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Regulated energy homeostasis is fundamental for maintaining life. Unfortunately, this critical process is affected in a high number of mentally ill patients. Eating disorders such as anorexia nervosa are prevalent in modern societies. Impaired appetite and weight loss are common in patients with depression. In addition, the use of neuroleptics frequently produces obesity and diabetes mellitus. However, the neural mechanisms underlying the pathophysiology of these behavioral and metabolic conditions are largely unknown. In this review, we first concentrate on the established brain machinery of food intake and body weight, especially on the melanocortin and neuropeptide Y (NPY) systems as illustration. These systems play a critical role in receiving and processing critical peripheral metabolic cues such as leptin and ghrelin. It is also notable that both systems modulate emotion and motivated behavior as well. Secondly, we discuss the significance and potential promise of multidisciplinary molecular and neuroanatomic techniques that will likely increase the understanding of brain circuitries coordinating energy homeostasis and emotion. Finally, we introduce several lines of evidence suggesting a link between the melanocortin/NPY systems and several neurotransmitter systems on which many of the psychotropic agents exert their influence.
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PMID:Body weight is regulated by the brain: a link between feeding and emotion. 1563 Apr 8

Effects on fatty acid profiles and milk fat yield due to dietary concentrate and supplemental 18:3n-3 were evaluated in 4 lactating Holstein cows fed a low- (35:65 concentrate:forage; L) or high- (65:35; H) concentrate diet without (LC, HC) added oil or with linseed oil (LCO, HCO) at 3% of DM. A 4 x 4 Latin square with four 4-wk periods was used. Milk yield and dry matter intake averaged 26.7 and 20.2 kg/d, respectively, across treatments. Plasma acetate and beta-hydroxybutyrate decreased, whereas glucose, nonesterified fatty acids, and leptin increased with high-concentrate diets. Milk fat percentage was lower in cows fed high-concentrate diets (2.31 vs. 3.38), resulting in decreases in yield of 11 (HC) and 42% (HCO). Reduced yields of 8:0-16:0 and cis9-18:1 fatty acids accounted for 69 and 17%, respectively, of the decrease in milk fat yield with HC vs. LC (-90 g/d), and for 26 and 33%, respectively, of the decrease with HCO vs. LCO (-400 g/d). Total trans-18:1 yield increased by 25 (HCO) and 59 (LCO) g/d with oil addition. Trans10-18:1 yield was 5-fold greater with high-concentrate diets. Trans11-18:1 increased by 13 (HCO) and 19 (LCO) g/d with oil addition. Trans13+14-18:1 yield increased by 9 (HCO) and 18 (LCO) g/d with linseed oil. Yield of total conjugated linoleic acids (CLA) in milk averaged 6 g/d with LC or HC compared with 14 g/d with LCO or HCO. Cis9,trans11-CLA yield was not affected by concentrate level but increased by 147% in response to oil. Feeding oil increased yields of trans11,cis13-, trans11,trans13-, and trans,trans-CLA, primarily with LCO. Trans10,cis12-CLA yield (average of 0.08 g/d) was not affected by treatments. Yield of trans11,cis15-18:2 was 1 g/d in cows fed LC or HC and 10 g/d with LCO or HCO. Yields of cis9,trans11-18:2, cis9,trans12-18:2, and cis9,trans13-18:2 were positively correlated (r = 0.74 to 0.94) with yields of trans11-18:1, trans12-18:1, and trans13+14-18:1, respectively. Plasma concentrations of biohydrogenation intermediates with concentrate or linseed oil level followed similar changes as those in milk fat. Milk fat depression was observed when HC induced an increase in trans10-18:1 yield. A correlation of 0.84 across 31 comparisons from 13 published studies, including the present one, was found among the increase in percentage of trans10-18:1 in milk fat and decreased milk fat yield. We observed, however, more drastic milk fat depression when HCO increased yields of total trans-18:1, trans11,cis15-18:2, trans isomers of 18:3, and reduced yields of 18:0 plus cis9-18:1.
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PMID:Relationship among trans and conjugated fatty acids and bovine milk fat yield due to dietary concentrate and linseed oil. 1565 39

Seasonal affective disorder (SAD) is a specific clinical entity characterized by recurrent episodes of depression, which typically occur during the winter with periods of remission during the spring and summer. These depression episodes are accompanied by hyperphagia with cravings for carbohydrates and moderate weight gain, and usually respond to light therapy. We examined potential relationships between leptin, a hormone known to affect appetite and weight regulation, and seasonal changes in mood and appetite by measuring plasma leptin, clinical severity of depression, appetite scores, and body mass index (BMI) in 19 women and 8 men with SAD and matched controls (20 women and 8 men) in the summer and winter. Plasma leptin was positively correlated with BMI in patients and controls during both seasons. Women and men with SAD both experienced depression in the winter, which was associated with increased appetite, caloric intake, and carbohydrate craving. Increased body weight during the winter in subjects with SAD was paralleled by a lack of concomitant changes in plasma leptin, which suggests that leptin sensitivity to changes in body weight may be influenced by seasons in subjects with SAD, similar to seasonal mammals.
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PMID:Plasma leptin in men and women with seasonal affective disorder and in healthy matched controls. 1682 28

Impaired leptin signalling in obesity is increasingly implicated in cardiovascular pathophysiology. To explore mechanisms for leptin activity in the heart, we hypothesized that physiological leptin signalling participates in maintaining cardiac beta-adrenergic regulation of excitation-contraction coupling. We studied 10-week-old (before development of cardiac hypertrophy) leptin-deficient (ob/ob, n=12) and C57Bl/6 (wild-type (WT), n=15) mice at baseline and after recombinant leptin infusion (0.3 mg kg-1 day-1 for 28 days, n=6 in each group). Ob/ob-isolated myocytes had attenuated sarcomere shortening and calcium transients ([Ca2+]i) versus WT (P<0.01 for both) following stimulation of the beta-receptor (with isoproterenol (isoprenaline)) or at the post-receptor level (with forskolin and dibutryl-cAMP). In addition, sarcoplasmic reticulum (SR) Ca2+ stores were depressed. Leptin replenishment in ob/ob mice restored each of these abnormalities towards normal without affecting gross (wall thickness) or microscopic (cell size) measures of cardiac architecture. Immunoblots revealed alterations of several proteins involved in excitation-contraction coupling in the ob/ob mice, including decreased abundance of Gsalpha-52 kDa, as well as alterations in the expression of Ca2+ cycling proteins (increased SR Ca2+-ATPase, and depressed phosphorylated phospholamban). In addition, protein kinase A (PKA) activity in ob/ob mice was depressed at baseline and correctable towards the activity found in WT with leptin repletion, a finding that could account for impaired beta-adrenergic responsiveness. Taken together, these data reveal a novel link between the leptin signalling pathway and normal cardiac function and suggest a mechanism by which leptin deficiency or resistance may lead to cardiac depression.
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PMID:Leptin repletion restores depressed {beta}-adrenergic contractility in ob/ob mice independently of cardiac hypertrophy. 1576 Sep 36

Depression is one of the most common psychiatric disorders. For a long time, clinicians suspected a causal link between depression and the endocrine system. The most frequently occurring endocrine abnormality in depressed subjects is hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. CRH and AVP are likely to play a substantial role in the pathophysiology of this disorder, and their receptors appear to be a specific target for future antidepressant drugs. Depression also affects the hypothalamic-pituitary-GH (HPGH) and -thyroid (HPT) axes. Alterations in the reproductive system may also play a role in the pathology of depression. In addition, there is increasing evidence that leptin and neurosteroids, such as DHEA, are implicated in mood disorders.
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PMID:Endocrine disturbances in depression. 1581 77

The aim of the present study was to evaluate serum leptin levels to demonstrate whether or not its eventual alterations might have an etiopathogenetic significance in patients with obsessive-compulsive disorder (OCD). Thus, it was planned to examine whether serum leptin levels were affected by pure OCD (OCD-D), pure depression (D) or the comorbidity of OCD and depression (OCD+D). Forty-four patients with OCD (27 with OCD-D and 17 with OCD+D), 38 depressed patients and 30 control subjects were enrolled and serum leptin and cortisol levels were measured. According to the mean leptin levels, no significant difference was found between the OCD-D and control groups and between the OCD+D and D groups, while statistically significantly lower levels were found in the OCD+D and D groups than in control group. Significant difference in the mean leptin levels was found among groups even after controlling for body mass index or sex. The present study confirms the strong relationship between serum leptin and cortisol values and suggests that reduced leptin levels, rather than having an etiopathogenetic significance in patients with OCD, seem to be associated with patients with OCD and depression but not with pure OCD patients, and that OCD may be a heterogeneous subtype containing some biological indications of anxiety and affective disorders.
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PMID:Serum leptin levels in obsessive-compulsive disorder. 1582 66

Leptin is a product of the obese gene and plays an important role in the regulation of body weight and food intake. Weight and appetite are frequently altered in depression. So far, inconsistent results have been reported in terms of leptin levels in depression. Therefore, the authors investigated serum leptin levels in patients with depression and in healthy controls, and whether there was any alteration throughout antidepressant treatment. Female patients showed significantly higher leptin levels than those of the control females both before and after the response to antidepressant treatment, whereas no difference was found between the male patients and the male controls. The improvement from depression with antidepressant treatment caused a further elevation on the leptin levels, in both female and male patients. These findings confirm an increase in leptin levels in depressive patients and presence of a sexual dimorphism. Moreover, clinical response to antidepressant treatment seems to have an additional increasing effect on leptin levels.
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PMID:Effects of antidepressant treatment and of gender on serum leptin levels in patients with major depression. 1586 59

Transdermal nicotine patches have been successfully introduced as a safe and powerful aid to smoking cessation; this has contributed to the rising interest in additional therapeutic applications for nicotine and synthetic nicotinic agonists. Nicotine and nicotinic agonists may have a therapeutic potential for a variety of disorders, including Alzheimer's and Parkinson's diseases, depression, attention deficit disorder, Tourette's syndrome and ulcerative colitis. These interests are partially fuelled by the urgent need of the tobacco industry to find new niches for nicotine in a world bound eventually to retire from cigarette smoking. At the same time, there is an increased interest in developing drugs for fighting obesity, a growing affliction of industrialised nations. This review presents data on the potential of nicotine, and in particular synthetic nicotinic agonists, for controlling body weight. Nicotinic agonists may become relatively safe, effective and inexpensive alternatives for several optional drugs currently being developed for treating human obesity, including beta-3-adrenergic agonists, leptin and its agonists, and neuropeptide Y antagonists.
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PMID:The therapeutic potential of nicotine and nicotinic agonists for weight control. 1599 28

The neurochemistry of feeding was a highlight of this meeting. A number of peptides are now known to participate in the control of nutrient balance, and many of them featured in the meeting, including the feeding suppressors alpha-melanocyte-stimulating hormone, leptin and corticotrophin releasing hormone, and the orexigenic agents, melanin-concentrating hormone, Agouti-related peptide, orexin A and neuropeptide Y. Other substances that play a role in feeding are amylin and its antagonist, AC-187, histamine, dopamine, serotonin, opiates, galanin and CART peptides. The hypothalamic and extrahypothalamic localization of these feedingrelated substances and their interactions with one another, and other brain regions, are beginning to be understood. Another symposium focused on sigma receptor ligands, such as (+)-pentazocine, PRE-084, the neurosteroid pregnanolone sulfate, NE-100, igmesine (JO-1784) and BD-1008 and related compounds. Results showed that sigma ligands may affect Ca(2+) signaling via two modes of action, one being at the endoplasmic reticulum and the other at the plasma membrane. Sigma receptors have been implicated in learning and memory, and may play a role in anxiety and depression.
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PMID:International Behavioral Neuroscience Society - Ninth meeting. Neurochemistry of feeding. 1608 42

It is becoming apparent that the hormone leptin plays an important role in modulating hippocampal function. Indeed, leptin enhances NMDA receptor activation and promotes hippocampal long-term potentiation (LTP). Furthermore, obese rodents with dysfunctional leptin receptors display impairments in hippocampal synaptic plasticity. Here we demonstrate that under conditions of enhanced excitability (evoked in Mg2+-free medium or following blockade of GABA(A) receptors), leptin induces a novel form of long-term depression (LTD) in area CA1 of the hippocampus. Leptin-induced LTD was markedly attenuated in the presence of D-(-)-2-Amino-5-Phosphonopentanoic acid (D-AP5), suggesting that it is dependent on the synaptic activation of NMDA receptors. In addition, low-frequency stimulus-evoked LTD occluded the effects of leptin. In contrast, metabotropic glutamate receptors (mGluRs) did not contribute to leptin-induced LTD as mGluR antagonists failed to either prevent or reverse this process. The signalling mechanisms underlying leptin-induced LTD were independent of the Ras-Raf-mitogen-activated protein kinase signalling pathway, but were markedly enhanced following inhibition of either phosphoinositide 3-kinase or protein phosphatases 1 and 2A. These data indicate that under conditions of enhanced excitability, leptin induces a novel form of homosynaptic LTD, which further underscores the proposed key role for this hormone in modulating NMDA receptor-dependent hippocampal synaptic plasticity.
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PMID:Leptin induces a novel form of NMDA receptor-dependent long-term depression. 1608 87


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