ECE2016 Guided Posters Obesity (10 abstracts)
1University Medical Center Schleswig-Holstein, Department of Internal Medicine I, Kiel, Germany; 2University Medical Center Schleswig-Holstein, Department of Neuroradiology, Kiel, Germany; 3University Medical Center Cologne, Department of Nuclear Medicine, Cologne, Germany.
Introduction: Obesity is associated with hypothalamic inflammation (HI) in animal models. While MRI studies in humans also found an increased intensity in the MBH in obese subjects, it remains unclear (1) if HI causes neuronal death and (2) if HI reverses during weight loss.
Patients and methods: n=50 obese subjects and n=50 age- and sex-matched controls where examined. MRI scans including spectroscopy were performed. Also, detailed nutritional questionnaires, serum lipidomics, 16s rRNA microbiome sequencing data as well as array-based genotyping data were obtained. n=10 obese subjects underwent bariatric surgery followed by a second MRI.
Results: Obese subjects exhibit an increased intensity in the left, but not the right MBH compared to non-obese controls. The NAA/Cr ratio, a marker for neuronal cell count in spectroscopy, did not differ between the two groups indicating that the number of neurons might not be affected by the inflammatory process. After bariatric surgery, BMI and HOMA showed a significant improvement in the mean follow-up time of 3 months. However, the MRI intensity in the MBH did not change in the same time period, suggesting that bariatric surgery might not beneficially affect HI.
Conclusion: Obese human subjects exhibit an increased MRI intensity of the MBH suggesting HI. While HI is not reversed by a significant weight loss due to bariatric surgery, the finding that the number of neurons is not altered in the MBH by HI might suggest that the function of the MBH in terms of appetite regulation might be reversible.