Background: Type 2 diabetes (T2D) is known to be a risk factor for invasive pancreatic ductal adenocarcinoma (PDAC). PDAC are characterized by prominent fibrosis called desmoplasia, but effective therapies targeting the stroma have not been forthcoming. PDAC pathogenesis with T2D remains to be elucidated. Pancreatic stellate cells (PSCs) are the origin of cancer-associated fibroblasts. T2D may promote PDAC, eliciting changes in the quiescent PSC (qPSC) population from the precancerous stage. However, the details are unknown. We evaluated the subpopulations of qPSCs and the impact of T2D. Methods: PSCs isolated from 8-week-old C57BL/6 mice and diabetic db/db mice were analyzed by single-cell RNA sequencing. Sorted qPSCs by FACS and PDAC cells were transplanted into allogenic mice. Results: The isolated qPSCs were broadly classified into mesothelial cell and pancreatic fibroblast (Paf) populations by single-cell RNA sequencing. Pafs were subclassified into inflammatory Pafs, myofibroblastic Pafs (myPafs) and a small novel population named tumor immunity- and angiogenesis promoting Pafs (tapPafs), expressing Cxcl13. In the subcutaneous transplantation model, the tumors transplanted with myPafs were significantly larger than the tumors transplanted with tapPafs. The tumors transplanted with tapPafs had more intrastromal immune cells than those transplanted with myPafs. In the tumors transplanted with tapPafs, CD3-positive and CD8-positive T cells and B220-positive B cells abundantly infiltrated the tumors. The microvascular density of tumors transplanted with tapPafs was greater than that of tumors transplanted with myPafs. In human PDAC specimen, T2D patients had higher PSC activation (PSCa) scores than non-T2D patients did, as evaluated by the intensity of aSMA staining around PanIN. The presence of CXCL13-positive stromal cells surrounding the PanIN in non-T2D patients was rich, while the number of CXCL13-positive stromal cell was dramatically decreased in T2D patients. RFS and OS were also shorter in patients with an absence of CXCL13-positive stromal cells and high PSCa scores than in patients with CXCL13-positive stromal cells and low PSCa scores. Conclusion: We revealed the subpopulation changes in qPSCs in T2D. A therapy that increases the number of tapPafs could be a novel therapeutic option for patients with PDAC and T2D, even those in a precancerous stage.