Diet-Induced Obesity (DIO) is a major risk 
factor for a number of disorders including non-insulin
dependent Type 2 Diabetes Mellitus (T2D). In our novel 
mouse model, the gene Atp10c is a strong candidate for 
metabolic disorders of Insulin Resistance (IR) and DIO. 
As such, we hypothesized that ATP10C has a key role in 
glucose
 metabolism
 via 
insulin-dependent
 and 
independent signaling pathways. We first examined the 
expression of Atp10c in both a genetic as well as an 
environmental mouse model of obesity. While our results 
showed that there were no significant changes in Atp10c 
expression in the genetic and environmental mouse 
models, our data does show high expression of Atp10c in 
key peripheral tissues namely skeletal muscle and adipose 
depots. Next, we performed western immunoblot analysis 
to detect potential targets of ATP10C in both the 
phosphatidyinosital-3-kinase (PI3K) and the mitogen
Activated Protein Kinase (MAPK) pathways. When 
accessing MAPK pathway proteins, the mutants showed a 
significant decrease in the ratio of activated to native 
forms of p38 and ERK1/2. Additionally, we observed 
differences in the PI3K pathway as there were significant results along with data from our investigations of skeletal 
muscle prove our hypothesis that Atp10c must play a role 
in glucose metabolism, and suggest that the action of 
Atp10c is potentially mediated via both the MAPK 
pathway as well as the PI3K pathway.