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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a great deal of information presently available documenting a cardiomyopathic condition in insulin-deficient models of diabetes. Less information is available documenting a similar status in non insulin-dependent models of diabetes. We have studied the functional integrity of the myofibrils isolated from hearts of JCR:LA rats. The JCR:LA rat is hyperinsulinemic, hyperlipidemic, glucose intolerant and obese. As such, it carries many of the characteristics found in humans with non insulin-dependent diabetes mellitus. These animals also have many indications of heart disease. However, it is not clear if the hearts suffer from vascular complications or are cardiomyopathic in nature. We examined Mg2+-dependent myofibrillar ATPase in hearts of JCR:LA-cp/cp rats and their corresponding control animals (+/?) and found no significant differences (P> 0.05). This is in striking contrast to the depression in this activity exhibited by cardiac myofibrils isolated from insulin-deficient models of diabetes. Our data demonstrate that myofibrillar functional integrity is normal in JCR:LA-cp rats and suggest that these hearts are not in a cardiomyopathic state. Insulin status may be critical in generating a cardiomyopathic condition in diabetes.
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PMID:Mg2+-dependent ATPase activity in cardiac myofibrils from the insulin-resistant JCR:LA-cp rat. 1190 Mar 75

In animal models of diabetes mellitus, such as the streptozotocin-diabetic rat (STZ-rat), spatial learning impairments develop in parallel with a reduced expression of long-term potentiation (LTP) and enhanced expression of long-term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ-diabetes and insulin treatment on the hippocampal post-synaptic glutamate N-methyl-D-aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post-synaptic density (PSD) fraction. In addition, the functional properties of the NMDA-receptor complex were examined. One month of STZ-diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr-dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and alphaCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ-rats compared with age-matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ-rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII-NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post-synaptic glutamatergic transmission is related to deficits in learning and plasticity in this animal model.
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PMID:Effects of streptozotocin-diabetes on the hippocampal NMDA receptor complex in rats. 1190 65

Depression is associated with an increased risk of developing cardiovascular disease and type 2 diabetes mellitus. Abdominal obesity is also a high risk factor for these diseases. Therefore, symptoms of depression and anxiety were examined in relation to abdominal obesity. A total of 59 middle-aged men volunteered for measurements with the Hamilton Depression Scale (HDS), the Montgomery-Asberg Depression Rating Scale (MADRS), the Beck Depression Inventory (BDI) and the Hamilton Anxiety Scale (HAS). These results were examined in relation to body mass index (BMI), waist/hip ratio (WHR) and sagittal abdominal diameter, a measurement of intra-abdominal fat mass, and metabolic variables. Men with WHR>1.0 (n=26) in comparison with men with normal WHR (<1.0, n=33) showed significantly higher sum scores in all the scales used. There were positive correlations between the sum scores of all the depression scales and the WHR or the sagittal abdominal diameter. BMI correlated comparatively weakly only with the HDS. The correlations with the WHR remained when the influence of BMI was eliminated, suggesting that obesity is less involved than centralization of body fat. Insulin and glucose were significantly related to the HDS. Morning cortisol levels were negatively related to the BDI and (borderline) to the MADRS, suggesting perturbations of the regulation of the hypothalamic-pituitary-adrenal axis. We conclude that men with abdominal obesity have symptoms of depression and anxiety.
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PMID:Depression and anxiety symptoms in relation to anthropometry and metabolism in men. 1242 56

Neonatal diabetes mellitus (NDM) is defined as hyperglycemia occurring in the first few weeks of life. It can be either transient (TNDM) or permanent (PNDM). A 25 days old newborn was brought to the hospital with restlessness, respiratory depression and cyanosis. He was born at term with a birth weight of 2,000 g. There was no consanguinity between his parents. His physical examination findings were as follows: Weight and height were under 3th percentile, he was hypoactive and dehydrated. Serum glucose level was 800 mg/dl; C-peptide was 0.41 ng/ml. Upon investigation for dyslipidemia in association with his neonatal diabetes, hyperchylomicronemia was found both in the patient and his father. Pancreatitis, anemia and cholestasis were also observed. Insulin treatment was started for his diabetes together with a special diet for dyslipidemia. At the end of 28 months of follow-up, dyslipidemia has resolved but the need for insulin therapy was still existing. However, TNDM was considered in differential diagnosis because he was small for gestational age (SGA) at birth and his symptoms had started at the 25th day of the neonatal period. Delayed recovery from insulin dependency brought out the possibility of PNDM. Furthermore, neonatal diabetes combined with hypechylomicronemia is a rare clinical picture. Reported cases of NDM with different clinical evaluation will help to better understanding of this disorder.
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PMID:Neonatal diabetes with hyperchylomicronemia. 1255 65

Insulin resistance is a metabolic syndrome commonly seen in obesity. Leptin, the obese gene product, plays a role in the regulation of cardiac function. Elevated leptin levels have been demonstrated under insulin-resistant states such as obesity and hypertension, although their role in cardiac dysfunction is unknown. This study was designed to determine the impact of prediabetic insulin resistance on leptin levels and leptin-induced cardiac contractile response. Whole-body insulin resistance was generated with a 10-week dietary sucrose feeding. Contractile and intracellular Ca(2+) properties were evaluated in ventricular myocytes using an IonOptix system. The contractile indices analyzed included peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR(90)), maximal velocity of shortening/relengthening (+/-dL/dt), fura-fluorescence intensity change (deltaFFI) and decay rate (tau). Sucrose-fed rats displayed significantly elevated body weight and plasma leptin levels, depressed PS, +/-dL/dt, shortened TPS, prolonged TR(90) and tau, as well as reduced deltaFFI compared to the starch-fed control group. Leptin (1-1000 nM) elicited a concentration-dependent depression of PS and deltaFFI in myocytes from both starch and sucrose groups. Leptin-induced contractile depression was abolished by the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyle ester, elevation of the extracellular Ca(2+) concentration, the Janus activated kinase 2 inhibitor AG-490 or the mitogen activated protein kinase inhibitor SB203580 in myocytes from both sucrose and starch groups. Moreover, AG-490 and SB203580 unmasked a positive response of PS in myocytes from both groups. These data indicate that insulin resistance directly induces hyperleptinemia and cardiac contractile dysfunction, without affecting leptin-mediated cardiac contractile function at the myocyte level.
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PMID:Insulin resistance induces hyperleptinemia, cardiac contractile dysfunction but not cardiac leptin resistance in ventricular myocytes. 1451 67

Growth hormone replacement in adult growth hormone deficient patients improves psychological well-being and the quality of life. The aim of this study was to investigate relationship between changes in mood, cognitive functioning, quality of life, changes in body composition and hormone concentration at baseline and six months after treatment with human recombinant growth hormone. Eighteen adult patients with growth hormone deficiency syndrome were recruited to the study. Growth hormone was administered in doses of 12 IU per week in an open design. After 6 months of growth hormone replacement therapy the psychological functioning improved significantly on mood scales (Profile of Mood State) and on a cognitive performance tests. Changes in quality of life scale were trivial. After growth hormone treatment serum concentration of Insulin like growth factor -1 (IGF-1) and triiodothyronine increased and concentration of serum free thyroxine decreased significantly in comparison to basal concentration. There were no significant differences in changes of plasma cortisol, thyrotropin and growth hormone concentrations. Improvement on Profile of Mood State global score as well as on Vigor-Activity subscale correlated significantly with increase in IGF-1 concentration. Improvement on Profile of Mood State Vigor-Activity subscale correlated with increase in water body mass and improvement on Hospital Anxiety and Depression scale depression subscale correlated with decrease in cortisol concentration. The study shows that growth hormone replacement improves mood and cognition in adult growth hormone deficient patients. This improvement is related to changes in water body mass as well as to endocrine changes.
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PMID:Psychological functioning after growth hormone therapy in adult growth hormone deficient patients: endocrine and body composition correlates. 1529 90

Twenty-four multiparous Holstein cows were used to determine the effects of dietary fat and glucose precursors on energy status and lactation. The treatment group (T) received 409 g/d (DM basis) of a combination of calcium salts of fatty acids, calcium propionate, and propylene glycol. The control group (C) received 409 g/d of a mixture of calcium salts of fatty acids and ground barley from 14 +/- 0.9 g/d before until 21 d after calving. Dry matter intake was greater (16.1 vs. 13.6 +/- 1.3 kg/d) for T than C during the last week prepartum and did not decrease for T from the previous week, whereas, in C, DM intakes decreased by 3.2 kg/d. Production of milk and milk fat did not differ. There was a tendency for lower protein and increased lactose concentrations in milk from T cows. Milk fat percentage was lower in T at d 7 (5.5 vs. 6.4 +/- 0.5%) and 28 (4.4 vs. 5.5 +/- 0.5%) of lactation. Liver lipid content was numerically lower (7.9 vs. 9.2 +/- 0.9%) and glycogen content was significantly higher (2.4 vs. 2.0 +/- 0.1%) in T vs. C cows on d 7 of lactation. Concentrations of nonesterified fatty acids were lower in blood of T cows on d 2 and 7 of lactation. Over all time points, blood glucose concentrations were higher in T cows pre- (70.75 vs. 62.1 +/- 1.3 mg/dL) and postpartum (60.1 vs. 56.2 +/- 1.1 mg/dL). Insulin concentrations in blood were greater for T (397 vs. 314 +/- 48 pg/mL) both pre- and postpartum. Feeding glucose precursors in combination with rumen inert lipids, compared with feeding barley in combination with the lipids for 2 wk before parturition and 3 wk postpartum helped avoid prepartum feed intake depression and increased blood glucose and insulin and decreased blood NEFA.
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PMID:Effects of dietary glucogenic precursors and fat on feed intake and carbohydrate status of transition dairy cows. 1532 25

The purpose of the study was to find out if snoring, sleep apnea and daytime sleepiness are independent indices of obesity related to type two diabetes (T2D), and whether depression is independently associated with features of sleep apnea. A population-based cohort study was conducted among 593 subjects (245 men and 348 women) born in 1935 and living in Oulu in 1996-1998. Glucose status was determined with a standard 2h oral glucose tolerance test, and sleeping disorders were recorded on the Epworth sleepiness scale (ESS) and in a questionnaire of five questions about sleeping and snoring. Depression was measured by the Zung self-rated depression scale. Insulin sensitivity was measured by quantitative insulin sensitivity check index. Habitual snoring was more common in diabetic subjects than in subjects with impaired glucose regulation (IGR) or normal glucose tolerance (NGT). All sleep disorders associated with neck circumference, waist circumference and body mass index (BMI). There was also a relationship between impaired insulin sensitivity and habitual snoring in bivariate analysis. In multiple logistic regression analysis, depression associated independently with daytime sleepiness (OR 3.00, 95% CI 1.40-6.46). Type 2 diabetes (T2D) (OR 1.93, 95% CI 1.04-3.57) and smoking (OR 1.69, 95% CI 1.00-2.84) associated independently with habitual snoring. BMI (OR 1.20, 95% CI 1.09-1.34) and male gender (OR 2.61, 95% CI 1.05-6.72) associated independently with sleep apnea. In a multiple regression model, BMI, neck circumference and habitual snoring associated independently with T2D. Habitual snoring was associated with T2D and impaired insulin sensitivity. Daytime sleepiness seemed to be linked with depression but not with using sleep medication, IGR and T2D.
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PMID:The relationship of glucose tolerance to sleep disorders and daytime sleepiness. 1562 Apr 38

Insulin and its receptor are both present in the central nervous system and are implicated in neuronal survival and hippocampal synaptic plasticity. Here we show that insulin activates phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB), and results in an induction of long-term depression (LTD) in hippocampal CA1 neurones. Evaluation of the frequency-response curve of synaptic plasticity revealed that insulin induced LTD at 0.033 Hz and LTP at 10 Hz, whereas in the absence of insulin, 1 Hz induced LTD and 100 Hz induced LTP. LTD induction in the presence of insulin required low frequency synaptic stimulation (0.033 Hz) and blockade of GABAergic transmission. The LTD or LTP induced in the presence of insulin was N-methyl-d-aspartate (NMDA) receptor specific as it could be inhibited by alpha-amino-5-phosphonopentanoic acid (APV), a specific NMDA receptor antagonist. LTD induction was also facilitated by lowering the extracellular Mg(2+) concentration, indicating an involvement of NMDA receptors. Inhibition of PI3K signalling or discontinuing synaptic stimulation also prevented this LTD. These results show that insulin modulates activity-dependent synaptic plasticity, which requires activation of NMDA receptors and the PI3K pathway. The results obtained provide a mechanistic link between insulin and synaptic plasticity, and explain how insulin functions as a neuromodulator.
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PMID:Insulin modulates hippocampal activity-dependent synaptic plasticity in a N-methyl-d-aspartate receptor and phosphatidyl-inositol-3-kinase-dependent manner. 1609 51

Insulin-like growth factor (IGF)-I is known to act on fibroblasts as a progression factor to push cells toward proliferation and activation to synthesize collagen. Subepithelial fibrosis, collagen deposition at the lamina reticularis, is part of the process of so-called remodeling and is a characteristic finding in the asthmatic airway. To study the role of IGF in the evolution of asthma, we used a model that involved immunization of mice with ovalbumin and alum, followed by an inhaled challenge of ovalbumin. IGF-I neutralizing antibody was continuously infused with an osmotic pump. Pulmonary function was analyzed using whole-body plethysmography before and after acetylcholine administration. It was found that OVA inhalation induced IGF-I expression at the site of the airway. IGF-I neutralizing Ab inhibited the elevation of airway resistance, airway inflammation, and an increase in airway wall thickening. The depression of ICAM-1 expression was accompanied by a diminution in airway inflammation. In conclusion, these results suggest that IGF-I is likely to be an important mediator of inflammation and remodeling in the asthmatic airway.
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PMID:Role of insulin-like growth factor-I in allergen-induced airway inflammation and remodeling. 1616 97


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