TH) in blood were detected by chemiluminascent immunoassay and competitive binding RIA methods. Thyroid morphology of mother and their young rats and the physical growth and nervous development of these off-springs were observed. The thickness of external granular layer in cerebellum was measured. The mRNA expression of myelin basic protein and Pcp-2 in cerebellum were detected by real-time fluorescence quantitative PCR, and the protein of those were detected by Western blot and immunohistochemical method. The mRNA expression of NIS and Pendrin were detected by real-time fluorescence quantitative PCR, too. The prolactin in blood of lactating rats was detected by enzyme-linked immunosorbnent assay.Results:1. The effect of different iodine supply on mother rats in lactation1.1 Severe iodine deficiency1.1.1 The urinary iodine excretion reduced:mother urine of severe iodine deficiency group had always been at a very low level compared with normal iodine group.1.1.2 The low iodine level in vivo:iodine in blood and in milk of severe iodine deficiency group were significantly lower than that of normal iodine group1.1.3 Thyroid goiter: thyroid of severe iodine deficiency group showed clear signs of hyperaemia, swelling. Thyroid absolute weight and relative weight were about 3 times more than the normal group. Histological studies have shown that a typical small follicular thyroid hyperplasia swollen.1.1.4 Hypothyroidism:severe iodine deficiency decreased serum TT4 and FT4 levels, TT3 and FT3 levels in the early compensatory increased slightly and then decreased, showing a significantly hypothyroidism and TSH stimulated.1.2 Mild iodine deficiency1.2.1 Reduction of urinary iodine excretion:mother urine iodine level of mild iodine deficiency group has always been at a low level compared with the NI group in order to ensure a normal blood iodine levels in vivo. 1.2.2 Low iodine status of the body alleviated:the mild iodine deficiency group, iodine in blood was 62.7% of the normal group, milk iodine was 51.2% of the normal group at 14 day of breast feeding, were significantly higher than those the proportion of iodine supply (50% of NI).1.2.3 A lesser goiter: mother rats of mild iodine deficiency group showed mild swelling of the thyroid (the thyroid weight was 1.5 times higher than the normal group), histological studies had shown individually small follicular hyperplasia.1.2.4 Thyroid function almost normal:the serum thyroid hormone levels of mother rats with mild iodine deficiency were closed to the NI group.1.3 Excessive iodineMother rat of excessive iodine group reduced the iodine content by increasing the urinary excretion of iodine:blood iodine content is 20 times higher than the NI group. Thyroid reduced iodine taking, T3 reduced synthesis, T4 relative increased in synthesis, serum T4 hormone level of ExI was higher, but T3 levels and T3/T4 were lower than the NI group. Changes in thyroid histology showed features of polymorphism, but the degree was light.2. The effect of different iodine supply on child rats in lactation2.1 Severe iodine deficiency2.1.1 The low level of iodine in vivo:by reducing urine excretion of iodine, iodine deficiency status had been partial remission, but the iodine intake was too little, the compensatory ability of body is not enough to alleviate the status of iodine deficiency, the child rats showed low blood iodine level unavoidably.2.1.2 Thyroid function reduced:child rat of severe iodine deficiency appeared hypothyroidism, serum TT4 levels were significantly lower than the normal group, thyroid histology observed with rats showed typical small goiter follicular hyperplasia similar to their mother.2.1.3 The growth and development of child rat delayed:representative of the physiological indicators, such as, ear standing, eyes opening, hair growning and body length, weight, and on behalf of the success rate of turning over on the plane, the success rate of negative geotaxis, as well as the hanging time of forelimb, SID group were significantly lagging behind compared with NI group, reflecting the "Cretinism" features.2.1.4 Cerebellar dysplasia: the proliferation and disappearance of EGL in SID were delayed, MBP and Pcp-2 mRNA and protein were significantly lower than NI group, that illustrated severe iodine deficiency that affects the normal development of cerebellum.2.2 Mild iodine deficiency2.2.1 Iodine level in vivo slightly lower: by reducing iodine urine excretion, iodine level in vivo of child rats of mild iodine deficiency group has been very good improvement.2.2.2 Thyroid function, physical growth and cerebellum development were close to normal group child rats:thyroid hormone levels in child rats of mild iodine deficiency were closed to the NI group, the histological change was only small follicular hyperplasia individually. EGL proliferation and regression, MBP and Pcp-2 mRNA and protein expression of mild iodine deficiency were slightly behind but no significant differences with the normal group.2.3 Excessive iodineBlood iodine of child rat in excessive iodine was only 3-4 times of NI group, and the ratio was far less than the milk iodine. TT4 levels, thyroid morphology, were not significantly differences, but cerebellum, growth and development were slightly behind compared with the normal group.3. The compensation of lactating mammary at different iodine supply3.1 Severe iodine deficiencyDecreased ability of iodine intake of mammary gland:a serious decline of NIS and Pendrin mRNA expressions of severe iodine deficiency group indicated that the thyroid capacity of iodine intake was into decompensated status.3.2 Mild iodine deficiencyCompensatory enhance in ability of iodine intake of mammary gland:NIS mRNA expression of mammary gland in lactation of mild iodine deficiency groups was increased. Although the expression of Pendrin mRNA was suppressed by low-iodine, but NIS has played a dominant position. Based on the above, the ability of breast taking in iodine of mild iodine deficiency groups was enhanced. 3.3 Excessive iodineCompensatory reduce in ability of iodine intake of mammary gland:The NIS and Pendrin mRNA expressions of mammary gland were significantly reduced, the ability of breast taking in iodine was declined.Conclusion:In conclusion, in severe iodine deficiency, the mother was into the decompensated state finally, appeard a significantly thyroid hypofunction and signs of TSH stimulation, which led to a typical follicular hyperplasia goiter, and the ability of breast taken in iodine descended, which affected the postnatal growth and development of offspring rat; in mild iodine deficiency, the lactating rats maintained their own normal thyroid function through compensatory, at the same time the capacity of iodine taken in breast enhanced to protect the offspring from iodine deficiency; for excessive iodine, mother rats had a strong ability to compensate to maintain normal thyroid function itself, and the capacity of iodine taken in breast reduced to protect the offspring from iodine excessive. But the breast ability of iodine accommodatation is limited, mainly through the infant's compensation (increase urine iodine excretion etc.) to mitigate the harm of iodine excessive.We also discovered:The compensatory way is various to abnormal iodine nutrition of the lactating mother. It exist certain regulation mechanism in mammary gland, but which plays the leading role are kidney, the mammary gland, the thyroid gland as well as the hypothalamus-gland pituitary gland- thyroid axis. Prompt us:it should not overlook iodine nutrition of breast-feeding women, supply iodine to them scientifically and rationally, and correct iodine deficiency or excessive iodine timely to prevent abnormal iodine nutrition on breast-feeding women and their offspring. |
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