Supporting data for "SH3 domain binding kinase 1 (SBK1) is a novel enhancer of hepatic insulin signaling."

The liver is the central organ for carbohydrate metabolism to maintain the blood glucose concentration within a normal range. Glucose breakdown or synthesis in the liver is tightly regulated by insulin via the insulin receptor (IR), insulin receptor substrate (IRS), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) pathway to enhance glucose uptake and glycogen synthesis. Hence, people with insulin resistance have a higher possibility of developing type II diabetes mellitus (T2DM). To date, about 451 million adults live with diabetes worldwide, which is expected to increase to 693 million by 2,045 if no effective prevention methods are adopted. Therefore, developing earlier stage treatment is crucial to prevent insulin resistance-induced metabolic syndrome. To dissect the molecular mechanism of insulin resistance, we generated a model of insulin resistance in nongenetically modified mice using high-fat diet (HFD) feeding regimen. Microarray analysis showed that the hepatic expression SH3 domain binding kinase 1 (SBK1), a novel kinase with unknown function, in HFD-fed mice was significantly higher than chow diet-fed mice. In this project, we will discuss the role of SBK1 in insulin signaling regulation and its potential role as a new therapeutic target against T2DM by biochemical assays, immunoblotting, and RT-PCR.