Insulin Resistance and Body Composition in Preterm Born Children During Prepubertal Ages

Feyza Darendeliler; Firdevs Bas; Ruveyde Bundak; Asuman Coban; Ozlem Sancakli; Sema Kabatas Eryilmaz; Banu Kucukemre; Rian Disci; Gulbin Gokcay; Semih Aki; Zeynep Ince; Nurten Eskiyurt

Disclosures

Clin Endocrinol. 2008;68(5):773-779. 

In This Article

Discussion

One of the main findings of this study is that premature AGA children are not insulin resistant when compared to term AGA children, provided that they have made a CUG appropriate for their target height and have normal BMI. The effect of intrauterine growth restraint and/or postnatal growth pattern on insulin resistance and insulin secretion in preterm born children in these age ranges in childhood has been studied in a few reports and have reported reduced insulin sensitivity.[15,16] In some studies, it was the postnatal weight gain that had an effect on later insulin levels,[17,32] and in a recent cohort study, the association between insulin levels in adulthood and birth weight was very weak in preterm infants but it was the adult obesity that had a greater impact on high insulin levels.[33] Thus, our preterm children may develop insulin resistance if they develop obesity. In fact, the association between the insulin levels and weight change is in favour of this assumption. One of the arguments may be the slightly younger age of the term AGA children than the preterm AGA group, but this should not have influenced insulin resistance which have been previously shown to be unaffected by age in the prepubertal age range.[34] It may also be argued that basal insulin and HOMA-IR may not be sensitive enough; however, among several parameters that can be used for insulin resistance, these have been recommended in childhood practice.[35] The most important point was that there were no differences between the BMI values between the preterm AGA and term AGA children.

The other major finding of this study is that preterm SGA children have similar insulin levels as preterm AGA children, that is, they are not more insulin resistant. Term SGA children, on the other hand, have much higher insulin levels than preterm SGA children who have similar anthropometric data. These findings point to the assumption that it is the intrauterine growth restriction in the third trimester that accounts for future metabolic abnormalities and the period before the third trimester does not have an important effect.

Hofman et al.[15] showed that preterm infants have reduced insulin sensitivity whether SGA or AGA when compared to controls, and being an SGA and preterm did not increase the risk of insulin resistance, similar to our study. In the study by Bazaes et al.[16] on the other hand, preterm SGA children had lower insulin sensitivity than the preterm AGA children, but they did not have term controls.

In our study, premature AGA and term AGA children were similar with respect to body composition, once more showing that premature AGA children are similar to the term AGA children. However, one could have expected that term SGA children who were more insulin resistant than premature SGA children and also more insulin resistant than term AGA children might have associated increased abdominal fat, but there were no differences in the mean values of total and truncal fat between these groups in this study. The main limitation of DEXA assessment of body composition is its inability to distinguish subcutaneous fat from intra-abdominal fat and truncal fat measured on DEXA is not the same as abdominal fat. However, it is difficult to perform body composition measurement in this age group, and we can conclude that there is no marked difference between the groups with respect to body composition in this group of preterm born children compared to term children. This finding is not in accordance with the data from term SGA children[9] which showed increased abdominal fat in term SGA children from 2 years of age in the presence of normal BMI. This may show that DEXA was not sensitive enough to detect the difference at these early ages in preterm children. This is the first study on body composition in preterm children in early childhood, and further studies may be needed for body composition data in preterm children.

Another finding in this study is that term SGA children have higher insulin levels than term AGA children in spite of having comparable BMI values which is in accordance with published reports.[8,9]

There were no differences between the IGF-I levels between preterm SGA and term SGA levels in consistence with their similar anthropometry. The lower IGF-1 levels in preterm AGA children may be due to their relatively lower weight SDS than that of term children, although their BMI were similar. There are not many studies on IGF axis in premature children, but in the study by Cutfield et al.,[36] premature AGA children had also lower IGF-1 levels than term AGA children. The children in that study had a height SDS of -0·8 and the low IGF-1 levels were attributed to growth hormone resistance. In our study, the height SDS of the preterm children was appropriate for their target height but slightly below the population mean and the lower IGF-1-values may well be due to GH resistance. Although there are several factors that affect the height of premature children, this may be one factor for the slightly compromised height in other studies which report a height deficit of 0·5-1·0 SD in childhood or older ages in preterm infants with similar range of gestational ages.[37,38]

Leptin levels may be high during the catch-up growth of term SGA children[14] at early ages, but they have been found usually low during childhood in thin SGAs when compared to normal AGA children.[39,40,41] On the other hand, serum leptin levels were found low in SGA born adults in some studies in spite of an increased adipose tissue and was related to altered adipose tissue.[13] Although leptin levels have been studied in SGA children in several studies, there are not many studies in premature children. In our study, serum leptin levels of the premature children were comparable to that of term children which shows that at comparable BMI levels, there is no pathology with respect to leptin levels. In healthy children, leptin levels show gender difference even after adjustment for body fat especially in puberty, but the gender difference may also be evident at prepubertal ages.[42,43] One noteworthy finding in our study was that gender difference in leptin levels was present only in term AGA children, whereas in term SGA and preterm children, there was no gender difference. The absence of gender difference in leptin levels in SGA children has been shown in some studies.[14]

It is noteworthy that although fasting glucose levels were in normal ranges in all groups, it has been found slightly but significantly high in term AGA children in our study. Although the underlying factors are not clear, it has been speculated that there may be evidence for a developmental adaptation of glucose metabolism in SGA children leading to reduced glucose concentrations.[44]

Insulin showed negative correlation with IGFBP-1 and was lowest in term SGA children with highest insulin values, which shows that the insulin-IGFBP-1 regulation is preserved in preterm children.

There were no significant differences in lipid levels in our study in compliance with some other studies in preterm children,[13] showing that these ages are too early for detection of lipid abnormalities, if any.

In conclusion, term SGA children have higher insulin levels compared to term AGA children as has been shown in previous studies even if they have normal and comparable BMI. Preterm AGA children, who have not experienced intrauterine growth insult, have similar insulin resistance compared to term AGA children, provided that they reach an appropriate height for their target height and have normal BMI. Preterm SGA children are not adversely affected and have similar insulin values as premature AGA children. These findings indicate that it is the intrauterine growth restriction in the last trimester that has an effect on future metabolic adverse outcome.


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