Journal
JOURNAL OF PINEAL RESEARCH
Volume 67, Issue 2, Pages -Publisher
WILEY
DOI: 10.1111/jpi.12580
Keywords
leptin receptor; leptin resistance; melatonin; melatonin receptor 1; metabolism; obesity
Categories
Funding
- NEI NIH HHS [R01 EY026291] Funding Source: Medline
- NHLBI NIH HHS [T32 HL103104] Funding Source: Medline
- NIH HHS [T-103104, EY026291, GM116760] Funding Source: Medline
- NIMHD NIH HHS [G12 MD007602, R25 MD007589] Funding Source: Medline
- NINDS NIH HHS [U54 NS034194] Funding Source: Medline
- Morehouse School of Medicine [S21MD000101, U54RR026137, 5U54NS083932, G12-RR03034] Funding Source: Medline
- Fundação de Amparo à Pesquisa do Estado de São Paulo [2014/50457-0, 2017/02983-2, 2017/01882, 2015/26190-6] Funding Source: Medline
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Recent studies have highlighted the involvement of melatonin in the regulation of energy homeostasis. In this study, we report that mice lacking melatonin receptor 1 (MT1KO) gained more weight, had a higher cumulative food intake, and were more hyperphagic after fasting compared to controls (WT). In response to a leptin injection, MT1KO mice showed a diminished reduction in body weight and food intake. To evaluate hypothalamic leptin signaling, we tested leptin-induced phosphorylation of the signal transducer and activator of transcription 3 (STAT3). Leptin failed to induce STAT3 phosphorylation in MT1KO mice beyond levels observed in mice injected with phosphate-buffered saline (PBS). Furthermore, STAT3 phosphorylation within the arcuate nucleus (ARH) was decreased in MT1KO mice. Leptin receptor mRNA levels in the hypothalamus of MT1KO were significantly reduced (about 50%) compared to WT. This study shows that: (a) MT1 deficiency causes weight gain and increased food intake; (b) a lack of MT1 signaling induces leptin resistance; (c) leptin resistance is ARH region-specific; and (d) leptin resistance is likely due to down-regulation of the leptin receptor. Our data demonstrate that MT1 signaling is an important modulator of leptin signaling.
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