Diabetologie und Stoffwechsel 2016; 11 - FV10
DOI: 10.1055/s-0036-1580757

Hypothalamic inflammation in humans is not reversed by a profound weight loss and an improved insulin sensitivity due to bariatric surgery

C Kreutzer 1, S Peters 2, DM Schulte 1, K Türk 1, S Wolff 2, A Rohr 2, T Kerby 2, C Riedel 2, T van Eimeren 3, S Schreiber 1, M Laudes 1
  • 1University Medical Center Schleswig-Holstein, Department of Internal Medicine 1, 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, 16 s 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 month. 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.