2022
DOI: 10.1016/j.sleep.2022.03.017
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Distribution of leptin receptors in the brain stem: possible route in the pathophysiology of neuromuscular control of airway resistance during sleep

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Cited by 6 publications
(3 citation statements)
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“…Leptin is a kind of hormones produced and secreted by adipose tissue that can bind to leptin receptors across the blood-brain barrier. Leptin receptors are mainly located in brain regions related to emotional control, such as the hippocampus, hypothalamus, and cerebral cortex, and they are partly found in serotonergic neurons in the brainstem [ 31 ]. The binding of leptin to the leptin receptor lead to changes in the structure and function of the hippocampus and the cerebral cortex to regulate the bodys’ mood [ 32 ].…”
Section: Discussionmentioning
confidence: 99%
“…Leptin is a kind of hormones produced and secreted by adipose tissue that can bind to leptin receptors across the blood-brain barrier. Leptin receptors are mainly located in brain regions related to emotional control, such as the hippocampus, hypothalamus, and cerebral cortex, and they are partly found in serotonergic neurons in the brainstem [ 31 ]. The binding of leptin to the leptin receptor lead to changes in the structure and function of the hippocampus and the cerebral cortex to regulate the bodys’ mood [ 32 ].…”
Section: Discussionmentioning
confidence: 99%
“…LP plays a crucial role in the regulation of hunger, appetite, satiety, energy balance, as well as glucose and lipid metabolism ( 4 , 5 ). Furthermore, LP also possesses the ability to modulate the diameter of the respiratory tract and contribute to the regulation of respiratory function ( 6 ). Studies have demonstrated that a considerable number of neurons implicated in the regulation of respiration possess long subtypes of leptin receptor (LepRb), namely within the nucleus of the solitary tract (NTS) and the dorsal medial hypothalamic nucleus ( 7 ).…”
Section: Introductionmentioning
confidence: 99%
“…CIH, independently of obesity, was shown to increase circulating insulin levels in Wistar rats (Olea et al., 2014; Sacramento et al., 2016) and mice (Wang et al., 2013), an effect that can be attributed to pancreatic β‐cell dysfunction and associated with a decrease in insulin content in CIH‐exposed β‐cells, and with increased proinsulin levels (Wang et al., 2013). Moreover, CIH increased leptin levels in Wistar and Sprague–Dawley rats (Ciriello et al., 2022; He et al., 2014; Olea et al., 2014), effects that were exacerbated by obesity (Martins et al., 2022; Olea et al., 2014) and decrease adiponectin levels (He et al., 2014; Thorn et al., 2017). Accumulating evidence suggests that hyperinsulinaemia and hyperleptinaemia and the consequent insulin and leptin resistance in CIH/OSA contributes to its cardiometabolic consequences either by promoting weight gain by deregulating satiety pathways (Ciriello et al., 2022) or by inducing oxidative stress and inflammation (for a review see Berger & Polotsky, 2018) or even through deregulation of sympathetic activity (Phillips et al., 2000).…”
Section: Introductionmentioning
confidence: 99%