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Leptin production capacity determines food intake and susceptibility to obesity-induced diabetes in Oikawa–Nagao Diabetes-Prone and Diabetes-Resistant mice – published online 19/06/2020

Akira Asai, Mototsugu Nagao, Koji Hayakawa, Teruo Miyazawa, Hitoshi Sugihara, Shinichi Oikawa

Even in the modern ‘obesogenic’ environment of plentiful food supply, not all people become obese by overeating. However, it remains poorly understood what determines individual differences in spontaneous meal size. In this issue, Asai and Nagao et al ( investigate the potential role of leptin production capacity in determining spontaneous meal size and consequent susceptibility to obesity-induced diabetes using selectively bred Oikawa–Nagao Diabetes-Prone (ON-DP) and Diabetes-Resistant (ON-DR) mice. The authors demonstrate that, prior to the development of obesity-induced diabetes, the spontaneously hyperphagic ON-DP mice had a lower circulating leptin level than the control ON-DR mice. ON-DP mice had a lower leptin production capacity in adipose tissue, probably because of the higher DNA methylation level in the Lep promoter region compared with that in ON-DR mice. The authors conclude that leptin production capacity, especially before the development of obesity, may have diagnostic potential for predicting individual risk of obesity and future onset of type 2 diabetes.

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