Purpose: Surgical resection of remnant gastric cancer (RGC) is technically challenging and difficult. Minimally invasive surgery (MIS) has been adopted for various procedures, but reports of MIS for RGC remain limited. Herein, we report the surgical techniques and short-term outcomes of MIS for RGC. Methods: We conducted a retrospective cohort study involving 61 consecutive RGC patients who underwent open or minimally invasive (laparoscopic or robotic) total gastrectomy for potentially curable RGC at our institution (January 1999–August 2025). A propensity scorematched cohort was used for an exploratory evaluation of the safety and efficacy of MIS for RGC, focusing on feasibility rather than superiority over open surgery. Results: Of these 61 patients, 53 underwent open surgery and eight underwent MIS gastrectomy for RGC. The median age was 70 years. The cohort comprised 53 men and eight women. The initial procedure was open surgery in 58 patients and MIS in three patients.Propensity score matching showed significantly reduced intraoperative blood loss in the MIS group compared with the open surgery group (39 mL vs. 576 mL, p < 0.05), and significantly longer operation time in the MIS group (352 minutes vs. 297 minutes, p < 0.05). Postoperative hospital stay was significantly shorter in the MIS group (12 days vs. 17 days, p < 0.05). The incidence of postoperative pancreatic fistula was lower in the MIS group, although not significantly different (0% vs. 16.7%). Conclusion MIS, including robotic gastrectomy, is feasible and safe for RGC, with potential perioperative benefits requiring multicenter validation.

BACKGROUND: Mitochondria, which harbor their own genome (mtDNA), have attracted attention due to the potential of mtDNA copy number (mtDNA-CN) as an indicator of mitochondrial dysfunction. Although mtDNA-CN has been proposed as a simple and accessible biomarker for metabolic disorders such as metabolic dysfunction-associated steatotic liver disease, the underlying mechanisms and the causal relationship remain insufficiently elucidated. In this investigation, we combined longitudinal epidemiological data, animal studies, and in vitro assays to elucidate the potential causal relationship between reduced mtDNA-CN and the development of steatotic liver disease (SLD). METHODS: We conducted a longitudinal study using data from a health examination cohort initiated in 1981 in Yakumo, Hokkaido, Japan. Data from examinations performed in 2015 and 2022 were analyzed, focusing on 76 subjects without SLD at baseline (2015) to assess the association between baseline mtDNA-CN and subsequent risk of SLD development. In addition, 28-day-old SD rats were fed ad libitum on a 45% high-fat diet and dissected at 2 and 8 weeks of age. Blood and liver mtDNA-CN were measured and compared at each feeding period. Additionally, in vitro experiments were performed using HepG2 cells treated with mitochondrial function inhibitors to induce mtDNA-CN depletion and to examine its impact on intracellular lipid accumulation. RESULTS: Epidemiological analysis showed that the subjects with low mtDNA-CN had a significantly higher odds ratio for developing SLD compared to high (odds ratio [95% confidence interval]: 4.93 [1.08-22.50]). Analysis of the animal model showed that 8 weeks of high-fat diet led to the development of fatty liver and a significant decrease in mtDNA-CN. A further 2 weeks of high-fat diet consumption resulted in a significant decrease in hepatic mtDNA-CN, despite the absence of fatty liver development, and a similar trend was observed for blood. Complementary in vitro experiments revealed that pharmacologically induced mitochondrial dysfunction led to a significant reduction in mtDNA-CN and was associated with increases in intracellular lipid accumulation in HepG2 cells. CONCLUSIONS Our findings suggest that reduced mtDNA-CN may contribute causally to SLD development and could serve as a convenient, noninvasive biomarker for early detection and risk assessment.
Animals ; DNA, Mitochondrial/genetics* ; Humans ; Male ; DNA Copy Number Variations ; Female ; Fatty Liver/blood* ; Rats ; Middle Aged ; Longitudinal Studies ; Rats, Sprague-Dawley ; Adult ; Japan/epidemiology* ; Aged ; Biomarkers/blood* ; Hep G2 Cells ; Diet, High-Fat/adverse effects*