Orexins, feeding, and energy balance

Girault, Elodie M.; Yi, Chun-Xia; Fliers, Eric; Kalsbeek, Andries

doi:10.1016/b978-0-444-59489-1.00005-7

Cited by 61 publications

(37 citation statements)

References 99 publications

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“…Moreover, orexin-A has pleiotropic effects, including increasing body temperature, heart rate, and blood pressure by stimulating the sympathetic nervous system (9,38). It has been shown that after a central orexin-A injection, body temperature increases and UCP-1 synthesis, which is thought to be a biomarker of peripheral thermogenesis, remains unaffected in mice (38).…”

Section: Orexin-a and Nesfatin-1 In Hyperthyroidismmentioning

confidence: 98%

“…It has been suggested that orexin-A increases both food intake and energy expenditure to prevent weight gain (5). Many publications have shown that orexin-A is related to sleep-wakefulness, arousal, energy balance, narcolepsy, glucose metabolism, gastric ulcers, and thermogenesis (4,(6)(7)(8)(9)(10)(11). The results of animal studies that investigated the relationship of orexin-A with the thyroid axis are contradictory (4,12,13).…”

Section: Introductionmentioning

confidence: 94%

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Circulating Levels of Orexin-A, Nesfatin-1, Agouti-Related Peptide, and Neuropeptide Y in Patients with Hyperthyroidism

Tohma

Aktürk

Altınova

et al. 2015

Thyroid

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Section: Orexin-a and Nesfatin-1 In Hyperthyroidismmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 94%

Circulating Levels of Orexin-A, Nesfatin-1, Agouti-Related Peptide, and Neuropeptide Y in Patients with Hyperthyroidism

Tohma

Aktürk

Altınova

et al. 2015

Thyroid

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show abstract

“…Conceivably, this change might participate in an adaptive mechanism to counteract the energy deficit by increasing OX efficiency. While in fasting experiments [35] , the OXR2 mRNA level remained constant, SWL mice exhibited a tendency to decrease indicative of a differential regulation of the 2 OXRs [36] .…”

Section: Adapted Changes In the Expression Of Hypothalamic Peptides Rmentioning

confidence: 99%

Long-Term Energy Deficit in Mice Causes Long-Lasting Hypothalamic Alterations after Recovery

Méquinion

Thuc²,

Zgheib

et al. 2016

Neuroendocrinology

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Although the short-term effects of fasting or energy deficit on hypothalamic neuropeptide circuitries are now better understood, the effects of long-term energy deficit and refeeding remain to be elucidated. We showed that after a long-term energy deficit,mice exhibited persistent hypoleptinemia following the refeeding period despite restoration of fat mass, ovarian activity, and feeding behavior. We aimed to examine the hypothalamic adaptations after 10 weeks of energy deficit and after 10 further weeks of nutritional recovery. To do so, we assessed the mRNA levels of the leptin receptor and the main orexigenic and anorexigenic peptides, and their receptors regulated by leptin. Markers of hypothalamic inflammation were assessed as leptin can also participate in this phenomenon.Long-term time-restricted feeding and separation induced significant increase in mRNA levels of hypothalamic orexigenic peptides, while both Y1 and Y5 receptor mRNAs were downregulated. No changes occurred in the mRNA levels of orexin (OX), melanin-concentrating hormone, pro-opiomelanocortin, 26RFa (26-amino acid RF-amide peptide), and their receptors despite an increase in the expression of melanocortin receptors (MC3-R and MC4-R) and OXR1 (OX receptor 1). The refeeding period induced an overexpression of leptin receptor mRNA in the hypothalamus. The other assessed mRNA levels were normalized except for Y2, Y5, MC3-R, and MC4-R, which remained upregulated. No convincing changes were observed in neuroinflammatory markers, even if interleukin-1β mRNA levels were increased in parallel with those of Iba1 (ionized calcium-binding adaptor molecule 1), a marker of microglial activation. Normalization of leptin-regulated functions and hypothalamic gene expressions in refed mice with low plasma leptin levels could be sustained by recalibration of hypothalamic sensitivity to leptin.

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“…The complementary functions of these two signaling molecules are crucially involved in regulating metabolism, feeding behavior and sleep/arousal. ORXs stimulate arousal, regulate glucose-lipid homeostasis, and increase energy expenditure [119,120]. Furthermore, disruption or loss of ORX/MCH signaling is associated with obesity and diabetes mellitus [119,120].…”

Section: The Orexin/melanin-concentrating Hormone Neuronal Systemmentioning

confidence: 99%

Circadian Clocks as Modulators of Metabolic Comorbidity in Psychiatric Disorders

Barandas

Landgraf

McCarthy

et al. 2015

Curr Psychiatry Rep

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Psychiatric disorders such as schizophrenia, bipolar disorder, and major depressive disorder are often accompanied by metabolic dysfunction symptoms, including obesity and diabetes. Since the circadian system controls important brain systems that regulate affective, cognitive, and metabolic functions, and neuropsychiatric and metabolic diseases are often correlated with disturbances of circadian rhythms, we hypothesize that dysregulation of circadian clocks plays a central role in metabolic comorbidity in psychiatric disorders. In this review paper, we highlight the role of circadian clocks in glucocorticoid, dopamine, and orexin/melanin-concentrating hormone systems, and describe how a dysfunction of these clocks may contribute to the simultaneous development of psychiatric and metabolic symptoms.3

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Orexins, feeding, and energy balance

Cited by 61 publications

References 99 publications

Circulating Levels of Orexin-A, Nesfatin-1, Agouti-Related Peptide, and Neuropeptide Y in Patients with Hyperthyroidism

Circulating Levels of Orexin-A, Nesfatin-1, Agouti-Related Peptide, and Neuropeptide Y in Patients with Hyperthyroidism

Long-Term Energy Deficit in Mice Causes Long-Lasting Hypothalamic Alterations after Recovery

Circadian Clocks as Modulators of Metabolic Comorbidity in Psychiatric Disorders

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