Beyond incretins: targeting neurokinin receptors for obesity treatment

A recent study in Nature identifies the neurokinin 2 receptor (NK2R), as a promising new target for treating obesity.  Through analyses of various existing human genetic association data, NK2R has been identified as a potential regulator of energy homeostasis with variants of this receptor gene being associated with glycaemic traits and obesity-related characteristics across different human populations.  Current obesity treatments target incretin receptors, but unlike incretin therapies that primarily affect food intake and insulin secretion, activation of NK2R was found to regulate both food intake (through neuronal signaling) and energy expenditure (probably through peripheral mechanisms).

A specific and long asting peptide activator for NK2R, EB1002, was deployed, which in diet induced obese mice reduces food intake and body weight (mainly fat mass), and improves insulin sensitivity, while increasing energy expenditure.  The mechanism appears to be partially dependent on the MC4R pathway but independent of leptin signaling.   EB1002 similarly reduces food intake, insulin levels, and body weight in obese macaques with effects even in diabetic individuals.

Targeting NK2R offers a novel strategy with a dual benefit of controlling appetite and boosting metabolism, and offers a potential new avenue for obesity treatment.

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