RESUMO
Objective@#To explore the relationship between prepregnancy body mass index, weight gain during pregnancy with preschool obesity and body composition in offspring, so as to provide evidence for gestational weight gain and childhood obesity prevention.@*Methods@#A total of 1 333 preschool children were recruited from 3 kindergartens in Tianjin from September to December 2020. Structured questionnaire was used to collect children s lifestyle information. Height, weight and body fat mass of children were assessed, and body fat percentage (FM%), fat mass index (FMI) and non fat mass index (FFMI) were calculated. Maternal medical records were collected and the mothers were grouped according to their prepregnancy weight status and weight gain during pregnancy. χ 2 test, t test, linear regression model and Logistic regression were used to analyze the differences of obesity and body composition among different groups.@*Results@#The prevalence of overweight and obesity in preschoolers was 12.7% and 7.7%. After adjusting maternal age and delivery, gestational age, gender, age and lifestyle of children, the correlation between maternal pre pregnancy BMI,gestational weight gain with obesity and body composition indexes of children in preschool age was statistically significant ( P <0.05). For mothers with normal weight before pregnancy, excessive weight gain during pregnancy increased risk of high FM% and high FMI in offspring ( OR=1.81, 1.68, P <0.05). There was no significant correlation between maternal weight gain during pregnancy with offspring obesity and body composition among mothers with prepregnant overweight or obesity.@*Conclusion@#Maternal weight status before pregnancy and weight gain during pregnancy are correlated with obesity and body composition in the preschool age of offspring. It is suggested that mothers should maintain appropriate weight status before and during pregnancy.
RESUMO
PIWI (P element induced wimpy testis) integrating RNAs (piRNAs) are small non-coding RNAs with the length of approximately 30 nucleotides that plays crucial roles in germ cells and adult stem cells. Recently, accumulating data have shown that piRNA and PIWI proteins are involved in tumorigenesis. However, the roles of PIWI proteins and piRNAs in pancreatic cancer are still elusive. Here, we showed that piR-017061 is significantly downregulated in pancreatic cancer patients' samples and pancreatic cancer cell lines. Furthermore, we studied the function of piR-017061 in pancreatic cancer and our data revealed that piR-017061 inhibits pancreatic cancer cell growth in vitro and in vivo. Moreover, we analyzed the genomic loci around piR-017061 and identified EFNA5 as a novel target of piR-017061. Importantly, our data further revealed a direct binding between piR-017061 and EFNA5 mRNA mediated by PIWIL1. Mechanically, piR-017061 cooperates with PIWIL1 to facilitate EFNA5 mRNA degradation and loss of piR-017061 results in accumulation of EFNA5 which facilitates pancreatic cancer development. Hence, our data provided novel insights into PIWI/piRNA-mediated gene regulation and their function in pancreatic cancer. Since PIWI proteins and piRNA predominately express in germline and cancer cells, our study provided novel therapeutic strategy for pancreatic cancer treatment.
