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

In the 2021 issue of the Journal of Biosciences in the article titled ''An in vitro mechanistic approach towards understanding the distinct pathways regulating insulin resistance and adipogenesis by apocynin'' by Sai Bharadwaja, Praveen Kumar Issac, Jocelyn Cleta, Rakesh Jeganathan, Sri Snehaa Chandrakumar and Sujatha Sundaresan (https://doi.org/10.1007/s12038-020-00134-2; Vol. 46, Article No. 008), the author Rakesh Jeganaathan's name was incorrectly mentioned as ''Rakesh Jeganathan''. The correct name should read as ''Rakesh Jeganaathan''.

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

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.

Molecular process of glucose uptake and glycogen storage due to hamamelitannin via insulin signalling cascade in glucose metabolism.

Understanding the mechanism by which the exogenous biomolecule modulates the GLUT-4 signalling cascade along with the information on glucose metabolism is essential for finding solutions to increasing cases of diabetes and metabolic disease. This study aimed at investigating the effect of hamamelitannin on glycogen synthesis in an insulin resistance model using L6 myotubes. Glucose uptake was determined using 2-deoxy-D-[1-3H] glucose and glycogen synthesis were also estimated in L6 myotubes. The expression levels of key genes and proteins involved in the insulin-signaling pathway were determined using real-time PCR and western blot techniques. The cells treated with various concentrations of hamamelitannin (20 µM to 100 µM) for 24 h showed that, the exposure of hamamelitannin was not cytotoxic to L6 myotubes. Further the 2-deoxy-D-[1-3H] glucose uptake assay was carried out in the presence of wortmannin and Genistein inhibitor for studying the GLUT-4 dependent cell surface recruitment. Hamamelitannin exhibited anti-diabetic activity by displaying a significant increase in glucose uptake (125.1%) and glycogen storage (8.7 mM) in a dose-dependent manner. The optimum concentration evincing maximum activity was found to be 100 µm. In addition, the expression of key genes and proteins involved in the insulin signaling pathway was studied to be upregulated by hamamelitannin treatment. Western blot analysis confirmed the translocation of GLUT-4 protein from an intracellular pool to the plasma membrane. Therefore, it can be conceived that hamamelitannin exhibited an insulinomimetic effect by enhancing the glucose uptake and its further conversion into glycogen by regulating glucose metabolism.