Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

Blais, Anne; Drouin, Gaëtan; Chaumontet, Catherine; Voisin, Thierry; Couvelard, Anne; Even, Patrick C.; Couvineau, Alain

doi:10.1371/journal.pone.0169908

Cited by 31 publications

(22 citation statements)

References 48 publications

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“…It is plausible that chronic sleep deprivation modified the feeding response to orexin‐A in the VLPO despite the fact that the effect of orexin‐A on feeding was null in rats with sufficient sleep . Finally, we acknowledge divergent effects of central and peripheral orexin‐A therapy on weight gain and energy expenditure. Further work is needed to resolve the specific mechanisms within and external to the VLPO that mediate the reduction in physical activity and its associated EE that leads to weight gain following sleep deprivation due to noise exposure.…”

Section: Discussionmentioning

confidence: 92%

Partial Sleep Deprivation Reduces the Efficacy of Orexin‐A to Stimulate Physical Activity and Energy Expenditure

DePorter

Coborn

Teske

2017

Obesity

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Objective: Sufficient sleep is required for weight maintenance. Sleep deprivation due to noise exposure stimulates weight gain by increasing hyperphagia and reducing energy expenditure (EE). Yet the mechanistic basis underlying the weight gain response is unclear. Orexin-A promotes arousal and negative energy balance, and orexin terminals project to the ventrolateral preoptic area (VLPO), which is involved in sleep-to-wake transitions. To determine whether sleep deprivation reduces orexin function in VLPO and to test the hypothesis that sleep deprivation would attenuate the orexin-A-stimulated increase in arousal, physical activity (PA), and EE. Methods: Electroencephalogram, electromyogram, distance traveled, and EE were determined in male Sprague-Dawley rats following orexin-A injections into VLPO both before and after acute (12-h) and chronic (8 h/d, 9 d) sleep deprivation by noise exposure. Results: Orexin-A in the VLPO significantly increased arousal, PA, total EE, and PA-related EE and reduced sleep and respiratory quotient before sleep deprivation. In contrast to after acute sleep deprivation in which orexin-A failed to stimulate EE during PA only, orexin-A failed to significantly increase arousal, PA, fat oxidation, total EE, and PA-related EE after chronic sleep deprivation. Conclusions: Sleep deprivation may reduce sensitivity to endogenous stimuli that enhance EE due to PA and thus stimulate weight gain.

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Section: Discussionmentioning

confidence: 92%

Partial Sleep Deprivation Reduces the Efficacy of Orexin‐A to Stimulate Physical Activity and Energy Expenditure

DePorter

Coborn

Teske

2017

Obesity

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“…Metabolic products that are produced in peripheral organs, such as estrogen, insulin, cortisol, and leptin, can cross the blood–brain barrier (BBB) and influence cognitive function. However, neuropeptides such as orexin (mice), allastostatin (drosophila), and neuropeptide Y (grass carp) modulate metabolic processes in different animals [ 26 ]. In a recent review, Yi et al suggested that neuropeptide Y receptors in humans can be a promising target for metabolic disorders [ 27 ].…”

Section: Relationship Between Metabolic Disorder and Alzheimer’s Dmentioning

confidence: 99%

Adiponectin: The Potential Regulator and Therapeutic Target of Obesity and Alzheimer’s Disease

Kim

Barua

Jeong

et al. 2020

IJMS

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Animal and human mechanistic studies have consistently shown an association between obesity and Alzheimer’s disease (AD). AD, a degenerative brain disease, is the most common cause of dementia and is characterized by the presence of extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles disposition. Some studies have recently demonstrated that Aβ and tau cannot fully explain the pathophysiological development of AD and that metabolic disease factors, such as insulin, adiponectin, and antioxidants, are important for the sporadic onset of nongenetic AD. Obesity prevention and treatment can be an efficacious and safe approach to AD prevention. Adiponectin is a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation. It has been shown to be inversely correlated with adipose tissue dysfunction and may enhance the risk of AD because a range of neuroprotection adiponectin mechanisms is related to AD pathology alleviation. In this study, we summarize the recent progress that addresses the beneficial effects and potential mechanisms of adiponectin in AD. Furthermore, we review recent studies on the diverse medications of adiponectin that could possibly be related to AD treatment, with a focus on their association with adiponectin. A better understanding of the neuroprotection roles of adiponectin will help clarify the precise underlying mechanism of AD development and progression.

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“…Previous studies showed that in human adipocytes isolated from subcutaneous, compared with intra-abdominal, adipose tissue, orexin-A is able to reduce adipogenesis in intra-abdominal but not subcutaneous adipocytes [15]. These results have been recently reinforced by the evidence of a small but significant reduction of visceral fat mass (FM) in orexin-A-treated mice not paralleled by differences in the subcutaneous fat, suggesting a lower sensitivity to orexin-A [16].…”

Section: Introductionmentioning

confidence: 96%

Effects of Very Low Calorie Ketogenic Diet on the Orexinergic System, Visceral Adipose Tissue, and ROS Production

et al. 2019

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Background: Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, thus influencing adipose tissue accumulation. Therapeutic diets in obesity treatment may combine the advantages of caloric restriction and dietary ketosis. The current study aimed to evaluate the effect of a very low calorie ketogenic diet (VLCKD) in a population of obese patients. Methods: Adiposity parameters and orexin-A serum profiling were quantified over an 8 week period. The effect of the VLCKD on reactive oxygen species (ROS) production and cell viability was evaluated, in vitro, by culturing Hep-G2 cells in the presence of VLCKD sera. Results: Dietary intervention induced significant effects on body weight, adiposity, and blood chemistry parameters. Moreover, a selective reduction in VAT was measured by dual-energy X-ray absorptiometry. Orexin-A levels significantly increased after dietary treatment. Hep-G2 cell viability was not affected after 24, 48, and 72 h incubation with patients’ sera, before and after the VLCKD. In the same model system, ROS production was not significantly influenced by dietary treatment. Conclusion: The VLCKD exerts a positive effect on VAT decrease, ameliorating adiposity and blood chemistry parameters. Furthermore, short-term mild dietary ketosis does not appear to have a cytotoxic effect, nor does it represent a factor capable of increasing oxidative stress. Finally, to the best of our knowledge, this is the first study that shows an effect of the VLCKD upon the orexinergic system, supporting the usefulness of such a therapeutic intervention in promoting obesity reduction in the individual burden of this disease.

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Impact of Orexin-A Treatment on Food Intake, Energy Metabolism and Body Weight in Mice

Cited by 31 publications

References 48 publications

Partial Sleep Deprivation Reduces the Efficacy of Orexin‐A to Stimulate Physical Activity and Energy Expenditure

Partial Sleep Deprivation Reduces the Efficacy of Orexin‐A to Stimulate Physical Activity and Energy Expenditure

Adiponectin: The Potential Regulator and Therapeutic Target of Obesity and Alzheimer’s Disease

Effects of Very Low Calorie Ketogenic Diet on the Orexinergic System, Visceral Adipose Tissue, and ROS Production

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