Weight loss after laparoscopic adjustable gastric banding surgery (LAGB) is associated with mobilization of adipose tissue from a variety of depots. We sought to evaluate and relate abdominal and hepatic lipid deposition in an obese female population 3 and 12 months after LAGB. We related changes in these depots to markers of insulin sensitivity. Eighteen female obese subjects underwent magnetic resonance imaging and spectroscopy before and 3 and 12 months after LAGB for the quantification of abdominal subcutaneous (ABSAT) and visceral (VAT) adipose tissue areas and liver fat content (LFAT). Fasting blood free fatty acids (FFA) were analyzed. Insulin sensitivity was assessed by the homeostasis model assessment of insulin resistance index (HOMA-R). Mean weight loss 3 and 12 months after LAGB was 9.8 +/- 1.1 kg and 20.0 +/- 2.2 kg, respectively. Postoperatively, VAT area loss exceeded ABSAT area loss in the cohort as a whole and when divided according to preoperative liver fat stores. Three months after LAGB, reductions had occurred in VAT and ABSAT areas (both P < .01) and in FFA (P < .05). Twelve months after LAGB, further significant reductions (P < .01) occurred in VAT and ABSAT areas but not in FFA. No significant reduction occurred in LFAT at either time point in the group as a whole. In those with preoperative hepatic steatosis (LFAT > approximately 5%, n = 7), LFAT fell by 42% (P = .036) 3 months after LAGB, with a total reduction of 50% (P = .027 cf baseline) occurring by 12 months. There was an improvement in HOMA-R at 12 months (1.9 +/- 0.3 cf 2.9 +/- 0.5 at baseline, P = .04) but not 3 months (2.7 +/- 0.4). Preoperatively, LFAT related significantly to VAT area (r = 0.67, P = .003) and HOMA-R (r = 0.497, P = .04) but not ABSAT area. Postoperatively at both 3 and 12 months, LFAT continued to relate to VAT area (r = 0.63, P < .01 at both time points) but not HOMA-R. The changes in LFAT and VAT area were unrelated postoperatively. Abdominal adipose tissue loss was greater from the visceral than subcutaneous depots, suggesting that insulin sensitivity may not be an important determinant of selective lipid depot loss. The lack of a significant change in liver fat in the group as a whole may relate to low preoperative liver fat stores and to high postoperative dietary fat intakes. Preoperative liver fat stores did not influence insulin sensitivity or abdominal lipid changes during weight loss. Liver fat content and VAT area interrelated more closely than either related to ABSAT area, suggesting differing regulatory pathways for fat mobilization from ABSAT and VAT depots but possibly similar pathways for storage and mobilization of fat in the liver and viscerally.