Birth weight concerning obesity and diabetes gene expression in healthy infants; a case- control study

Abstract

Abstract Background: Since obesity and diabetes are prevalent worldwide; identifying the factors affecting these two conditions can effectively alter them. We decided to investigate the expression of obesity and diabetes genes in infants with birth weight lower than 2500 g. Methods: The current case-control study was performed on 215 healthy infants aged 5-6 months, referring to Kermanshah's health and treatment centers. After measuring the weight and height of the infant, the values were compared with the diagram of WHO to assure being healthy and well-grown and infants who were healthy, were selected to the study. 78 infants was in case group and 137 infants was in control group. 5 cc of intravenous blood was collected from all infants. Blood samples were collected in Ethylenediaminetetraacetic acid (EDTA) coated vials to evaluate the expression of MC4R, MTNR1B, PTEN, ACACB, PPAR-γ, PPAR-α, (NRXN3 (NTRK2), (PCSK1), (A2BP1), (TMEM18), (LXR), (BDNF), (TCF7L2),(FTO) and (CPT1A) genes. The data was analyzed by Chi square, Mann-Whitney U and Spearman tests. Results: a significant inverse correlation between birth weight and obesity and diabetes genes, including MTNR1B, NTRK2, PCSK1, and PTEN genes (r= -0.221, -0.235, -0.246, and -0.418, respectively). In addition, the LBW infant's expression level was significantly up-regulated than the normal weight infants (P= 0.001, 0.007, 0.001, and <0.001, respectively). The expression level of the PPAR-a gene had a significantly positive correlation with birth weight (r= 0.19, P= 0.005). The expression level of the PPAR-a gene in the normal weight infants was significantly up-regulated than the LBW infants (P= 0.049). Conclusion: expression levels of MTNR1B, NTRK2, PCSK1, and PTEN genes were up-regulated in the LBW infants; however, the expression level of PPAR-a gene was significantly down-regulated in the LBW infants compared to the infants with normal birth weight.