Long-chain fatty acid uptake is upregulated in omental adipocytes from patients undergoing bariatric surgery for obesity

SUBJECTS: A total of 10 obese patients (BMI 49.8711.9 (s.d.) kg/m 2 ) undergoing laparoscopic bariatric surgery, and 10 nonobese subjects (BMI 24.272.3 kg/m 2 ) undergoing other clinically indicated laparoscopic abdominal surgical procedures. MEASUREMENTS: Cell size distribution and [ 3 H]oleic acid uptake kinetics were studied in adipocytes isolated from omental fat biopsies obtained during surgery. Adipocyte surface area (SA) was calculated from the measured cell diameters. Plasma leptin and insulin concentrations were measured by RIA in fasting blood samples obtained on the morning of surgery. RESULTS: The mean SA of obese adipocytes (41 50875381m 2 /cell) was increased 2.4-fold compared to that of nonobese adipocytes (16 92876529m 2 /cell; Po0.01). LCFA uptake in each group was the sum of saturable and nonsaturable components. Both the Vmax of the saturable component (21.376.3 vs 5.171.9 pmol/s/50 000 cells) and the rate constant k of the nonsaturable component (0.01570.002 vs 0.006670.0023 ml/s/50 000 cells) were increased (Po0.001) in obese adipocytes compared with nonobese controls. When expressed relative to cell size, Vmax/m 2 SA was greater in obese than nonobese adipocytes (Po0.05), whereas k/m 2 SA did not differ between the groups. CONCLUSION: The data support the concepts that (1) adipocyte LCFA uptake consists of distinct facilitated (saturable) and diffusive processes; (2) increased saturable LCFA uptake in obese adipocytes is not simply a consequence of increased cell size, but rather reflects upregulation of a facilitated transport process; and (3) the permeability of adipocyte plasma membranes to LCFA is not appreciably altered by obesity, and increased nonsaturable uptake in obese adipocytes principally reflects an increase in cell SA. Regulation of saturable LCFA uptake by adipocytes may be an important control point for body adiposity.