In a recent Science article Czupryn et al. reported on obesity treatment in leptin-receptor deficient obese mice by restoration of hypothalamic circuitries through neurotransplantation [1]. However, this experimental approach in not novel as the concept already has been developed by several research groups more than a decade ago providing the proof of principle and a wealth of technical details. Surprisingly, the authors of the Science paper did not refer to the previously published data. Indeed, after the initial discovery of the impact of the ventromedial hypothalamus (VMH) in obesity and following extensive use of neurotransplantation as experimental and even clinical approaches in mainly neurodegenerative disorders, such as Parkinson's disease, transplantation of embryonic hypothalamic tissue in obese VMH-lesioned rats were performed and showed anti-obesity effects [2, 3]. Further, hypothalamic transplantation in leptin-receptor deficient obese Zucker rats has also been performed, resulting in substantial decrease in body weight and insulinemia, supporting the restoration of hypothalamic leptin signaling by the grafted neurons [4, 5].
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