Metformin could be used to lower cholesterol levels, new research carried out at Helmholtz Zentrum München and the German Diabetes Centre in Dusseldorf has revealed.
The study looked at blood samples from more than 1,800 participants. These were split into several groups – one given metformin and four control groups who were not given the drug.
The researchers were looking for metabolites that would provide evidence of blood lipid profiles. They discovered lower concentrations of three metabolites in the metformin group. The metabolites were all associated with lower levels of low-density lipoprotein (LDL) cholesterol.
Lower levels of LDL cholesterol could be explained by genes associated with AMPK, a molecular mechanism activated by metformin, the researchers believe. By activating AMPK, metformin controls the genes associated with LDL cholesterol levels.
Together with colleagues in the Netherlands, the scientists aligned the metabolite concentrations with the genetic information, thereby identifying metabolites and genes involved in the respective pathways.
"We speculate that metformin intake affects the levels of LDL cholesterol via AMPK, leading to a down-regulation of the genes FADS1 and 2,” said Dr Rui Wang-Sattler, head of the group 'Metabolism' in the Research Unit of Molecular Epidemiology at the Institute of Epidemiology II of the Helmholtz Zentrum München. “This is also supported by the fact that three lipid metabolites, which are dependent on FADS, are decreased. Presumably, this is the mechanism how the production of LDL cholesterol is repressed by metformin."
First author of the report, Dr Tao Xu, added: "Our study suggests that metformin might indeed have an additional beneficial effect with regards to cardiovascular diseases among the diabetes patients."
Moreover, the Helmholtz scientists aim to elucidate how metformin, which has been used for more than 50 years, works on the molecular level. "Until now the exact mechanism is unclear,” added co-first author Dr Stefan Brandmaier added. “Thus, we want to continue our contribution to its decryption."