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. 2019 Dec 10;122(2):258–265. doi: 10.1038/s41416-019-0665-5

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Model of effect of metformin on lipid metabolism on breast cancer cells. Triglyceride is synthesised from fatty acid derived from carbon sources including glucose and glutamine and also exogenous fatty acid, requiring modification by elongases and desaturases prior to storage in lipid droplets. Metformin inhibits complex 1 disrupting electron transfer required to catalyse the final dehydrogenation step of fatty acid oxidation resulting in the accumulation of triglyceride in lipid droplets. AMPK is known to be an activator of fatty acid oxidation and metformin’s predominant effects on lipid metabolism in breast cancer cells are via an AMPK-independent pathway and secondary to its more direct mitochondrial effect on Complex 1. FA fatty acid, TG triglyceride, TCA Cycle tricarboxylic acid cycle.