sLepR plays a crucial role in regulating circulating leptin levels without increasing leptin transcription in adipose tissue.[37, 38] The levels of sLepR were inversely correlated with obesity and altered glucose and lipid metabolism in humans.[39] In this study, paternally BPA‐exposed offspring also exhibited similar food intake but lower energy expenditure when compared to the controls, suggesting that paternal exposure to BPA attenuated hepatic Lepr signaling and induced leptin resistance in the offspring. The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.