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Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
Cold exposure restores the decrease in leptin receptors (OB-Rb) caused by neonatal leptin treatment in 30-day-old
S C P Dutra1, E G Moura, A L Rodrigues
1Department of Physiological Sciences, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Neonatal leptin exposure programs thyroid function, leading to altered responses to cold in adult rats. Cold exposure normalized leptin receptor levels and enhanced thyroid hormone release in leptin-treated rats.
Area of Science:
- Endocrinology
- Metabolism
- Developmental Biology
Background:
- Neonatal leptin treatment influences adult thyroid function.
- Both leptin and thyroid hormones (TH) are involved in thermogenesis.
Purpose of the Study:
- To investigate the effect of cold exposure on thyroid function in neonate rats previously treated with leptin.
- To evaluate the role of leptin receptors (OB-Rb) in mediating thyroid hormone responses to cold.
Main Methods:
- Neonatal rats received leptin or saline injections for 10 days.
- At 30 days old, rats were exposed to cold (8°C) or thermoneutrality (25°C).
- Serum leptin, TH, TSH, liver deiodinase (D1), and mitochondrial glycerol-3-phosphate dehydrogenase (mGPD) activities were measured. Hypothalamic and thyroidal OB-Rb levels were assessed via western blot.
Main Results:
- Leptin-treated rats exhibited hyperleptinemia and lower free tri-iodothyronine (FT3) levels.
- Cold exposure increased thyroid hormones (FT4, FT3) in both leptin-treated and control groups.
- Leptin treatment reduced D1 and mGPD activities, which were restored by cold exposure. OB-Rb levels were decreased by neonatal leptin but normalized with cold exposure.
Conclusions:
- Neonatal leptin programming alters thyroid hormone levels and responses to cold.
- Cold exposure normalizes OB-Rb levels and enhances thyroid hormone response in leptin-programmed rats.
- OB-Rb plays a role in the adaptive thyroid hormone response to cold stress.
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