Reduction in total plasma ghrelin levels following catecholamine depletion: Relation to bulimic and depressive symptoms

Homan, Philipp; Grob, Simona; Milos, Gabriella; Schnyder, Ulrich; Hasler, Gregor

doi:10.1016/j.psyneuen.2012.12.024

Cited by 13 publications

(9 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The high gastric ghrelin cell β1AR expression, coupled with previous reports identifying gastric ghrelin cells as the predominant source of circulating ghrelin [45] and atenolol as a β1AR-selective β-blocker with a hydrophilic nature that restricts its actions to the periphery, suggest that the current finding of atenolol-induced lowering of plasma ghrelin in the setting of CSDS is mediated via blocking β1ARs expressed by the gastric ghrelin cells. Also, although not a β-blocker, the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine, which causes transient catecholamine depletion, lowers total plasma ghrelin when administered to human subjects; these reduced total ghrelin levels negatively correlate with depressive symptoms [46].…”

Section: Discussionmentioning

confidence: 99%

β1-adrenergic receptors mediate plasma acyl-ghrelin elevation and depressive-like behavior induced by chronic psychosocial stress

Gupta

Chuang

Mani

et al. 2019

Neuropsychopharmacol.

View full text Add to dashboard Cite

The ghrelin system is a key component of the mood and metabolic responses to chronic psychosocial stress. For example, circulating acyl-ghrelin rises in several rodent and human stress models, administered acyl-ghrelin induces antidepressant-like behavioral responses in mice, and mice with deleted ghrelin receptors (GHSRs) exhibit exaggerated depressive-like behaviors, changed eating behaviors, and altered metabolism in response to chronic stress. However, the mechanisms mediating stressinduced rises in ghrelin are unknown and ghrelin's antidepressant-like efficacy in the setting of chronic stress is incompletely characterized. Here, we used a pharmacological approach in combination with a 10-day chronic social defeat stress (CSDS) model in male mice to investigate whether the sympathoadrenal system is involved in the ghrelin response to stress. We also examined the antidepressant-like efficacy of administered ghrelin and the synthetic GHSR agonist GHRP-2 during and/or after CSDS. We found that administration of the β1-adrenergic receptor (β1AR) blocker atenolol during CSDS blunts the elevation of plasma acyl-ghrelin and exaggerates depressive-like behavior. Neither acute injection of acyl-ghrelin directly following CSDS nor its chronic administration during or after CSDS nor chronic delivery of GHRP-2 during and after CSDS improved stress-induced depressive-like behavior. Thus, β1ARs drive the acyl-ghrelin response to CSDS, but supplementing the natural increases in acyl-ghrelin with exogenous acyl-ghrelin or GHSR agonist does not further enhance the antidepressant-like actions of the endogenous ghrelin system in the setting of CSDS.

show abstract

Section: Discussionmentioning

confidence: 99%

β1-adrenergic receptors mediate plasma acyl-ghrelin elevation and depressive-like behavior induced by chronic psychosocial stress

Gupta

Chuang

Mani

et al. 2019

Neuropsychopharmacol.

View full text Add to dashboard Cite

show abstract

“… 38 Ghrelin, a hormone that has been recognized as an appetite-stimulating peptide, might be involved in the prevention or mitigation of depressive symptoms in animals and humans. 39 – 41 Moreover, both skipping breakfast and eating at night have been characterized as circadian delays in daily food intake that could lead to disrupted sleep. 42 , 43 Participants with such circadian and sleep disturbances are more prone to mood disorders.…”

Section: Discussionmentioning

confidence: 99%

Independent and combined relationship of habitual unhealthy eating behaviors with depressive symptoms: A prospective study

Huang¹,

Momma²,

Chen³

et al. 2017

Journal of Epidemiology

View full text Add to dashboard Cite

BackgroundUnhealthy eating has been found to be associated with the prevalence of depressive symptoms. However, prospective evidence of the combined effects of unhealthy eating and depressive symptoms has not been reported. This study aimed to elucidate the prospective relationship between habitual unhealthy eating habits and depressive symptoms.MethodsA 2-year prospective cohort study of 376 Japanese adults aged 24–83 years without depressive symptoms at baseline was conducted. Information about participants' eating behaviors was obtained via a self-administered questionnaire, in which skipping breakfast, eating dinner shortly before bedtime, and snacking after dinner were recorded. Depressive symptoms were assessed using the Japanese version of the Zung Self-rating Depression Scale.ResultsThe 2-year incidence of depressive symptoms was found to be 23.7% (89/376). Covariate-adjusted multivariate Poisson regression analyses showed that habitual snacking after dinner was significantly associated with the incidence of depressive symptoms (relative risk [RR] 1.77; 95% confidence interval [CI], 1.00–3.14, p = 0.049), whereas no relationship was found between skipping breakfast or eating dinner shortly before bedtime and depressive symptoms. On the other hand, there was an interaction effect of snacking after dinner and dinner before bedtime on depressive symptoms (p for the interaction = 0.044). Participants with more than two unhealthy eating behaviors had a higher incidence of depressive symptoms compared to those with fewer than two unhealthy eating behaviors (RR 1.71; 95% CI, 1.06–2.77, p = 0.028).ConclusionsThis prospective study is the first to reveal the combined relationship between unhealthy eating and the incidence of depressive symptoms.

show abstract

“…The study protocol was approved by the ethics committee of the Canton Zurich. The sample of this study overlaps with the sample of prior published data (22,23). We used a randomized, doubleblind, placebo-controlled, crossover design in which each subject underwent 2 identical sessions separated by at least 7 days in which they received either AMPT or placebo.…”

Section: Methodsmentioning

confidence: 99%

Behavioral Responses to Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa and Healthy Subjects

Grob¹,

Stern

Gamper³

et al. 2015

Biological Psychiatry

Self Cite

View full text Add to dashboard Cite

show abstract

Reduction in total plasma ghrelin levels following catecholamine depletion: Relation to bulimic and depressive symptoms

Cited by 13 publications

References 54 publications

β1-adrenergic receptors mediate plasma acyl-ghrelin elevation and depressive-like behavior induced by chronic psychosocial stress

β1-adrenergic receptors mediate plasma acyl-ghrelin elevation and depressive-like behavior induced by chronic psychosocial stress

Independent and combined relationship of habitual unhealthy eating behaviors with depressive symptoms: A prospective study

Behavioral Responses to Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa and Healthy Subjects

Contact Info

Product

Resources

About