Background and Aims : T lymphocytes (T cells) accumulate in the adipose tissue during obesity and their activation is paralleled by a switch in their metabolism towards anaerobic glycolysis with elevated amount of lactate production, which should be eliminated properly to limit cytotoxic effects. Aim of this project is to investigate the relevance of a key lactate transporter, namely MCT1 in T cells during obesity.Methods: MCT1f/fCD4-cre mice, which undergo the specific deletion of MCT1 in both CD4 and CD8 T lymphocytes during thymic development, were fed with an high fat diet (HFD) for 20 weeks. Adipose tissue immunophenotyping and gene expression were performed at 20 weeks. Proteomics on T lymphocytes after activation from our animal model was performed.Results: MCT1 is highly expressed in CD8+T cells after activation. Compared to controls, MCT1 deficient CD8+T cells showed a switch toward oxidative phosphorylation, coupled to increased mithochondria presence. MCT1f/f CD4-cre mice on HFD, despite a similar weight gain and glucose response, presented less CD8+T effector memory cells (Tem) in VAT (Tem CD8+: MCT1f/f 41653cells/g±32894, MCT1f/fCD4-cre 10169cells/g±7509, p<0.001), independently of cell death. Furthermore, MCT1f/f CD4-cre mice presented a significantly lower expression of visceral adipose tissue (VAT) preadipogenic markers (e.g. PPARγ, PPARδ, cEBPδ; p<0.001) associated with decreased VAT accumulation and reduced adipocytes area compared to MCT1f/f.Conclusions: Our data demonstrates that MCT1 transporter deficiency affects metabolic reprogramming of activated CD8+ T cells and their recruitment in adipose tissue during obesity. Background and Aims : T lymphocytes (T cells) accumulate in the adipose tissue during obesity and their activation is paralleled by a switch in their metabolism towards anaerobic glycolysis with elevated amount of lactate production, which should be eliminated properly to limit cytotoxic effects. Aim of this project is to investigate the relevance of a key lactate transporter, namely MCT1 in T cells during obesity. Methods: MCT1f/fCD4-cre mice, which undergo the specific deletion of MCT1 in both CD4 and CD8 T lymphocytes during thymic development, were fed with an high fat diet (HFD) for 20 weeks. Adipose tissue immunophenotyping and gene expression were performed at 20 weeks. Proteomics on T lymphocytes after activation from our animal model was performed. Results: MCT1 is highly expressed in CD8+T cells after activation. Compared to controls, MCT1 deficient CD8+T cells showed a switch toward oxidative phosphorylation, coupled to increased mithochondria presence. MCT1f/f CD4-cre mice on HFD, despite a similar weight gain and glucose response, presented less CD8+T effector memory cells (Tem) in VAT (Tem CD8+: MCT1f/f 41653cells/g±32894, MCT1f/fCD4-cre 10169cells/g±7509, p<0.001), independently of cell death. Furthermore, MCT1f/f CD4-cre mice presented a significantly lower expression of visceral adipose tissue (VAT) preadipogenic markers (e.g. PPARγ, PPARδ, cEBPδ; p<0.001) associated with decreased VAT accumulation and reduced adipocytes area compared to MCT1f/f. Conclusions: Our data demonstrates that MCT1 transporter deficiency affects metabolic reprogramming of activated CD8+ T cells and their recruitment in adipose tissue during obesity.