Impaired leptin responsiveness in the nucleus accumbens of leptin-overexpressing transgenic mice with dysregulated sucrose and lipid preference independent of obesity

Hidenari Nomura, Cheol Son, Daisuke Aotani, Yoshiyuki Shimizu, Goro Katsuura, Michio Noguchi, Toru Kusakabe, Tomohiro Tanaka, Takashi Miyazawa, Kiminori Hosoda, Kazuwa Nakao

研究成果: ジャーナルへの寄稿学術誌査読

2 被引用数 (Scopus)

抄録

While hypothalamic leptin resistance can occur prior to establishment of obesity, clarification is needed as to whether the impaired response to leptin in the reward-related nuclei occurs independently of obesity. To answer this question, we attempted to dissociate the normally coexisting leptin resistance from obesity. We investigated phenotypes of leptin-overexpressing transgenic mice fed for 1 week with 60 % high-fat diet (HFD) (LepTg-HFD1W mice). After 1 week, we observed that LepTg-HFD1W mice weighed as same as wild type (WT) mice fed standard chow diet (CD) for 1 week (WT-CD1W mice). However, compared to WT-CD1W mice, LepTg-HFD1W mice exhibited attenuated leptin-induced anorexia, decreased leptin-induced c-fos immunostaining in nucleus accumbens (NAc), one of important site of reward system, decreased leptin-stimulated pSTAT3 immunostaining in hypothalamus. Furthermore, neither sucrose nor lipid preference was suppressed by leptin in LepTg-HFD1W mice. On the contrary, leptin significantly suppressed both preferences in WT mice fed HFD (WT-HFD1 W mice). These results indicate that leptin responsiveness decreases in NAc independently of obesity. Additionally, in this situation, suppressive effect of leptin on the hedonic feeding results in impaired regulation. Such findings suggest the impaired leptin responsiveness in NAc partially contributes to dysregulated hedonic feeding behavior independently of obesity.

本文言語英語
ページ(範囲)94-102
ページ数9
ジャーナルNeuroscience Research
177
DOI
出版ステータス出版済み - 4月 2022
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 神経科学一般

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