Obesity-associated metaflammation drives the development of insulin resistance and type 2 diabetes, notably through modulation of innate and adaptive immune cells in metabolic organs. Although macrophages are generally considered as central players in regulating tissue-specific insulin sensitivity, dendritic cells (DCs) also accumulate in white adipose tissue and the liver during obesity. DCs are specialized antigen presenting cells that govern T cell responses. The priming of effector, helper and regulatory T cells by DCs is driven by specific cell-intrinsic metabolic rewiring in response to microenvironmental cues, leading to modulation of co-stimulatory molecule and cytokine expression that shape T cell polarization. Although the nutrient sensor LKB1 has been recently shown to control cellular metabolism and T cell priming functions of DCs for maintaining anti-tumor immunity, little was known in the context of metaflammation. In the framework of this presentation, we will mainly focus on our recent work investigating the role of LKB1 in DC-mediated T helper cell priming in metabolic tissues and its impact on metabolic homeostasis during obesity. Altogether, we show that LKB1 signaling in DCs protects against obesity-induced metabolic dysfunctions by limiting DC-mediated hepatic Th17 responses through both AMPKα1 and SIK-dependent mechanism(s).