Relationship between serum adiponectin and bone mineral density in preterm infants / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To examine serum adiponectin level in preterm infants and to evaluate the relationship between serum adiponectin and bone mineral density in preterm infants.</p><p><b>METHODS</b>Seventy-two appropriate-for-gestational-age neonates were classified into three groups according to their gestational ages: early preterm (31-33(+6) weeks, 13 cases), late preterm (34-36(+6) weeks, 16 cases), and full-term (37-42 weeks, 43 cases). Venous blood was collected at one week of their life to measure serum adiponectin concentration. During the period, omnisense ultrasound bone sonometer was applied to measure speed of sound (SOS) of the left tibia.</p><p><b>RESULTS</b>The median of tibia SOS in the early preterm group was significantly lower than in the late preterm and full term groups (P<0.05), and the median of tibia SOS in the late preterm group was lower than in the full-term group (P<0.05). Serum adiponectin level was lowest in the early preterm group, and the full-term group had the highest serum adiponectin level. Serum adiponectin level was positively correlated with tibia SOS in preterm infants (r=0.664, P<0.05). According to the result of multivariate linear stepwise regression analysis, serum adiponectin and birth weight were independent predictor of tibia SOS in preterm infants.</p><p><b>CONCLUSIONS</b>Serum adiponectin level is lower in preterm infants than that in full-term infants. There is a positive correlation between serum adiponectin and bone mineral density in preterm infants.</p>

Relationship between bone turnover markers and bone sound of speed in appropriate-for-gestational-age neonates / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the correlation of gestational age (GA) with carboxyterminal propeptide of type I procollagen (PICP), deoxypyridinoline (DPD), and bone sound of speed (SOS) in appropriate-for-gestational-age (AGA) neonates, as well as the relationship between bone turnover markers and bone SOS.</p><p><b>METHODS</b>Sixty-five AGA neonates were included in the study. The neonates were divided into three groups: preterm infant (GA ≤3 4 weeks, 14 cases), late preterm infant (34 weeks<GA<37 weeks, 13 cases), and full-term infant (GA ≥ 37 weeks, 38 cases). Birth weight and length were measured in all cases, and Ponderal index (PI) was used to estimate their nutritional status. Venous blood was collected within 7 days after birth to measure blood PICP concentration. Urine was collected to measure urinary DPD and creatinine (Cr) levels. Omnisense 7000P ultrasound bone sonometer was applied to measure the SOS of the left tibia in all cases within 7 days after birth.</p><p><b>RESULTS</b>There were significant differences in GA (F=140.199, P<0.001), birth weight (F=47.042, P<0.001), birth length (F=46.877, P<0.001), and PI (F=11.898, P<0.001) between the three groups; the higher the GA, the higher the birth weigh, birth length, and PI. There were significant differences in PICP (F=30.384, P<0.001), DPD/Cr (F=21.761, P<0.001), and SOS (F=20.052, P<0.001) between the three groups; the higher the GA, the lower the PICP and DPD/Cr and the higher the bone SOS. PICP and DPD/Cr were negatively correlated with GA, birth weight and bone SOS (P<0.01), while bone SOS was positively correlated with GA and birth weight (P<0.01), which still held true after adjustment for GA and birth weight.</p><p><b>CONCLUSIONS</b>Among AGA neonates, bone turnover markers are negatively correlated with GA, birth weight and bone SOS. High bone turnover is bad for bone health in AGA neonates.</p>

Relationships between Low Birth Weight and Insulin Resistance and Adult Cardiovascular Disease / 实用儿科临床杂志

The nutritional status in early life have been gradually recognized that it can change the status of development and metabolism of adults.Epidemiological evidence and animal model study have found that low birth weight is the risk factors of adult metabolic syndrome and cardiovascular disease.Insulin resistance is a common pathophysiological basis.Renin-angiotensin system and insulin signaling systems interact to promote the development of insulin resistance.