Body Weight, Metabolism, and Clock Genes

doi:10.1201/b17253-9

Cited by 4 publications

(4 citation statements)

References 73 publications

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“…In addition to their important role regulating metabolic activity in the periphery, there are profound interactions between GCs and appetite control . Feeding is a major synchroniser of HPA axis rhythmicity , and the amount of food ingested is associated with GC secretion . Reciprocally, increased food intake and body weight gain in humans are associated with increases in circulating GCs associated with the therapeutic administration of GCs or Cushing's disease .…”

Section: Gcs In the Control Of Food Intakementioning

confidence: 99%

Novel Aspects of Glucocorticoid Actions

Uchôa

Aguilera

Herman

et al. 2014

J Neuroendocrinology

125

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Normal hypothalamic-pituitary-adrenal (HPA) axis activity leading to rhythmic and episodic release of adrenal glucocorticoids is essential for body homeostasis and survival during stress. Acting through specific intracellular receptors in the brain and periphery, glucocorticoids regulate behavior, metabolic, cardiovascular, immune, and neuroendocrine activities. In contrast to chronic elevated levels, circadian and acute stress-induced increases in glucocorticoids are necessary for hippocampal neuronal survival and memory acquisition and consolidation, through inhibiting apoptosis, facilitating glutamate transmission and inducing immediate early genes and spine formation. In addition to its metabolic actions leading to increasing energy availability, glucocorticoids have profound effects on feeding behavior, mainly through modulation of orexigenic and anorixegenic neuropeptides. Evidence is also emerging that in addition to the recognized immune suppressive actions of glucocorticoids by counteracting adrenergic proinflammatory actions, circadian elevations have priming effects in the immune system, potentiating acute defensive responses. In addition, negative feedback by glucocorticoids involves multiple mechanisms leading to limiting HPA axis activation and preventing deleterious effects of excessive glucocorticoid production. Adequate glucocorticoid secretion to meet body demands is tightly regulated by a complex neural circuitry controlling hypothalamic corticotrophin releasing hormone (CRH) and vasopressin secretion, the main regulators of pituitary adrenocorticotrophic hormone (ACTH). Rapid feedback mechanisms, likely involving non-genomic actions of glucocorticoids, mediate immediate inhibition of hypothalamic CRH and ACTH secretion, while intermediate and delayed mechanisms mediated by genomic actions involve modulation of limbic circuitry and peripheral metabolic messengers. Consistent with their key adaptive roles, HPA axis components are evolutionarily conserved, being present in the earliest vertebrates. Understanding these basic mechanisms may lead to novel approaches for the development of diagnostic and therapeutic tools for disorders related to stress and alterations of glucocorticoid secretion.

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Section: Gcs In the Control Of Food Intakementioning

confidence: 99%

Novel Aspects of Glucocorticoid Actions

Uchôa

Aguilera

Herman

et al. 2014

J Neuroendocrinology

125

View full text Add to dashboard Cite

show abstract

“…see Noguchi et al ; Oitzl et al ; Ridder et al ; Shishkina et al ; Veldhuis et al ). Not only does glucocorticoid secretion lead to increased food seeking and appetite (McEwen ), but food consumption in turn is known to modulate HPA axis function (Leal & Moreira ). In Addison's disease, glucocorticoid levels are low and this is associated with symptomatic anorexia and loss of appetite (Nieman & Chanco Turner ).…”

Section: Part 4: Potential Molecular Mechanisms Underlying Stress Modmentioning

confidence: 99%

Integrated circuits and molecular components for stress and feeding: implications for eating disorders

Hardaway

Crowley

Bulik

et al. 2015

Genes Brain and Behavior

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Eating disorders are complex brain disorders that afflict millions of individuals worldwide. The etiology of these diseases is not fully understood, but a growing body of literature suggests that stress and anxiety may play a critical role in their development. As our understanding of the genetic and environmental factors that contribute to disease in clinical populations like anorexia nervosa, bulimia nervosa and binge eating disorder continue to grow, neuroscientists are using animal models to understand the neurobiology of stress and feeding. We hypothesize that eating disorder clinical phenotypes may result from stress-induced maladaptive alterations in neural circuits that regulate feeding, and that these circuits can be neurochemically isolated using animal model of eating disorders.

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“…Periodic factors, such as light/dark, sleep/wake, food ingestion, rest/activity cycles, and social cues synchronize the circadian rhythms (1)(2)(3). In mammals, the adult circadian oscillators are synchronized by the suprachiasmatic nucleus (SCN), known as "master" clock, which receive direct photic input from the retina by the light/dark cycle.…”

mentioning

confidence: 99%

Postnatal Ontogeny of the Circadian Expression of the Adrenal Clock Genes and Corticosterone Rhythm in Male Rats

et al. 2017

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The postnatal synchronization of the circadian variation of the adrenal clock genes in mammals remains unknown. We evaluated the postnatal ontogeny of daily variation of clock genes (Clock/Bmal1/Per1/Per2/Per3/Cry1/Cry2/Rorα/Rev-Erbα) and steroidogenesis-related genes (Star and Mc2r) in rat adrenals and its relationship with the emergence of plasma corticosterone rhythm using cosinor analysis. Plasma corticosterone circadian rhythm was detected from postnatal day (P)1, with morning acrophase, between zeitgeber time (ZT)0 and ZT2. From P14, there was a nocturnal acrophase of corticosterone at ZT20, which was associated with pups' eye opening. From P3 there was a circadian variation of the mRNA expression of Bmal1, Per2, Per3, and Cry1 genes with morning acrophase, whereas Rev-Erbα had nocturnal acrophase. From P14, Bmal1, Per2, Per3, and Cry1 acrophases advanced by approximately 10 hours, as compared with early neonatal days, becoming vespertine-nocturnal. In all postnatal ages, Per2 and Cry1 circadian profiles were synchronized in phase with the circadian rhythm of plasma corticosterone, whereas Bmal1 was in antiphase. An adult-like Star circadian rhythm profile was observed only from P21. In conclusion, our original data demonstrated a progressive postnatal maturation of the circadian variation of the adrenal clock genes in synchrony with the development of the corticosterone circadian rhythm in rats.

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Body Weight, Metabolism, and Clock Genes

Cited by 4 publications

References 73 publications

Novel Aspects of Glucocorticoid Actions

Novel Aspects of Glucocorticoid Actions

Integrated circuits and molecular components for stress and feeding: implications for eating disorders

Postnatal Ontogeny of the Circadian Expression of the Adrenal Clock Genes and Corticosterone Rhythm in Male Rats

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