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. 2021 Jan 21;11:1932. doi: 10.1038/s41598-020-80563-z

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Knockdown of ADH1B yields a decrease in insulin-stimulated glucose uptake within adipocytes. Knockdown of ADH1B was performed by transfection of differentiating pre-adipocytes with ADH1B-specific pooled siRNA or non-targeting (Scramble) control siRNA. Cultured adipocytes were starved for 12 h and then treated with 1 µM insulin (+ Insulin) to stimulate uptake of exogenous 2-deoxyglucose (2-DG) which is metabolized to 2-DG 6 phosphate (2-DG6P). Accumulated 2-DG6P was oxidized to generate a proportional amount of NADPH, yielding an oxidized product that was detected at OD = 412 nm. Data is presented as the mean ± s.e.m. *P < 0.05.