A 56-year-old man who had been receiving medication for hypertension for 5 years was referred to our hospital for further investigation of a pancreatic tumor detected by abdominal ultrasonography screening. His initial body weight and body mass index (BMI) were 94.0 kg and 37.2 kg/m2, respectively. Contrast computed tomography (CT) revealed an enhanced tumor measuring 15 mm on the pancreatic body and severe fat deposition. The thickness of the pancreas parenchyma at the bifurcation of the superior mesenteric and splenic veins was 32 mm, and the PV was evaluated as 148 ml. The subcutaneous and visceral fat volumes were 337.4 cm2, and 276.1 cm2, respectively. An endoscopic ultrasonographic fine needle aspiration (EUS-FNA) revealed a rosette-like aggregation of small round monotonous cells, and immunohistochemical staining showed that the tumor cells were positive for synaptophysin. The Ki-67 proliferation percentage score (index) was approximately 1%. We also confirmed that every serum hormonal status of insulin, glucagon, and gastrin did not increase. Therefore, we diagnosed the pancreatic tumor as being non-functioning PNET-G1. Based on these examinations, we planned to perform LSG first and wait approximately 6 months after LSG to evaluate weight loss and metabolic effects before performing LSPDP for the PNET. We performed LSG, as previously reported [] and sprayed a liquid antiadhesive agent for LSPDP (AdSpray, Terumo Corporation, Tokyo, Japan). The patient was discharged on postoperative day 5 without any perioperative complications. We followed him closely, monitoring weight loss effects and PNET size, for 6 months after LSG. His body weight and BMI decreased dramatically to 64.0 kg and 25.3 kg/m2, respectively. Contrast CT revealed that the pancreas parenchyma thickness and the PV also decreased to 17 mm and 99 mL, respectively, with no tumor growth, and the subcutaneous and visceral fat volumes decreased to 98.6 cm2 and 93.2 cm2, respectively. CT attenuations of the pancreas also improved after LSG in pancreatic head (− 28.5 HU to 37.3 HU), body (− 56.5 HU to 17.3 HU), and tail (− 58.3 HU to 1.4 HU). From these changes, pancreatic fat reduction was successfully brought by LSG. Based on these weight loss effects, we conducted that LSG had dramatically reduced the perioperative risk factors of LSPDP. Due to the improvement in his hypertension, the attending physician advised the patient he could discontinue all antihypertensive medications. We also evaluated metabolic effects, because the reduction of the pancreas parenchyma was the most concerning factor in relation to T2D onset after LSPDP. The results of a 75-g oral glucose tolerance test at baseline and 6 months after LSG are shown in Fig.. The time to peak glucose level changed from 60 to 30 min, and the time to peak immunoreactive insulin level changed from 90 to 30 min, respectively. In addition, the homeostatic model assessment of insulin resistance (2.6 to 0.5) and insulinogenic index scores (1.26 to 2.45) improved dramatically. Based on these evaluations, we confirmed a dramatic improvement in both insulin resistance and the recovery of islet β cell function. Therefore, we deemed the reduction of risk factors sufficient and decided to perform LSPDP for PNET-G1 as a second-stage surgery. Under general anesthesia, the patient was placed in the right semi-lateral position. Carbon dioxide pneumoperitoneum pressure was set at 10 mmHg, and we inserted 4 trocars in total. For this LSPDP, we had to preserve the splenic vessels, because we had already transected the short gastric vessels during LSG. As there were some adhesions between the gastric sleeve and the omentum, we separated these adhesions and confirmed the pancreas mass. We then dissected and mobilized the caudal side of the pancreas body and tail. We dissected and taped the splenic artery at the suprapancreatic side and mobilized the pancreas body while transecting small branches of the splenic vessels. After confirming the tumor location by ultrasonography, we compressed the pancreas for 3 min and transected it using a linear stapler (Endo GIA™ 60 mm Articulating Extra Thick Reinforced Reload with Tri-Staple™ Technology, Medtronic plc, Dublin, Ireland). The operating time and blood loss were 257 min and 70 mL, respectively. Histopathological examination revealed that the tumor was compatible with PNET-G1 being 14 × 11 mm in size on the basis of no mitosis being observed and a very low Ki-67 proliferation index (1.15%). Immunohistochemical staining also revealed that the tumor was positive for chromogranin A, synaptophysin, and CD56. The postoperative course was unremarkable. Postoperative enhanced CT examination revealed that there were not any splenic/portal vein thrombi. The patient was discharged on postoperative day 14 without symptomatic POPF. During 6 months of the follow-up, no recurrence or T2D onset were observed after LSPDP.