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. 2023 Dec 18;21:504. doi: 10.1186/s12916-023-03227-5

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© The Author(s) 2023

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Mendelian randomization estimates for the association of genetically proxied SLC13A5 inhibition with biomarkers of glucose and lipid metabolism, and inflammation. Mendelian randomization estimates are scaled per 1-standard deviation (SD) increase in plasma citrate through genetically proxied SLC13A5 inhibition. The units for fasting glucose is mmol/l, the units for C-reactive protein (CRP) is standard deviation (SD) change of log transformed levels, and the remaining exposures are measured in SD units. HDLc: high-density lipoprotein cholesterol, IL6: interleukin 6, LDLc: low-density lipoprotein cholesterol