Another limitation is the lack of further vascular disease measurements e.g. inflammatory markers such as ICAM-1, VCAM-1, IL-8, MCP-1, etc. Furthermore exploring liver disease formation i.e. NASH or NAFLD would have been interesting in our animal model due to the existing association between the components of MetS (i.e. visceral obesity, insulin resistance and dyslipidemia) and NALD/NASH. This evidence concerns the gene CCL2 and metabolic dysfunction-associated steatotic liver disease.