Abdominal adiposity and liver fat content 3 and 12 months after gastric banding surgery.

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.

Rapid significant weight loss and regional lipid deposition: Implications for insulin sensitivity.

AIM: To compare regional lipid deposition and insulin sensitivity after differing weight loss strategies: very low calorie diet (VLCD) and laparoscopic adjustable gastric banding (LAGB). METHOD: Thirty-nine obese women underwent anthropometry, proton magnetic resonance (MR) spectroscopy for assessment of liver fat (LFAT) and MR imaging for visceral (VAT) and subcutaneous abdominal fat volume (SAT) determination. Fasting blood was taken for insulin, glucose and free fatty acid (FFA) analysis. Measurements were repeated after 6-weeks Optifast VLCD (n = 14) or 3 months after LAGB (n = 25). RESULTS: Similar, significant (p < 0.001) weight loss occurred after VLCD (8%) and LAGB (9%). Both interventions induced significant (p < 0.001) and similar reductions in body mass index (BMI) and waist circumference, and in SAT and VAT (VLCD p < 0.05, LAGB p < 0.001). LFAT fell only after VLCD (p < 0.05). Plasma FFA only fell after LAGB (p < 0.05). Homeostasis model assessment (HOMA-R) improved only following VLCD (p < 0.05). No relations were detected between the changes in LFAT, VAT and SAT. The change in LFAT related to the change in HOMA-R in both interventions combined (r = 0.410, p = 0.013) and in the VLCD group (r = 0.660, p = 0.020). There was no change in relative dietary fat intake after LAGB (p = 0.11). CONCLUSION: Caloric and fat restriction for 6 weeks (VLCD) reduces weight, SAT, VAT, LFAT and HOMA-R. Less severe caloric restriction for 12 weeks (LAGB) causes significant loss of weight, VAT and SAT but no detectable change in LFAT and HOMA-R. Following weight loss, a change in LFAT is related more to changes in insulin sensitivity or dietary fat than to abdominal adiposity loss.

The early effects of weight loss surgery on regional adiposity.

BACKGROUND: Weight loss beyond 6 months following laparoscopic adjustable gastric banding (LAGB) is associated with a preferential mobilization of visceral adipose tissue and an improvement in insulin sensitivity in insulin resistant subjects. Because the rate of weight loss is greatest in the first 3 months after LAGB, we investigated the impact of LAGB on changes in regional lipid deposition and insulin sensitivity over this period. METHODS: 10 female obese non-diabetic subjects underwent magnetic resonance (MR) imaging and spectroscopy before and 12 weeks after LAGB (using the Swedish band), for the quantification of abdominal subcutaneous and visceral adipose tissue areas and intrahepatic lipid. Fasting blood free fatty acids were analyzed. Insulin sensitivity was monitored by fasting insulin and homeostasis model assessment (HOMA). RESULTS: Median weight loss 12 weeks after gastric banding was 9.5 kg [interquartile range (IQR): -16.5 to -6]. There were significant reductions in median abdominal subcutaneous (-20% [IQR: -24 to -13]) and visceral (-15% [IQR: -49 to -8]) adipose tissue depots as well as plasma free fatty acids (-34% [IQR: -79 to -8]). The amount of weight lost was directly proportional to the initial BMI (r=0.778; P=0.008). Visceral fat loss was proportional to initial visceral adiposity (r=0.80, P=0.01). There was no significant improvement in insulin sensitivity. CONCLUSION: Significant fat loss occurs 3 months after LAGB. The absence of a concurrent improvement in insulin sensitivity may reflect the relatively small reduction in visceral adipose tissue at this stage. Improvement in insulin sensitivity beyond 3 months after LAGB may be due to the continued loss of visceral adipose tissue.