Abstract
AIMS/HYPOTHESIS: Intra-abdominal transplantation of non-visceral adipose tissue in rodents, simulating increased abdominal fat in obesity, paradoxically improves glucose tolerance and insulin sensitivity. We hypothesised that this improvement is due to transplant-induced enhanced uptake of fatty acids by adipose tissue, thus reducing fatty acid flux into, and triacylglycerol storage in, the liver. METHODS: In Experiment 1, mice were sham-operated or received heterologous epididymal white adipose tissue (WAT; EWAT) or visceral WAT (VWAT) transplantation to the portal and splanchnic circulation regions in the visceral cavity. In Experiment 2, inguinal WAT (IWAT) or EWAT was removed and subsequently transplanted to the visceral cavity of the same mouse (autotransplant). IWAT and EWAT autotransplants were repeated in Experiment 3 and compared with heterotransplants. RESULTS: Heterotransplantation of VWAT did not alter glucose tolerance, whereas auto- or hetero-transplantation of EWAT or IWAT significantly improved glucose tolerance. Transplantation-induced improvements in glucose tolerance 4 weeks after surgery coincided with decreased liver triacylglycerol, decreased portal plasma lipids and increased hepatic insulin sensitivity. By 8 weeks, these changes were apparent only in mice with autotransplantation. Heterologous EWAT transplantation-induced glucose improvement persisted without altered liver metabolism. CONCLUSIONS/INTERPRETATION: Increases in visceral fat, via transplantation of visceral or non-visceral adipose tissue, is not a major risk factor for glucose intolerance. In fact, there are dynamic metabolic improvements following transplantation that include decreased portal lipids and improved liver metabolism, but these improvements are transient under certain circumstances.