scholarly journals Stress as a potential moderator of ovarian hormone influences on binge eating in women

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 222 ◽  
Author(s):  
Natasha Fowler ◽  
Phuong T. Vo ◽  
Cheryl L. Sisk ◽  
Kelly L. Klump

Previous research has demonstrated significant associations between increased levels of ovarian hormones and increased rates of binge eating (BE) in women. However, whereas all women experience fluctuations in ovarian hormones across the menstrual cycle, not all women binge eat in response to these fluctuations, suggesting that other factors must contribute. Stress is one potential contributing factor. Specifically, it may be that hormone-BE associations are stronger in women who experience high levels of stress, particularly as stress has been shown to be a precipitant to BE episodes in women. To date, no studies have directly examined stress as a moderator of hormone-BE associations, but indirect data (that is, associations between BE and stress and between ovarian hormones and stress) could provide initial clues about moderating effects. Given the above, the purpose of this narrative review was to evaluate these indirect data and their promise for understanding the role of stress in hormone-BE associations. Studies examining associations between all three phenotypes (that is, ovarian hormones, stress, and BE) in animals and humans were reviewed to provide the most thorough and up-to-date review of the literature on the potential moderating effects of stress on ovarian hormone–BE associations. Overall, current evidence suggests that associations between hormones and BE may be stronger in women with high stress levels, possibly via altered hypothalamic–pituitary–adrenal axis response to stress and increased sensitivity to and altered effects of ovarian hormones during stress. Additional studies are necessary to directly examine stress as a moderator of ovarian hormone–BE associations and identify the mechanisms underlying these effects.

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Elisabetta Catalani ◽  
Clara De Palma ◽  
Cristiana Perrotta ◽  
Davide Cervia

Neuropeptides drive a wide diversity of biological actions and mediate multiple regulatory functions involving all organ systems. They modulate intercellular signalling in the central and peripheral nervous systems as well as the cross talk among nervous and endocrine systems. Indeed, neuropeptides can function as peptide hormones regulating physiological homeostasis (e.g., cognition, blood pressure, feeding behaviour, water balance, glucose metabolism, pain, and response to stress), neuroprotection, and immunomodulation. We aim here to describe the recent advances on the role exerted by neuropeptides in the control of autophagy and its molecular mechanisms since increasing evidence indicates that dysregulation of autophagic process is related to different pathological conditions, including neurodegeneration, metabolic disorders, and cancer.


2015 ◽  
Vol 46 (1) ◽  
pp. 27-45 ◽  
Author(s):  
E. Appiah-Kusi ◽  
E. Leyden ◽  
S. Parmar ◽  
V. Mondelli ◽  
P. McGuire ◽  
...  

The aim of this article is to summarize current evidence regarding alterations in the neuroendocrine stress response system and endocannabinoid system and their relationship in psychotic disorders such as schizophrenia. Exposure to stress is linked to the development of a number of psychiatric disorders including psychosis. However, the precise role of stress in the development of psychosis and the possible mechanisms that might underlie this are not well understood. Recently the cannabinoid hypothesis of schizophrenia has emerged as a potential line of enquiry. Endocannabinoid levels are increased in patients with psychosis compared with healthy volunteers; furthermore, they increase in response to stress, which suggests another potential mechanism for how stress might be a causal factor in the development of psychosis. However, research regarding the links between stress and the endocannabinoid system is in its infancy. Evidence summarized here points to an alteration in the baseline tone and reactivity of the hypothalamic–pituitary–adrenal (HPA) axis as well as in various components of the endocannabinoid system in patients with psychosis. Moreover, the precise nature of the inter-relationship between these two systems is unclear in man, especially their biological relevance in the context of psychosis. Future studies need to simultaneously investigate HPA axis and endocannabinoid alterations both at baseline and following experimental perturbation in healthy individuals and those with psychosis to understand how they interact with each other in health and disease and obtain mechanistic insight as to their relevance to the pathophysiology of schizophrenia.


2020 ◽  
pp. 216770262095153 ◽  
Author(s):  
Megan E. Mikhail ◽  
Pamela K. Keel ◽  
S. Alexandra Burt ◽  
Cheryl L. Sisk ◽  
Michael Neale ◽  
...  

Ovarian hormones significantly influence dysregulated eating in females. However, most women do not develop appreciable disordered eating, which suggests that ovarian hormones may not affect all women equally. We examined whether individual differences in trait negative affect (NA) moderate ovarian hormone–dysregulated eating associations in 446 women who provided saliva samples for hormone measurements and ratings of NA and emotional eating daily for 45 consecutive days. Women were at greatest risk for emotional eating when they had high trait NA and experienced a hormonal milieu characterized by low estradiol or high progesterone. Although effects were evident in all women, the combination of high trait NA and high progesterone was particularly risky for women with a history of clinically significant binge-eating episodes. These findings provide initial evidence that affective and hormonal risk interact to promote emotional eating and that effects may be amplified in women with clinically significant binge eating.


2009 ◽  
Vol 101 (6) ◽  
pp. 3192-3198 ◽  
Author(s):  
Matthew R. Campioni ◽  
Ming Xu ◽  
Daniel S. McGehee

Stress hormones released in the CNS following exposure to unavoidable, aversive stimuli have been shown to alter the physiology of neurons in multiple brain regions including hippocampus, amygdala, prefrontal cortex, and ventral tegmental area. The nucleus accumbens (NAc), a motor-limbic interface linked to motivation and reward, receives inputs from each of these stress-affected brain regions, raising the possibility that its function might also be altered in response to stress. To assess potential stress-induced plasticity in the NAc, we exposed adult mice to daily cold water forced swim for 2 consecutive days and conducted electrophysiological experiments assessing glutamate receptor function in brain slices taken 18–24 h following the second swim. We found that AMPA receptor (AMPAR)/ N-methyl-d-aspartate receptor (NMDAR) ratios, a measure of synaptic strength, were increased in the NAc shell but not core medium spiny neurons (MSNs) in stressed animals relative to controls. This effect was blocked by preadministration of glucocorticoid receptor (GR) antagonist RU486, suggesting that the observed changes are dependent on corticosteroid signaling. The role of corticosterone (CORT) in the observed plasticity was confirmed, because exogenous administration of 10 mg/kg CORT also enhanced AMPAR/NMDAR ratios in the NAc shell. The synaptic changes in NAc shell MSNs reflect an enhancement of AMPAR-mediated currents, as we observed increased AMPAR miniature postsynaptic current (mEPSC) amplitude following stress but no change in NMDAR mEPSCs. We hypothesize that altered information processing via plasticity of excitatory inputs might contribute to reward-related behaviors such as stress-induced reinstatement of drug seeking in animals and relapse in humans.


2020 ◽  
Vol 21 (10) ◽  
pp. 3687
Author(s):  
Donata Figaj ◽  
Paulina Czaplewska ◽  
Tomasz Przepióra ◽  
Patrycja Ambroziak ◽  
Marta Potrykus ◽  
...  

The Lon protein is a protease implicated in the virulence of many pathogenic bacteria, including some plant pathogens. However, little is known about the role of Lon in bacteria from genus Dickeya. This group of bacteria includes important potato pathogens, with the most aggressive species, D. solani. To determine the importance of Lon for pathogenicity and response to stress conditions of bacteria, we constructed a D. solani Δlon strain. The mutant bacteria showed increased sensitivity to certain stress conditions, in particular osmotic and high-temperature stresses. Furthermore, qPCR analysis showed an increased expression of the lon gene in D. solani under these conditions. The deletion of the lon gene resulted in decreased motility, lower activity of secreted pectinolytic enzymes and finally delayed onset of blackleg symptoms in the potato plants. In the Δlon cells, the altered levels of several proteins, including virulence factors and proteins associated with virulence, were detected by means of Sequential Window Acquisition of All Theoretical Mass Spectra (SWATH-MS) analysis. These included components of the type III secretion system and proteins involved in bacterial motility. Our results indicate that Lon protease is important for D. solani to withstand stressful conditions and effectively invade the potato plant.


2008 ◽  
Vol 38 (12) ◽  
pp. 1749-1757 ◽  
Author(s):  
K. L. Klump ◽  
P. K. Keel ◽  
K. M. Culbert ◽  
C. Edler

BackgroundSignificant associations between changes in ovarian hormones and binge eating are present across the menstrual cycle in women with bulimia nervosa. However, no study has examined these relationships in a non-clinical sample, despite the need for these data for designing risk-factor studies.MethodIn study 1, we modified several continuous measures of binge eating and identified those that were most sensitive to menstrual-cycle fluctuations in a non-clinical sample of 10 women who completed measures for 35 days. In study 2, we explored associations between ovarian hormones and binge-eating scores in nine women who completed these same measures for 65 days and provided daily saliva samples for assays of estradiol and progesterone concentrations.ResultsIn study 1, the Emotional Eating subscale of the Dutch Eating Behavior Questionnaire exhibited superior reliability and was most sensitive to predicted menstrual-cycle changes in binge eating (i.e. increased scores in the mid-luteal/premenstrual compared with follicular/ovulatory phases). In study 2, this scale showed predicted inverse associations with estradiol and positive associations with progesterone across the menstrual cycle that could not be accounted for by changes in negative affect.ConclusionAssociations between ovarian hormones and binge eating are robust and present in clinical and non-clinical samples. Findings support the ability to examine the role of ovarian hormones as risk factors for binge eating in large-scale prospective studies and twin studies.


2011 ◽  
Vol 300 (1) ◽  
pp. E28-E36 ◽  
Author(s):  
S. M. Herod ◽  
A. M. Dettmer ◽  
M. A. Novak ◽  
J. S. Meyer ◽  
J. L. Cameron

Stress-induced reproductive dysfunction is a relatively common cause of infertility in women. In response to everyday life stress, some individuals readily develop reproductive dysfunction (i.e., they are stress sensitive), whereas others are more stress resilient. Female cynomolgus monkeys, when exposed to mild combined psychosocial and metabolic stress (change in social environment + 20% reduced calorie diet), can be categorized as stress sensitive (SS; they rapidly become anovulatory in response to stress), medium stress resilient (MSR; they slowly become anovulatory in response to prolonged stress), or highly stress resilient (HSR; they maintain normal menstrual cycles in response to stress). In this study, we examined whether increased sensitivity to stress-induced reproductive dysfunction is associated with elevated adrenal axis activity by measuring 1) the diurnal release of ACTH and cortisol, 2) ACTH and cortisol in response to an acute psychological stress, 3) the percent suppression of cortisol in response to dexamethasone negative feedback, 4) the diurnal release of ACTH and cortisol following exposure to mild psychosocial and metabolic stress, 5) the concentration of cortisol in hair, and 6) adrenal weight. SS monkeys ( n = 5) did not differ from MSR ( n = 5) or HSR ( n = 7) monkeys in any measurement of baseline HPA axis activity or the integrated measurements of chronic HPA axis activity. However, MSR + SS monkeys ( n = 10) did secrete more cortisol than HSR monkeys during the daytime hours (1000–1800) following exposure to a novel social environment and reduced diet. We conclude that increased activity of the HPA axis is unlikely to be the primary mechanism causing increased sensitivity to stress-induced reproductive dysfunction.


Reproduction ◽  
2001 ◽  
pp. 493-501 ◽  
Author(s):  
M McLean ◽  
R Smith

Corticotrophin-releasing hormone (CRH), the hypothalamic peptide that controls function of the pituitary-adrenal axis in response to stress, is expressed in abundance in the human placenta and is present in high concentrations in maternal and fetal plasma during late pregnancy. A number of lines of evidence now imply a role for this hormone in the control of parturition and fetal maturation in humans. It has been proposed that CRH, through interactions with oestrogen, adrenal steroids, prostaglandins and oxytocin, establishes positive-feedback loops that initiate parturition and labour. Excessive production of placental CRH has also been linked to preterm labour. However, there are a number of significant gaps in our knowledge of the function of this peptide in pregnancy. This review examines current evidence regarding the putative role of CRH in human parturition.


Physiology ◽  
2006 ◽  
Vol 21 (2) ◽  
pp. 134-145 ◽  
Author(s):  
Kurt R. Stenmark ◽  
Neil Davie ◽  
Maria Frid ◽  
Evgenia Gerasimovskaya ◽  
Mita Das

An increasing volume of experimental data indicates that the adventitial fibroblast, in both the pulmonary and systemic circulations, is a critical regulator of vascular wall function in health and disease. A rapidly emerging concept is that the vascular adventitia acts as biological processing center for the retrieval, integration, storage, and release of key regulators of vessel wall function. In response to stress or injury, resident adventitial cells can be activated and reprogrammed to exhibit different functional and structural behaviors. In fact, under certain conditions, the adventitial compartment may be considered the principal injury-sensing tissue of the vessel wall. In response to vascular stresses such as overdistension and hypoxia, the adventitial fibroblast is activated and undergoes phenotypic changes, which include proliferation, differentiation, upregulation of contractile and extracellular matrix proteins, and release of factors that directly affect medial smooth muscle cell tone and growth and that stimulate recruitment of inflammatory and progenitor cells to the vessel wall. Each of these changes in fibroblast phenotype modulates either directly or indirectly changes in overall vascular function and structure. The purpose of this review is to present the current evidence demonstrating that the adventitial fibroblast acts as a key regulator of pulmonary vascular function and structure from the “outside-in.”


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