The hepatic overexpression of C2-AKT ameliorates obesity-induced insulin resistance

Metabolic disorders, such as obesity and diabetes, have become increasingly prevalent worldwide, posing significant challenges to public health. Insulin resistance, a hallmark of these disorders, is characterized by an impaired response to insulin in target tissues, leading to dysregulated glucose and lipid metabolism. Although the pathogenesis of insulin resistance is complex and multifactorial, mounting evidence suggests that disrupted intracellular calcium (Ca2+) homeostasis plays a crucial role in its development. To elucidate the molecular mechanisms underlying the improved metabolic profiles in C2-AKT overexpression mice, we performed RNA-seq on liver tissues from both control and C2-AKT mice To examine the effects of C2-AKT specifically in hepatocytes, we crossed ROSA26-C2-AKT mice with Alb-Cre mice. In this cross, Cre recombinase, driven by the liver-specific albumin (Alb) promoter, enables targeted C2-AKT expression in hepatocytes, providing a valuable tool for studying its function and regulation in liver physiology. At 8 weeks of age, we fed 8-week-old male C2-AKT mice or control mice with a high-fat diet (HFD) for 10 weeks.