Obesity is associated with chronic low-grade inflammation, yet the early immunological events that precede overt metabolic disease remain poorly defined — despite representing an important therapeutic window. Here we show that short-term high-fat diet (HFD) feeding for one to three weeks is sufficient to impair systemic glucose handling, as evident by altered glucose and insulin tolerance, demonstrating that metabolic perturbation precedes the onset of obesity. Concomitant with these early metabolic changes, we observed a loss of conventional type 1 dendritic cells (cDC1) across adipose tissue, lung and bone marrow (BM), accompanied by functional alterations in the residual cDC compartment. Mechanistically, impaired cDC1 development is driven by reduced IRF8 expression in common dendritic cell progenitors (CDPs) and pre-cDC1, two stages that are critically dependent on FLT3L signalling. Consistent with this, serum FLT3L levels were significantly reduced in HFD-fed mice, suggesting that limited cytokine availability constrains IRF8-driven cDC1 specification. Using a newly generated Flt3l-mCherry reporter mouse, we identify lymphoid cells as the dominant cellular source of FLT3L in vivo, and a lymphocyte-specific Flt3l conditional knockout recapitulates the reduction of cDC1, establishing lymphoid-derived FLT3L as a non-redundant rheostat of steady-state cDC1 output. In parallel, early HFD feeding drove a marked expansion of IL-17–producing RORγt⁺ γδ T cells and RORγt⁺ Th17 cells across tissues, indicating cDC1 loss and altered antigen-presenting cell function in shaping early obesity associated type 17 bias. Ongoing work uses lymphoid Flt3l cKO mice to elucidate whether cDC1 deficiency drives diet-induced obesity and loss of glucose tolerance, complemented by in vitro DC–T cell co-culture assays and assessment of DC/T cell colocalization under CD versus HFD to define a potential DC–Th17 axis governing obesity onset.