Brain free fatty acid uptake is elevated in morbid obesity, and is irreversible 6 months after bariatric surgery: A positron emission tomography study

Aim: To investigate whether there are differences in brain fatty acid uptake (BFAU) between morbidly obese and lean subjects, and the effect of weight loss following bariatric surgery. Materials and methods: We measured BFAU with 14(R, S)-[18F]fluoro-6-thia-heptadecanoic acid and positron emission tomography in 24 morbidly obese and 14 lean women. Obese subjects were restudied 6 months after bariatric surgery. We also assessed whether there was hypothalamic neuroinflammation in the obese subjects using fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging. Results: Obese subjects had a higher BFAU than lean subjects (1.12 [0.61] vs. 0.72 [0.50] μmol 100 g−1 min−1, P = 0.0002), driven by higher fatty acid uptake availability. BFAU correlated positively with BMI (P = 0.006, r = 0.48), whole body fatty acid oxidation (P = 0.006, r = 0.47) and leptin levels (P = 0.001, r = 0.54). When BFAU, leptin and body mass index (BMI) were included in the same model, the association between BFAU and leptin was the strongest. BFAU did not correlate with FLAIR-derived estimates of hypothalamic inflammation. Six months after bariatric surgery, obese subjects achieved significant weight loss (−10 units of BMI). BFAU was not significantly changed (1.12 [0.61] vs. 1.09 [0.39] μmol 100 g−1 min−1, ns), probably because of the ongoing catabolic state. Finally, baseline BFAU predicted worse plasma glucose levels at 2 years of follow-up. Conclusions: BFAU is increased in morbidly obese compared with lean subjects, and is unchanged 6 months after bariatric surgery. Baseline BFAU predicts worse plasma glucose levels at follow-up, supporting the notion that the brain participates in the control of whole-body homeostasis.