School of Medicine

As the prevalence of childhood obesity increases in the United States, the prevalence of obesity-related co-morbidities, such as type 2 diabetes mellitus, has increased as well. However, there is currently limited published data on the role of genes and signaling pathways in childhood obesity. Obesity is described as a cause of type 2 diabetes mellitus mediated by chronic inflammation. Our goal is to determine the role of genes in adipose tissue in insulin resistance amongst young pubertal mice by investigating the gene expression profiles of young and adult murine adipose tissue in diet-induced obesity. In our study, we hypothesized that adipose tissue gene profiles differ between young and adult mouse populations. To investigate these differences in adipose tissue between young and adult mice, we utilized genome-wide transcriptional microarray analysis. Results from this study showed that adult mice on high fat diet (HFD) have increased fat mass in comparison to their age-matched controls on normal chow diet (NCD). In contrast, young mice do not significantly increase their fat mass when placed on HFD compared to their age-matched controls on NCD. Furthermore, we found that adult mice exhibit an increase in fasting blood glucose and fasting insulin following HFD. Fasting blood glucose and fasting insulin values in young mice do not differ between NCD and HFD groups. This data suggest that young mice are protected from HFD-induced insulin resistance. In order to illuminate why young mice are protected from HFD-induced insulin resistance, we used microarray analysis and found candidate genes and signaling pathways that could be responsible for mitigating HFD-induced insulin resistance.