Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The noradrenergic and specific serotoninergic antidepressant mirtazapine improves sleep, modulates hormone secretion including blunting of hypothalamic-pituitary-adrenocortical (HPA) activity, and may prompt increased appetite and weight gain. The simultaneous investigation of sleep electroencephalogram (EEG) and hormone secretion during antidepressive treatment helps to further elucidate these effects. We examined sleep EEG (for later conventional and quantitative analyses) and the nocturnal concentrations of cortisol, adrenocorticotropin (ACTH), growth hormone (GH), prolactin, melatonin and the key factors of energy balance, ghrelin, and leptin before and after 28 days of treatment of depressed patients (seven women, three men, mean age 39.9+/-4.2 years) with mirtazapine. In addition, a sleep EEG was recorded at day 2 and the dexamethasone-corticotropin-releasing hormone (DEX-CRH) test was performed to assess HPA activity at days -3 and 26. Psychometry and mirtazapine plasma concentrations were measured weekly. Already at day 2, sleep continuity was improved. This effect persisted at day 28, when slow-wave sleep, low-delta, theta and alpha activity, leptin and (0300-0700) melatonin increased, and cortisol and ghrelin decreased. ACTH and prolactin remained unchanged. The first two specimens of GH collected after the start of quantitative EEG analysis were reduced at day 28. The DEX-CRH test showed, at day 26, a blunting of the overshoot of ACTH and cortisol found at day -3. The Hamilton Depression score decreased from 32.1+/-7.3 to 15.5+/-6.7 between days -1 and 28. A weight gain of approximately 3 kg was observed. This unique profile of changes is compatible with the action of mirtazapine at 5-HT-2 receptors, at presynaptic adrenergic alpha 2 receptors, at the HPA system, and on ghrelin and leptin.
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PMID:Changes of sleep architecture, spectral composition of sleep EEG, the nocturnal secretion of cortisol, ACTH, GH, prolactin, melatonin, ghrelin, and leptin, and the DEX-CRH test in depressed patients during treatment with mirtazapine. 1623 93

Pro-inflammatory factors such as the adipokine leptin and cytokine tumor necrosis factor-alpha (TNFalpha) have been implicated in the onset of myocardial dysfunction in ischemia-reperfusion injury, sepsis, heart failure, viral myocarditis and cardiac allograft rejection. Although circulating TNFalpha and leptin levels are both elevated under a variety of inflammatory conditions, it remains unknown whether TNFalpha and leptin depress cardiac contractile function independently or synergistically. We examined the effect of acute (30 min) and short-term (24h) exposure of TNFalpha, leptin or both on cardiac contractile function in adult rat ventricular myocytes. Contractile properties were evaluated using an Ionoptix Softedge system including peak shortening (PS), maximal velocity of shortening/relengthening (+/-L/t), time-to-PS (TPS) and time-to-90% relengthening (TR(90)). Both TNFalpha (0.5-500 pg/ml) and leptin (1-100 nm) exerted concentration-dependent inhibitions in PS and +/-L/t following a 30-min exposure. TNFalpha but not leptin prolonged TR(90). Interestingly, TNFalpha-induced depression of cell shortening was masked by leptin and vice versa. Following a 24-h incubation, both TNFalpha and leptin significantly inhibited PS and +/-L/t without affecting TPS and TR(90). There was no additive or synergistic response by the two pro-inflammatory factors. The nitric oxide synthase inhibitor l-NMMA abolished depression of myocyte shortening elicited by TNFalpha, leptin or both. In summary, this study demonstrated that the inhibitory effect on cardiac contraction by TNFalpha and leptin may mask each other and share a common mechanism(s), probably dependent on NO.
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PMID:Interaction between tumor necrosis factor-alpha and leptin-induced inhibition of cardiac contractile function in isolated ventricular myocytes. 1629 37

Leptin is thought to be related to vegetative symptoms of depression such as alterations in food intake and weight. Fifty-seven drug-free patients and 26 healthy controls were enrolled in this study. We have found that the serum leptin levels were higher in patients with atypical depressive disorder than in controls, but not in patients with non-atypical depressive disorder, however, body mass index, age, and gender were not significantly different between these groups. Probably, these findings seem to be associated with some features of the atypical depressive disorders such as weight gain, a result of hyperphagia.
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PMID:High serum leptin levels in depressive disorders with atypical features. 1640 Dec 52

Leptin, a hormone secreted from adipose tissue, was originally discovered to regulate body weight. The localization of the leptin receptor in limbic structures suggests a potential role for leptin in emotional processes. Here, we show that rats exposed to chronic unpredictable stress and chronic social defeat exhibit low leptin levels in plasma. Systemic leptin treatment reversed the hedonic-like deficit induced by chronic unpredictable stress and improved behavioral despair dose-dependently in the forced swim test (FST), a model widely used for screening potential antidepressant efficacy. The behavioral effects of leptin in the FST were accompanied by increased neuronal activation in limbic structures, particularly in the hippocampus. Intrahippocampal infusion of leptin produced a similar antidepressant-like effect in the FST as its systemic administration. By contrast, infusion of leptin into the hypothalamus decreased body weight but had no effect on FST behavior. These findings suggest that: (i) impaired leptin production and secretion may contribute to chronic stress-induced depression-like phenotypes, (ii) the hippocampus is a brain site mediating leptin's antidepressant-like activity, and (iii) elevating leptin signaling in brain may represent a novel approach for the treatment of depressive disorders.
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PMID:Leptin: a potential novel antidepressant. 1642 96

Patients with bulimia nervosa (BN) have bulimic and depressive symptoms, which have been associated with abnormalities in the neuroendocrine and vagal systems. Subjects included twenty-four female drug-free outpatients with BN that were selected from patients seeking treatment for eating behavior in our hospital along with twenty-five age-matched healthy females who served as controls. We investigated ghrelin and leptin levels, cardiac vagal tone and sympathovagal balance, frequency of sets of binge-eating and vomiting episodes per week and the Profile of Mood States (POMS) depression scale in BN before and after a 16-week administration of the serotonin selective reuptake inhibitor (SSRI) paroxetine combined with cognitive-behavioral therapy. Compared to controls, the BN group had higher ghrelin levels and resting cardiac vagal tone, and lower leptin levels and resting cardiac sympathovagal balance before treatment, although there was a significant difference between the two groups for the body mass index (BMI). The elevated ghrelin levels (301.7 +/- 18.9 pmol/l, mean +/- SEM vs. 202.8 +/- 15.6 pmol/l, P < 0.01), cardiac vagal tone (2246.4 +/- 335.5 ms(2) vs. 1128.5 +/- 193.3 ms(2), P < 0.01), frequency of sets of binge-eating and purging episodes and T scores for the POMS depression scale were all significantly decreased after treatment despite similar BMI, percent body fat and leptin levels. In close association with cardiac vagal function and ghrelin recoveries, abnormal eating behavior and depressive symptoms improved, indicating the usefulness of these indexes in the assessment of clinical condition and therapeutic efficacy in BN.
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PMID:Ghrelin concentrations and cardiac vagal tone are decreased after pharmacologic and cognitive-behavioral treatment in patients with bulimia nervosa. 1664 14

It is well documented that the hormone leptin plays a pivotal role in regulating food intake and body weight via its hypothalamic actions. However, leptin receptors are expressed throughout the brain with high levels found in the hippocampus. Evidence is accumulating that leptin has widespread actions on CNS function and in particular learning and memory. Recent studies have demonstrated that leptin-deficient or-insensitive rodents have impairments in hippocampal synaptic plasticity and in spatial memory tasks performed in the Morris water maze. Moreover, direct administration of leptin into the brain facilitates hippocampal long-term potentiation (LTP), and improves memory performance in mice. There is also evidence that, at the cellular level, leptin has the capacity to convert hippocampal short-term potentiation (STP) into LTP, via enhancing NMDA receptor function. Recent data indicates that leptin can also induce a novel form of NMDA receptor-dependent hippocampal long-term depression. Here, we review the evidence implicating a key role for the hormone leptin in modulating hippocampal synaptic plasticity and discuss the role of lipid signaling cascades in this process.
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PMID:Leptin and its role in hippocampal synaptic plasticity. 1667 6

The longer life expectancy of women than that of men and, therefore, the longer exposure to fracture risk has, at least partially, led to neglect of osteoporosis in men. Recently, unipolar depression, which is 2 times more frequent in women than in men, has been linked to osteoporosis. However, it is quite possible that this diagnosis may escape detection in men because of a different behavioral phenotype between the genders. A potential mechanism of bone loss in depression has been proposed, involving concurrent activation of the hypothalamo-pituitary-adrenal and sympatho-adrenal axes, suppression of the gonadal and somatotrophic axes, and high interleukin-6 and low leptin levels. We suggest that similar neurohormonal changes may cause osteoporosis in men.
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PMID:Depression and osteoporosis in men: association or casual link? 1672 81

This study describes: 1. The therapeutic effects on anorexia nervosa (AN) and bulimia nervosa (BN) patients of a psycho-nutritional intensive day-hospital program; 2. The possible correlation between the changes observed in the psychometric tests and the variations of a number of biological parameters. Forty-six female patients (24 AN and 22 BN) were assessed through a semi-structured clinical interview based on DSM-IV criteria for Eating Disorders (ED) and a number of psychometric tests (SCL-90R, BDI, EDI-2, EAT-40, BITE, BAT) at the beginning and at the end of treatment, and after a 6-month follow-up. At these three times, we also assessed the plasma level of leptin, cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and 17beta-estradiol together with body mass index (BMI) and menstrual cycle. From beginning to discharge, the scores on all psychometric tests improved in the whole sample, except for the Perfectionism subscale of EDI-2 in both groups (AN and BN), the Anger-Hostility, Phobic Anxiety and Paranoid Ideation subscales of SCL-90 and the Interpersonal Distrust subscale of EDI-2 in the BN group. At follow-up, there was a worsening of the BITE scores and of a number of EDI-2 subscales, especially in the AN subgroup - with these changes correlating with the trend of BMI. In AN patients, plasma leptin levels changed from the beginning to the end of treatment and at follow-up according to BMI changes. The mean plasma leptin level in the BN subgroup was higher than in the AN one. We found a statistically significant correlation with the scores of BDI, SCL-90R Depression and Ineffectiveness subscales, EAT-40, BITE-Symptom subscale and the trend of menses dividing these patients into two subgroups (according to the plasma leptin concentration, higher or lower than the top leptin level in the anorexics). These data seem to confirm that leptin secretion doesn't correlate univocally to BMI.
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PMID:Correlation between psychometric and biological parameters in anorexic and bulimic patients during and after an intensive day hospital treatment. 1675 67

To characterize microvascular function, candidate risk pathways, and metabolic syndrome prevalence in women with cardiac syndrome X, 52 nondiabetic women with angiographically normal epicardial arteries but >1 mm of planar ST depression during exercise testing (patients) and 24 healthy controls of similar age were recruited. In addition to fasting blood samples and anthropometric measurements, forearm cutaneous microvascular function after iontophoresis of acetylcholine and sodium nitroprusside was assessed by laser Doppler imaging. Despite body mass index correction and a larger proportion on statin therapy, patients had high levels of insulin (p=0.016), triglycerides (p=0.018), intercellular adhesion molecule-1 (p=0.021), von Willebrand factor (p=0.005), and leptin (p=0.005) and lower levels of high-density lipoprotein cholesterol (p=0.042) compared with controls. Consistent with these data, 30% of patients but only 8% of controls fulfilled criteria for the metabolic syndrome as defined by the National Cholesterol Education Program (p=0.015). Endothelium-dependent and -independent microvascular functions were markedly impaired in patients (p<0.001), and the odds ratio for cardiac syndrome X was 7.38 (95% confidence interval 2.2 to 24.7) if the acetylcholine response was <8,710 flux units. In conclusion, women with cardiac syndrome X more commonly have metabolic syndrome and related adiposity, metabolic, and inflammatory derangements. They also have significantly impaired skin microvascular function as assessed by laser Doppler imaging, consistent with generalized vascular dysfunction, a finding with potential diagnostic implications.
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PMID:Microvascular function, metabolic syndrome, and novel risk factor status in women with cardiac syndrome X. 1676 22

Supplementation with a high dose (600 g/d) of rumen inert conjugated linoleic acids (RI-CLA) inhibits milk fat synthesis in total mixed ration (TMR)-fed dairy cows immediately post partum. However, effects of RI-CLA on milk fat and bioenergetic parameters during the transition period in grazing cows have not been investigated. Multiparous Holstein cows (n=39) grazing pasture were randomly assigned to one of three treatments: (1) pasture (PAS), (2) PAS+540 g/d Hyprofat (palm oil; HYPRO) and (3) PAS+600 g/d RI-CLA. HYPRO and RI-CLA supplements were isoenergetic, fed twice daily at 7.00 and 16.00 and provided 0 and 125 g CLA/d, respectively. Treatments began 27+/-10 d prepartum and continued until 36+/-1 days in milk (DIM). There was little or no overall effect of RI-CLA on content or yield of milk protein and lactose. RI-CLA supplementation decreased overall milk fat content and yield with RI-CLA-induced milk fat depression (MFD) becoming significant by day 3 when compared with PAS and by day 6 when compared with HYPRO. MFD continued to increase in severity during the first 24 d post partum after which MFD reached a plateau (approximately 40%; RI-CLA v. HYPRO). Pasture-fed cows produced less milk (19.4 kg/d) than the lipid-supplemented groups and although there were no overall differences in milk yield between RI-CLA and HYPRO (22.3 kg/d) a curvilinear relationship (R2=0.57) existed between the RI-CLA-induced milk yield response and extent of MFD. RI-CLA tended to increase milk yield (1.8 kg/d) compared with HYPRO until MFD exceeded 35% (approximately day 21), after which point the positive milk yield response was eliminated. Milk fat trans-10, cis-12 CLA content averaged 0.25 g/100 g in the RI-CLA treatment, was temporally independent, and was undetectable in PAS and HYPRO treatments. Based on the milk fat 14ratio1/14ratio0 ratio, RI-CLA decreased the overall Delta9-desaturase system compared with PAS and HYPRO. Compared with HYPRO, RI-CLA had no effect on plasma glucose, insulin, leptin, or NEFA concentrations. Results indicate that a high RI-CLA dose decreases milk fat synthesis and tends to increase milk yield immediately post partum in pasture-fed cows; however, excessive MFD (>35%) appears to be associated with a diminished milk yield response.
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PMID:Effects of dietary conjugated linoleic acid on production and metabolic parameters in transition dairy cows grazing fresh pasture. 1683


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