Corrigendum to “IDF2022-1217 Evaluation of the COBLL1 intron variant SNP rs6712203 in adipocytes of obese female risk and non-risk allele carriers” [Diabet. Res. Clin. Pract. 197(1) (2023) 110289] (Diabetes Research and Clinical Practice (2023) 197(S1), (S0168822723001341), (10.1016/j.diabres.2023.110289))

The authors regret that the wrong version of the above-mentioned abstract was published. The correct version is now reproduced below. The authors would like to apologise for any inconvenience caused. Background Epigenetic maps revealed a cell-type-specific enhancer in proximity to the rs6712203 SNP. A previous study showed a putative link between this intronic rs6712203 C-to T single-nucleotide polymorphism and a disrupted POU2F2 activator motif in risk C-allele carriers in adipocyte cells. In particular, the rs6712203 T non-risk-variant enhancer increased the expression of COBLL1 in adipocytes. In turn, perturbed COBLL1 expression led to disturbed actin remodeling during adipogenesis and reduction of insulin-stimulated glucose uptake, triglyceride storage and response to lipolytic stimulation. Aim We focus on the relation between COBLL1 expression and T2D in adipocytes studying the expression of selected marker genes of fat metabolism and the metabolome in obese female risk and non-risk allele carriers. Methods 11 female participants at an age of 18 up to 65 with a mean BMI of 48.41 were included. Subcutaneous cells from the participants were cultured and differentiated into adipocytes. At distinct stages of differentiation cells were analyzed for expression of selected marker genes by RT-qPCR. Metabolomic parameters were determined using DI-FT-ICR-MS analysis with ultra-high resolution and high mass accuracy. Results Expression of selected marker genes by RT-qPCR analysis displayed no significant changes between risk and non-risk allele carriers. In Phase 1, day 0–3 to day 3, metabolomic analysis by DI-FT-ICR-MS of several compound classes in rs6712203 risk allele carriers, revealed a decrease of organooxygens, and an increase in prenol lipids, glycerophospholipids, and sex-hormone related steroids/steroid derivatives. In Phase 2, day 3 to day 14, there were no longer any significant results. Mass difference enrichment analysis (MDEA) demonstrated that Phase 1 metabolism of risk pre-adipocytes is characterized by active primary metabolism, faster lipid production and intact actin-related metabolism. Primary metabolism, including TCA, glycolysis, and actin-related processes are down-regulated in Phase 2, while the metabolism of lipids and steroids is enhanced. Conclusion A synergy of novel bioinformatic technologies and comprehensive biological validation was used as powerful and exciting new tools to understand how genetic variants and disease are associated.