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

Leptin is known to regulate food intake and energy expenditure. Since loss of appetite and bodyweight are important signs and symptoms of major depression we studied leptin plasma concentrations in both depressed patients (n = 24) suffering from loss of appetite and a healthy control group (n = 33). To rule out the possibility of inferences with other endocrine parameters known to be changed in depression or suspected to be related to leptin, we also studied cortisol, insulin, growth hormone (GH) and GH-binding protein (GHBP). We found that leptin plasma concentrations did not differ between depressed patients and healthy controls. However, leptin was positively associated with female gender, body mass index (BMI) and morning insulin. 24-hour mean cortisol was not related to leptin. Also, GH and GHBP were not related to leptin when controlled for BMI in an ANCOVA model. We conclude that leptin plasma concentrations are unchanged in depression and that there is no evidence for leptin playing a major role in loss of appetite and body weight in depressed patients.
 ...
PMID:Plasma leptin in depressed patients and healthy controls. 901 49

Leptin, the protein product of the obese (ob) gene, has been suggested to play a role in the regulation of food intake. As depressive episodes are frequently characterized by loss of appetite, reduced food intake and weight loss, altered leptin secretion might also be expected in patients with depression. Therefore, we examined nocturnal (10.00 p.m. to 7.00 a.m.) secretion of leptin, cortisol, ACTH and growth hormone (GH) in a group of 15 patients with depression and age- and sex-matched controls (age range 23-71 years). In addition, the effects of pulsatile administration of growth hormone-releasing hormone (GHRH), thought to be an endogenous antagonist of corticotropin-releasing hormone (CRH), which in turn is believed to play a critical role for the pathophysiology of depression, on nocturnal hormone secretion were assessed. Patients with depression showed a trend towards elevated nocturnal cortisol secretion (F = 3.8, p < 0.05). Nocturnal serum leptin was significantly higher in patients, despite a reported weight loss (F = 8, p < 0.05), but showed the same sexual dimorphism as in controls (F = 20.9, p < 0.01). No significant differences were seen between patients and controls with regard to plasma GH and ACTH. GHRH treatment increased GH secretion in both patients and controls, while the other hormones were not affected. Furthermore, serum leptin was correlated with body mass index (BMI) in controls, but not in patients with depression, supporting an altered regulation of leptin secretion in depressive illness. Finally, we provide some evidence that in young female patients the normal nocturnal leptin surge is blunted. As glucocorticoids can prevent the fasting-induced decline in serum leptin, we propose that hypercortisolism in depression might counteract the reduction in leptin secretion caused by decreased food intake and weight loss. Elevated serum leptin in depression might in turn further promote CRH release, as shown in animals and, hence, contribute to HPA system hyperactivity seen in depression.
 ...
PMID:Elevated nocturnal profiles of serum leptin in patients with depression. 984 57

Diabetes mellitus is a common disease in older people, with almost 50% of Type 2 diabetic patients being over 60 years of age; despite this, half of older people with frank diabetes are not diagnosed. While insulin resistance is common in older people, large numbers also have impaired insulin secretion. Age, body habitus and physical activity all play a role in the pathogenesis of hyperglycaemia associated with diabetes mellitus. Leptin levels relate to insulin resistance in older people and amylin secretion is associated with delayed return of glucose levels to baseline. Depression, impaired cognitive function, and lack of recognition of thirst and subsequent dehydration are important factors to be taken into account in the management of older diabetic patients, who may also have impaired physical function, an increased rate of injurious falls, and increased prevalence of pressure ulcers, amputations and tuberculosis. Hyperglycaemia can result in a decreased pain threshold and incontinence. Dietary management plays less of a role in older diabetic patients but exercise, with a particular emphasis on balance and stability, is an important component of the management and treatment of older diabetic patients. The use of metformin as a treatment should be avoided in patients over 80 years of age because of declining kidney function. Insulin therapy is an option but as hypoglycaemia is related to advancing age, patients should be monitored carefully for the development of hypoglycaemia. Care providers also play an important role in the management of older people with diabetes mellitus. Glycaemic control can be obtained with minimal side-effects in most older diabetics including those patients in nursing homes.
 ...
PMID:The elderly Type 2 diabetic patient: special considerations. 986 91

Human obesity leads to an increase in respiratory demands. As obesity becomes more pronounced some individuals are unable to compensate, leading to elevated arterial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidity and mortality (Pickwickian syndrome). The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depression of central respiratory control mechanisms. Here we report that obese C57BL/6J-Lepob mice, which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p < 0. 0001). A role for leptin in restoring ventilation in these obese, mutant mice was investigated. Three days of leptin infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, but particularly during rapid eye movement (REM) sleep when respiration was otherwise profoundly depressed. The effect of leptin was independent of food intake, weight, and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory control centers. Furthermore, leptin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4.0 +/- 0.5 to 5.6 +/- 0.4 ml/min/%CO2; p < 0.01) and REM (-0.1 +/- 0.5 to 3.0 +/- 0.8 ml/min/%CO2; p < 0.01) sleep. We also demonstrate in wild-type mice that ventilation is appropriately compensated when obesity is diet-induced and endogenous leptin levels are raised more than tenfold. These results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects. O'Donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR, Smith PL. Leptin prevents respiratory depression in obesity.
 ...
PMID:Leptin prevents respiratory depression in obesity. 1022 14

Appetite, food intake and weight are frequently altered in psychiatric disorders such as major depression and schizophrenia. The few studies investigating weight and the body mass index (BMI) have yielded variable results. Leptin, a fat cell-derived hormone signalling to the brain the size of the adipose tissue, plays a pivotal role in the regulation of weight and food intake. Moreover, leptin is involved in the control of other behaviors and in brain development. There is almost no information about the amounts of circulating leptin in major depression or schizophrenia. We investigated the BMI and plasma leptin levels in patients with major depression (n = 62), schizophrenia (n = 42), and in healthy controls (n = 64). Mean BMIs did not differ between groups. However, leptin levels were significantly lower in both patient groups compared to healthy controls. Moreover, patients suffering from schizophrenia showed significantly lower leptin levels than depressed patients. Decreased leptin levels were independent of psychotropic medication. We conclude that depression and schizophrenia go along with decreased systemic leptin concentrations that cannot be explained by medication or an altered BMI. Hence, leptin might play an important pathophysiological role in these psychiatric disorders that deserves further scientific attention.
 ...
PMID:Low leptin levels but normal body mass indices in patients with depression or schizophrenia. 1134 Mar 38

In this chapter we have reviewed the evidence for physiological anorexia of aging and stressed that its pathophysiology involves both central and peripheral mechanisms. Early satiation in the older person appears to involve signals predominantly arising in the stomach. The increased feeling of satiety in older persons is mainly related to changes in the central feeding drive, in particular a decrease in the opioid rewarding properties for fatty foods. Increased cytokines, secondary to inflammatory conditions which are common in old age, may further increase the anorexia seen in older persons. Leptin, the fat hormone, is an excellent indicator of fat mass in women, in whom leptin concentrations correlate with the MNA. In men, testosterone inhibits leptin, and the fall in testosterone with age results in an increase in leptin concentrations. In males the MNA is not related to leptin concentrations. Finally, we have examined the interrelation of two nutritional screening indices, MNA and SCALES. The two indices were well correlated and were both predictive of poor basic function. We conclude that the MNA is an excellent predictor of nutritional status. These findings suggest that malnutrition is a major predictor of frailty or the "failure to thrive" syndrome in older persons. Depression is a major cause of poor nutritional status in older persons.
 ...
PMID:Anorexia of aging, leptin, and the Mini Nutritional Assessment. 1149 May 97

The anorexic effect of exposure to high altitude may be related to the reduction in the arterial oxygen content (Ca(O2)) induced by hypoxemia and possibly the associated decreased convective oxygen transport (COT). This study was then performed to evaluate the effects of either transfusion-induced polycythemia or previous acclimation to hypobaria with endogenously induced polycythemia on the anorexic effect of simulated high altitude (SHA) in adult female rats. Food consumption, expressed in g/d/100 g body weight, was reduced by 40% in rats exposed to 506 mbar for 4 d, as compared to control rats maintained in room air. Transfusion polycythemia, which significantly increased hematocrit, hemoglobin concentration, Ca(O2), and COT, did not change the anorexic response to the exposure to hypobaric air. Depression of food intake during exposure to SHA also occurred in rats fasted during 31 h before exposure and allowed to eat ad libitum for 2 h during exposure. Body mass loss was similar in 48-h fasted rats that were either hypoxic or normoxic. Body mass loss was similar in normoxic and hypoxic rats, the former eating the amount of food freely eaten by the latter. Hypoxia-acclimated rats with endogenously induced polycythemia taken to SHA again had diminished food intake and lost body mass at rates that were very close to those found in nonacclimated ones. Exposure to SHA also led to a decrease in food consumption, body weight, and plasma leptin in adult female mice. Analysis of data suggest that body mass loss that accompanies SHA-induced hypoxia is due to hypophagia and that experimental manipulation of the blood oxygen transport capacity cannot ameliorate it. Leptin does not appear to be an inducer of the anorexic response to hypoxia, at least in mice and rats.
 ...
PMID:Failure of polycythemia-induced increase in arterial oxygen content to suppress the anorexic effect of simulated high altitude in the adult rat. 1200 64

Leptin is well known to be involved in the control of feeding, reproduction and neuroendocrine functions through its action on the hypothalamus. However, leptin receptors are found in brain regions other than the hypothalamus (including the hippocampus and cerebral cortex) suggesting extrahypothalamic functions. We investigated hippocampal long-term potentiation (LTP) and long-term depression (LTD), and the spatial-memory function in two leptin receptor-deficient rodents (Zucker rats and db/db mice). In brain slices, the CA1 hippocampal region of both strains showed impairments of LTP and LTD; leptin (10(-12) M) did not improve these impairments in either strain. These strains also showed lower basal levels of Ca(2+)/calmodulin-dependent protein kinase II activity in the CA1 region than the respective controls, and the levels did not respond to tetanic stimulation. These strains also showed impaired spatial memory in the Morris water-maze test (i.e. longer swim-path lengths during training sessions and less frequent crossings of the platform's original location in the probe test. From these results we suggest that the leptin receptor-deficient animals show impaired LTP in CA1 and poor spatial memory due, at least in part, to a deficiency in leptin receptors in the hippocampus.
 ...
PMID:Impairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents. 1215 Jul 80

Leptin (L) is associated with body-weight-regulating and adipostatic functions. Its receptors also may be found centrally. Thyroid hormones regulate metabolic processes mainly by binding at peripheral receptors. Aim of this study was to show if there is a link between those central and peripheral regulation systems and to investigate the influence of different training intensities on L and the hypothalamic-thyroid-axis (HTA) in highly trained rowers. Six rowers (18.9 +/- 2.6 y; BMI 22.8 +/- 2.1 kg/m (2)) undertook high intensity resistance training (RT) for three weeks followed by three weeks of endurance training (ET). After each training cycle the subjects had one week for recovery (R1, R2). Blood samples were taken before and at the end of RT, R1, ET and R2. L, thyroid stimulating hormone (TSH), free T3 (fT3) and free T4 (fT4) were measured. After RT, a significant reduction in L, TSH and fT3 was found (p < 0.05). fT4 was unchanged. L remained decreased until the end of R1. After ET, a significant increase of TSH was found. L correlated to basal TSH levels (r = 0.49, p = 0.006) during R. BMI and body fat were unchanged throughout the study and were not correlated with hormonal levels. We speculate a high energy flux during intensified training (RT) caused the decrease of L and the HTA, independent of BMI or body fat. Thus, we conclude a depression of L and HTA is associated with training intensity.
 ...
PMID:Training intensity influences leptin and thyroid hormones in highly trained rowers. 1221 61

Weight gain is a frequent adverse effect associated with lithium use. Leptin is an adipocyte hormone, regulating food intake and energy balance providing the hypothalamus with information on the amount of body fat. Therefore, we planned to evaluate whether lithium administration was associated with weight gain, and leptin levels. The study consisted of 15 consecutive inpatients with bipolar I disorder according to DSM-III-R. The fasting serum leptin levels were measured. The patients were evaluated at baseline and at the eighth week according to the body mass index, weight, Young Mania Rating (YMRS) and Hamilton Depression Rating (HAM-D) scales, and serum leptin levels. With respect to the leptin levels, a significant difference was observed after lithium treatment. There was a significant positive correlation between the changes in leptin levels and the duration of illness. The change in total YMRS scores correlated with change in leptin levels and that in weight. In conclusion, our result suggest that leptin may be associated with lithium-induced weight gain.
 ...
PMID:Weight gain and serum leptin levels in patients on lithium treatment. 1237 22


1 2 3 4 5 6 Next >>