UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. There are major changes in progesterone, oestrogen, cortisol and beta-endorphin level associated with parturition, and as all these can be psychoactive it is likely that they contribute to the mood changes that can occur at this time. However evidence for their involvement is, at present, indirect. 2. Postnatal depression itself appears to be a heterogeneous condition with different times of onset, and it is probable that various biological and social factors play a role to a differing degree in different individuals. 3. About half of postnatal depression appears to arise in the first two weeks after childbirth. Some cases follow a period of early euphoria. 4. A different subgroup is associated with thyroid dysfunction, which peaks two to five months postpartum. 5. The tyramine test does not predict vulnerability to postnatal depression. 6. It is suggested that in future research the time course of onset of the depression, and the nature of the mood changes that occur in the first postpartum week, are investigated as possibly relevant variables.
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PMID:Do biochemical factors play a part in postnatal depression? 149 22

The relationships between mood change, obstetric experience and alterations in plasma cortisol, beta-endorphin (beta-EP) and corticotrophin-releasing hormone (CRH) were examined in a prospective study of 97 primiparous Australian women. Psychological measures were administered between the 28th week of pregnancy and the 3rd postnatal month, including the Profile of Mood States (POMS) and the Montgomery Asberg Depressive Rating Scale (MADRS). Blood samples were collected for cortisol, beta-EP and CRH assay on most of these occasions and during labour. Factor analysis was used to identify key subsets of psychological variables for use in the subsequent analyses. 'Mood disturbance' and 'tiredness' factors peaked at 38 weeks' gestation, while 'difficulty falling asleep' was greatest around the time of birth. Cortisol, beta-EP and CRH concentrations rose significantly as pregnancy advanced and peaked at birth; plasma CRH correlated with plasma cortisol (r = 0.54) and beta-EP (r = 0.32). Women with the highest 'mood disturbance' and MADRS depression scores at 28 weeks' gestation received significantly more pain relief during labour. Those women whose mood deteriorated from 38 weeks' gestation to postnatal day 2 had larger falls in plasma beta-EP after delivery (p less than 0.01) than those women whose mood improved or remained constant. Women in this mood-deteriorated subgroup also had significantly higher MADRS depression scores at 3 months (p less than 0.01). Mild antenatal depression (MADRS greater than 13) occurred in 5.2% of women and mild postnatal depression in 4.7%. Overall, these data suggest a role for circulating CRH in the regulation of maternal cortisol secretion and significant relationships between maternal postnatal mood states and beta-EP and between antenatal mood states and obstetric events.
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PMID:Mood changes, obstetric experience and alterations in plasma cortisol, beta-endorphin and corticotrophin releasing hormone during pregnancy and the puerperium. 213 27

The stress system coordinates the adaptive responses of the organism to stressors of any kind.(1). The main components of the stress system are the corticotropin-releasing hormone (CRH) and locus ceruleus-norepinephrine (LC/NE)-autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. CRH inhibits appetite and activates thermogenesis via the catecholaminergic system. Also, reciprocal interactions exist between the amygdala and the hippocampus and the stress system, which stimulates these elements and is regulated by them. CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. Interestingly, all three of these functions receive and depend on positive catecholaminergic input. The end-hormones of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, on the other hand, have multiple roles. They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. In addition, they directly inhibit pituitary gonadotropin, GH and TSH secretion, render the target tissues of sex steroids and growth factors resistant to these substances and suppress the 5' deiodinase, which converts the relatively inactive tetraiodothyronine (T(4)) to triiodothyronine (T(3)), contributing further to the suppression of reproductive, growth and thyroid functions. They also have direct as well as insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome X) and direct effects on the bone, causing "low turnover" osteoporosis. Central CRH, via glucocorticoids and catecholamines, inhibits the inflammatory reaction, while directly secreted by peripheral nerves CRH stimulates local inflammation (immune CRH). CRH antagonists may be useful in human pathologic states, such as melancholic depression and chronic anxiety, associated with chronic hyperactivity of the stress system, along with predictable behavioral, neuroendocrine, metabolic and immune changes, based on the interrelations outlined above. Conversely, potentiators of CRH secretion/action may be useful to treat atypical depression, postpartum depression and the fibromyalgia/chronic fatigue syndromes, all characterized by low HPA axis and LC/NE activity, fatigue, depressive symptomatology, hyperalgesia and increased immune/inflammatory responses to stimuli.
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PMID:Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. 1237 95

This review examines proposed endocrine-based etiologies of postpartum depression (PPD) and how knowledge of these etiologies may affect future treatments. It is based on a review of papers shedding light on the etiology of PPD with special emphasis on research into endocrine-related depression. A picture of PPD is starting to emerge that suggests a variety of endocrine root causes as well as psychosocial risk factors. Hormones reviewed include progesterone, estradiol and estriol, cortisol, corticotropin-releasing hormone, prolactin, thyroid-stimulating hormone and triiodothyronine/thyroxine. Other substances examined include 3 antithyroid autoantibodies. Better understanding of the physiologic bases for depressive symptoms may lead to correction of the underlying pathology of PPD rather than treatment of symptoms.
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PMID:Endocrine factors and postpartum depression. A selected review. 1285 9

Postpartum depression (PPD) affects at least 10% to 15% of postpartum women, including more than 600,000 American mothers in 2003 alone. Dramatic changes in the hypothalamic-pituitary-adrenal (HPA) system in the transition from pregnancy to postpartum coupled with research on the psychobiology of depression provided the foundation for this study. The purpose of this study was to compare the reactivity and regulation of the HPA axis components, adrenocorticotropic hormone (ACTH) and cortisol, in depressed and nondepressed postpartum women. A comparative, longitudinal study design was used with 22 normal, healthy, nondepressed pregnant women. Physiologic and postpartum depression data were collected at 6 and 12 weeks postpartum at a university clinical research center. Maximal treadmill exercise stimulated plasma ACTH and serum cortisol levels which were measured before, during, and after 20 min of exercise. Postpartum depression was measured with the Postpartum Depression Screening Scale. Lag within-subject ACTH levels predicting cortisol regression slopes were significantly different between the depressed and nondepressed groups at both 6 and 12 weeks. The depressed group showed no relationship between their ACTH and cortisol levels, with higher ACTH and lower cortisol levels when compared with the nondepressed group. The expected regulated relationship with cortisol levels rising in response to rising ACTH levels was found in the non-depressed group. These findings indicate that the HPA axis was dysregulated in the depressed group, but regulated in the nondepressed group at 6 and 12 weeks postpartum. This pattern of higher ACTH levels to stimulate less cortisol is similar to patterns found in women with early life stresses.
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PMID:Dysregulation of the hypothalamic-pituitary-adrenal axis in postpartum depression. 1717 20

The endogenous opioid system is involved in modulating a number of behavioral and physiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis. In humans, a functional variant in the OPRM1 gene (OPRM1 A118G) is associated with a number of outcomes, including attenuated HPA axis responses to stress. A nonsynonymous variant (OPRM1 C77G) in the rhesus macaque has been shown to have similar effects in vivo to the human variant. The current study investigated whether OPRM1 C77G influences HPA axis response to stress in rhesus macaques. We analyzed plasma adrenocorticotropic hormone (ACTH) and cortisol levels measured in response to three different stressors: (1) maternal separation in infant subjects at 6 months of age, (2) acute ethanol administration in adolescent subjects at 4 years of age, and (3) postpartum HPA axis function in adult rhesus macaque females. For the maternal separation paradigm, ACTH and cortisol levels were determined at baseline as well as peak levels during each of 4 consecutive separation episodes. For the acute ethanol administration paradigm, hormone levels were determined at baseline and again at 5 min, 10 min, and 60 min following the ethanol infusion. For postpartum sampling, hormone levels were determined at postpartum days 7, 14, 21, 30, 60, 90, 120, and 150. Infants carrying the 77G allele exhibited lower levels of cortisol across all 4 separation episodes. Furthermore, adolescents carrying the 77G allele exhibited lower cortisol levels at 5 and 10 min following acute ethanol administration. Adult females with prior reproductive experience and who carry the 77G allele exhibited lower cortisol levels across the postpartum period. No significant genotype effects were found for ACTH, although there were some trends for lower ACTH levels in 77G allele carriers. These data are consistent with human studies that have demonstrated attenuated cortisol responses to stress among carriers of the OPRM1 118G allele, lending further support to the argument that the rhesus and human allelic variants are functionally similar. Our results also suggest that OPRM1 variation may influence coping style, as well as alcohol-induced and postpartum levels of HPA axis activity and, as such, may modify vulnerability to alcohol use disorders and postpartum depression.
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PMID:OPRM1 gene variation influences hypothalamic-pituitary-adrenal axis function in response to a variety of stressors in rhesus macaques. 2145 16

Three decades of research point to both biological and psychological risk factors for postpartum depression, but very little research integrates the two. This study bridged this gap by testing whether prenatal social support predicted depressive symptoms at 8 weeks postpartum in a multiethnic sample of 210 women and whether the stress hormone placental corticotropin-releasing hormone (pCRH), measured at 19, 29, and 37 weeks' gestation, mediated this relationship. We found that prenatal family support predicted significantly fewer depressive symptoms postpartum and more gradual increases in pCRH from 29 to 37 weeks' gestation. Furthermore, steeper increases in pCRH during this same period predicted more depressive symptoms postpartum. Finally, these changes in pCRH in late pregnancy mediated the relationship between prenatal family support and postpartum depressive symptoms. These results suggest that social and biological risk factors for postpartum depressive symptoms are intertwined and move us closer to an integrated biopsychosocial understanding of postpartum depression.
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PMID:Placental Corticotropin-Releasing Hormone Mediates the Association Between Prenatal Social Support and Postpartum Depression. 2399 96

Postpartum depression affects 10-20% of women following birth and exerts persisting adverse consequences on both mother and child. An incomplete understanding of its etiology constitutes a barrier to early identification and treatment. It is likely that prenatal hormone trajectories represent both markers of risk and also causal factors in the development of postpartum depression. During pregnancy the maternal hypothalamic-pituitary-adrenal axis undergoes dramatic alterations, due in large part, to the introduction of the placenta, a transient endocrine organ of fetal origin. We suggest that prenatal placental and hypothalamic-pituitary-adrenal axis dysregulation is predictive of risk for postpartum depression. In this model the positive feedback loop involving the systems regulating the products of the HPA axis results in higher prenatal levels of cortisol and placental corticotropin-releasing hormone. Greater elevations in placental corticotropin-releasing hormone are related to a disturbance in the sensitivity of the anterior pituitary to cortisol and also perhaps to decreased central corticotropin-releasing hormone secretion. Secondary or tertiary adrenal insufficiencies of a more extreme nature, which emerge during the prenatal period, may be predictive of an extended or more pronounced postpartum hypothalamic-pituitary-adrenal refractory period, which in turn represents a risk factor for development of postpartum depression. In addition to reviewing the relevant existing literature, new data are presented in support of this model which link elevated placental corticotropin-releasing hormone with low levels of ACTH at 3-months postpartum. Future research will further elucidate the role of hypothalamic-pituitary-adrenal axis dysregulation in postpartum depression and also whether prenatal placental and hypothalamic-pituitary-adrenal profiles might prove useful in the early identification of mothers at risk for postpartum mood dysregulation.
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PMID:New insights into the role of perinatal HPA-axis dysregulation in postpartum depression. 2421 Jan 35

In the period of gestation, delivery and post-delivery, fear and tension produced in puerperae are likely to evolve into depression as they worry too much about delivery pain. In recent years, it has been noted that stressful events during this period aggravate postpartum depression. To discuss the effect of these childbirth-related stressful events on neuroendocrine functions of patients with postpartum depression, 300 full-term puerperae who had been admitted to the Beijing Obstetrics and Gynecology Hospital, Capital Medical University between October, 2011 and October, 2013 and who had suffered from stressful childbirth-related events were enrolled as a study group. This group was divided into six subgroups, i.e., A, B, C, D, E and F, based on the number of stressful events they had suffered which were labeled by numbers 1 to 6. Additionally, 100 puerperae from the same hospital who had not suffered from childbirth-related stressful events were taken as controls. Relevant clinical indexes, including serum adrenocorticotropic hormone (ACTH), plasma 5-hydroxytryptamine (5-HT), noradrenaline ELISA (NE), dopamine (DA) and cortisol level were measured and compared. It was found that incidence probability of postpartum depression was significantly different between the study group (13.67%, 41/300) and the control group (7%, 7/100). Moreover, the incidence probability of postpartum depression of puerperae suffering from no less than 4 childbirth-related stressful events was higher than those suffering from no more than 3, and the difference was statistically significant (P<0.05). Thus, stress disorders caused by these events are one of the important pathogenic factors of postpartum depression.
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PMID:NEUROENDOCRINE FUNCTIONS OF PUERPERAE WITH POSTPARTUM DEPRESSION AGGRAVATED BY STRESSFUL CHILDBIRTH-RELATED EVENTS. 2640 8

Maternal depression has been shown to negatively impact offspring development. Investigation into the impact of maternal depression and offspring behavior has relied on correlative studies in humans. Further investigation into the underlying mechanisms has been hindered by the lack of useful animal models. We previously characterized a mouse model which exhibits depression-like behaviors restricted to the postpartum period and abnormal/fragmented maternal care (Gabrd (-/-) mice). Here we utilized this unique mouse model to investigate the mechanism(s) through which maternal depression-like behaviors adversely impact offspring development. Cross-fostering experiments reveal increased anxiety-like and depression-like behaviors in mice reared by Gabrd (-/-) mothers. Wild type and Gabrd (-/-) mice subjected to unpredictable stress during late pregnancy exhibit decreased pup survival and depression-like behavior in the postpartum period. Exogenous corticosterone treatment in wild type mice during late pregnancy is sufficient to decrease pup survival and induce anxiety-like and depression-like behaviors in the offspring. Further, the abnormal behaviors in juvenile mice reared by Gabrd (-/-) mice are alleviated by treatment of the mothers with the corticotropin-releasing hormone (CRH) antagonist, Antalarmin. These studies suggest that hyperresponsiveness of the HPA axis is associated with postpartum depression and may mediate the adverse effects of maternal depression on offspring behavior.
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PMID:Behavioral Deficits in Juveniles Mediated by Maternal Stress Hormones in Mice. 2681 62

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