An in vitro mechanistic approach towards understanding the distinct pathways regulating insulin resistance and adipogenesis by apocynin

Abstract

Adipogenesis is a cascade of processes that entail the differentiation of fibroblasts into mature adipocytes, which results in the accumulation of triglycerides in the adipose cells due to high dietary supplements. This physiological condition increases the risk of type 2 diabetes. Apocynin (4-hydroxy-3-methoxyacetophenone), an organic compound from the root extracts of the medicinal herb Picrorhiza kurroa, has been used in various experimental studies. The current study focuses on deciphering the cellular and molecular mechanisms interlinking obesity and diabetes by validating the various key targets involved in insulin signaling and adipogenesis. Apocynin exhibited enhanced glucose uptake and decreased lipid accumulation in the adipocytes. Furthermore, the expression of molecular markers involved in the insulin signaling pathway, such as IRTK, IRS-1, PI3K, GLUT-4, and the adipogenic pathway, such as PPAR α, adiponectin, C/EBP-α and SREBP1C, by qPCR supported our hypothesis largely. Apocynin mimicked insulin in the insulin-signaling pathway by showing equivalent gene expression. It ameliorated adipogenesis by downregulating the key markers in the adipogenic pathway. Corroborating the hypothesis that Apocynin is antihyperlipidemic in nature, it reduced the expression of PPARα and adiponectin. These results substantiate that Apocynin exerts anti-diabetic and anti-adipogenic effects by regulating resistin and antioxidant enzyme levels in vitro.