Abstract
In the mouse, the osteoblast-derived hormone Lipocalin-2 (LCN2) suppresses food intake and acts as a satiety signal. This study now shows that a meal challenge increases serum LCN2 levels in humans with normal or overweight, but not in those with obesity. Postprandial LCN2 serum levels correlate inversely with hunger sensation in challenged subjects. Brain PET scans show that injected radiolabelled recombinant human LCN2 (rh-LCN2) crosses the blood-brain barrier and localizes to the hypothalamus. Daily treatment of lean monkeys with rh-LCN2 decreased food intake by 21%, without overt side effects, suggesting that LCN2 may be a novel target for obesity treatment.
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