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 purpose of this study was to determine if exogenous insulin-like growth factor-I (IGF-I) would improve growth rate or body composition of young broiler chickens. Broiler cockerels were given a daily intramuscular (im) injection of sodium acetate buffer (buffer control), 100 or 200 micrograms recombinant-derived human IGF-I (rhIGF-I) per kg body weight from 11 to 24 days of age. Exogenous IGF-I did not affect the average daily gain, average daily feed consumption, or the gain-to-feed ratio of broiler chickens. Although daily injection of 200 micrograms/kg of rhIGF-I reduced (P less than 0.05) body ash content, there was no significant effect of IGF-I treatment on either body fat or protein content. Plasma GH levels were depressed (P less than 0.05) by chronic treatment with rhIGF-I. In contrast, plasma levels of T3 and T4 were not affected by rhIGF-I treatment. The half-life of rhIGF-I in plasma was determined at 25 days of age in naive control or chronically-injected chickens after a single intravenous dose of 50 micrograms rhIGF-I/kg. We found a single compartment, first-order disappearance pattern of rhIGF-I from chicken plasma. The half-life (t1/2) of rhIGF-I in plasma was similar (t1/2 = 32.5 min) for naive controls (injected once) or chronically-treated chickens which had received a daily injection of rhIGF-I (100 or 200 micrograms/kg) for 14 d. These data indicate that daily injection of IGF-I cannot be used to enhance growth performance or body composition of broiler chickens when given during the early growth period. The depression of plasma GH levels in rhIGF-I-injected chickens supports a negative-feedback role of IGF-I on pituitary GH secretion.
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PMID:Response of young broiler chickens to chronic injection of recombinant-derived human insulin-like growth factor-I. 178 8

Insulin-like growth factor-I (IGF-I) and IGF-II have been measured in plasma obtained from male and female pigs of two strains during daily administration of pituitary-derived porcine GH (pGH; 100 micrograms/kg) from 60 to 90 kg body weight. Each plasma sample was first chromatographed to separate the IGF from binding proteins in order to obtain reliable measurements. IGF-I concentrations showed no differences between strains, but were higher in untreated males (497 +/- 43 (S.E.M.) micrograms/l) than females (299 +/- 15 micrograms/l). GH-treated animals had two-fold higher concentrations of IGF-I. IGF-II concentrations were not significantly different between sexes or strains, but were decreased in pigs treated with pGH (299 +/- 28 micrograms/1) compared with controls (431 +/- 32 micrograms/l). Binding protein concentrations, measured as interference in the IGF-I and IGF-II assays, were not different between sexes or strains, but were increased in pGH-treated animals. Taken together, these results indicate that in addition to the expected increase in IGF-I concentrations, exogenous administration of pGH to pigs leads to an increase in IGF-binding protein and a depression in IGF-II concentrations.
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PMID:Growth hormone increases insulin-like growth factor-I (IGF-I) and decreases IGF-II in plasma of growing pigs. 215 87

Insulin-like growth factor-I elicits a long-term depression of the glutamate-induced GABA release in the adult rat cerebellum that lasts at least several hours. We studied whether protein kinase C and nitric oxide may be involved in this effect of insulin-like growth factor-I on GABA release since both signalling pathways have been implicated in other forms of neuromodulation in the cerebellum. By using microdialysis in the adult rat cerebellum, we found that either an inhibitor of protein kinase C (staurosporine) or of nitric oxide synthase (Nw-nitro-L-arginine methyl ester) counteracted the long-term, but not the acute effects of insulin-like growth factor-I on glutamate-induced GABA release. On the contrary, when either an activator of protein kinase C (phorbol ester), or an nitric oxide donor (L-arginine), were given with glutamate, they mimicked only the acute effects of insulin-like growth factor-I on glutamate-induced GABA release. Finally, when both protein kinase C and nitric oxide-synthase were simultaneously inhibited by conjoint administration of staurosporine and Nw-nitro-L-arginine methyl ester, a complete blockage of both the short and the long-term effects of insulin-like growth factor-I on GABA release was obtained. These results, indicate that: (i) activation by insulin-like growth factor-I of either the protein kinase C or nitric oxide-signalling pathways is sufficient for the short-term inhibition of glutamate-induced GABA release; and (ii) simultaneous activation of both the protein kinase C and the nitric oxide signalling pathways is necessary for insulin-like growth factor-I to induce a long-term depression of GABA responses to glutamate. Thus, long-term depression of glutamate-induced GABA release by insulin-like growth factor-I in the cerebellum is mediated by simultaneous activation of both protein kinase C and nitric oxide-signalling pathways.
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PMID:Involvement of protein kinase C and nitric oxide in the modulation by insulin-like growth factor-I of glutamate-induced GABA release in the cerebellum. 884 70

This study was undertaken to determine if human recombinant growth hormone (hrGH, 6 mg/d for 2 wk) would stimulate muscle protein synthesis in AIDS wasting. Healthy controls were compared with patients who were HIV+, had AIDS without weight loss, and had AIDS with > 10% weight loss. Before hrGH, rates of skeletal muscle protein synthesis, measured with l-[2H5]phenylalanine, were the same in controls and in all stages of disease. Rates of myofibrillar protein degradation, however, assessed from urinary excretion of 3-methyl histidine, were higher in AIDS and AIDS wasting than in HIV+ or healthy individuals. The group with weight loss had significantly higher TNFalpha levels but not higher HIV viral loads. Muscle function, as determined by isokinetic knee extension and shoulder flexion, was significantly higher in controls than all infected individuals. After GH, rates of protein synthesis were stimulated 27% in controls, with a smaller increase (11%) in HIV+, and a significant depression (42%) in AIDS with weight loss, despite fourfold elevation in insulin-like growth factor-I in all groups. There was a significant correlation of hrGH-induced changes in muscle protein synthesis with severity of disease (P = 0.002). The results indicate increased basal muscle protein degradation and decreased responsiveness of muscle protein synthesis to GH in the later stages of disease.
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PMID:Responsiveness of muscle protein synthesis to growth hormone administration in HIV-infected individuals declines with severity of disease. 932 79

The present study evaluates the effects of 2 years of growth hormone (GH) replacement therapy on psychological well-being and cognitive performance in adults with childhood-onset growth hormone deficiency (CO-GHD). A total of 48 GHD adult men (mean age: 27 years) were randomly assigned to one of four treatment groups: placebo treatment, or GH replacement in a dose of 1, 2, or 3 IU/m2, respectively. Placebo treatment was given for 6 months. Psychological assessments were made every 6 months. Assessments included somatic and psychological complaints, depression, fatigue, vigor, tension, state/trait anxiety, iconic memory, short-term memory, long-term memory and perceptual-motor skill. GH treatment was considered physiological if the observed insulin-like growth factor-I (IGF-I) levels were within the normal range. It was considered supraphysiological if serum IGF-I rose to a value exceeding the upper normal limit. During the placebo-controlled phase of the study the changes in memory performance were positively correlated to the GH induced changes in serum IGF-I concentration and, more weakly, to the daily GH substitution dose. At 6 months memory only had improved in the group receiving supraphysiological GH treatment, but not in the group of patients who had a normalization of serum IGF-I. However, after 1 year of treatment a normalization of memory functioning was found in both groups of patients and this was preserved during the 2nd year of treatment. No changes were observed in psychological well-being and perceptual-motor skill. We conclude that GH replacement improves memory function in adults with CO-GHD. It has no effect on psychological well-being or perceptual-motor skill. Supraphysiological treatment accelerates the recovery of memory performance. However, the long-term effects are not different from those achieved with physiological GH replacement.
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PMID:Cognitive changes during growth hormone replacement in adult men. 961 51

A multistage protozoan parasitic disease was used as a cachexia model to study the effects of daily administration of bovine growth hormone (GH) on endocrine and body composition changes of young calves from the onset of the acute phase response (APR). Male calves averaging 127.5 +/- 2.0 kg body weight were assigned to control, ad libitum fed, noninfected (C); ad libitum fed, infected (250,000 oocysts Sarcocystis cruzi, per os, I); noninfected, pair-fed (PF) to matched I-treatment calves and these respective same treatments in calves injected daily with GH (USDA-bGH-B1), 12.5 mg/calf/day, im) designated as CGH, IGH and PFGH. GH injections were initiated on Day 20 postinfection (PI), 3 to 4 d before the onset of clinical signs of APR, and continued to Day 56 PI, at which time animals were euthanized for tissue collections. Abrupt increases in rectal temperature commensurate with up to 70% reduction in voluntary feed intake were observed in I and IGH beginning 23-25 d PI. For the trial period between Days 20 and 56 PI, average daily carcass protein gains were 123, 52, 109, 124, 48, and 67 g/d and average daily carcass fat gains were 85, 11, 43, 71, -23, and 29 g/d for C, I, PF, CGH, IGH, and PFGH, respectively. Effects of GH were significant for fat accretion and plasma urea depression. Rectus femoris was highly refractory to catabolic effects of infection while psoas major was significantly catabolized during infection. Plasma concentrations of insulin-like growth factor-I (IGF-I) increased significantly in all GH-treated calves between Day 20 and 23 PI. Plasma IGF-I declined well below Day 20 values in all infected calves from the onset of the APR through the end of the study. The decrease in plasma IGF-I concentrations in I and IG was highly correlated with the magnitude of the fever response. Hepatic mRNA for GH receptor and IGF-I was decreased in infected calves. Hepatic microsomal membrane binding of 125I-GH did not differ between groups. The data suggest that effects of GH and parasitism on tissue metabolism during disease may vary among different specific tissue pools. The data demonstrate that daily GH administration in young calves does not prevent lean tissue losses and may accelerate fat depletion associated with cachectic parasitism. Furthermore, the onset of APR overrode the capacity for GH to maintain elevated plasma concentrations of IGF-I, an effect not readily explained through changes of GH-receptor binding.
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PMID:Changes in somatotropic axis response and body composition during growth hormone administration in progressive cachectic parasitism. 967 56

Abdominal obesity, anxiety, and depression have been found to cluster in several studies. To further characterize these associations, the following study was performed. In a population of 51-year-old men (N = 284), measurements of obesity (body mass index [BMI]) and body fat distribution (waist to hip ratio [WHR] and sagittal trunk recumbent diameter [D]) were analyzed in relation to dexamethasone (0.5 mg) inhibition of cortisol secretion, measured as salivary cortisol. Symptoms of anxiety and depression were defined by a validated questionnaire. Furthermore, testosterone, insulin-like growth factor-I (IGF-I), insulin, glucose, and serum lipid levels were measured. Twenty-five men (8.8%) had symptoms of anxiety and depression. BMI, WHR, and D correlated negatively with testosterone, except for BMI in the anxio-depressive (ADP) group. IGF-I showed no significant relationship. Furthermore, fasting insulin and the insulin to glucose ratio correlated positively and high-density lipoprotein (HDL) cholesterol correlated negatively with BMI, WHR, and D in the total study population and in the subgroups. Total and low-density lipoprotein (LDL) cholesterol showed no significant relationships. Correlation coefficients tended to be higher in ADP men. Dexamethasone inhibition showed a negative significant relationship with BMI (rho = -.47, P = .025), WHR (borderline, rho = -.37, P = .086), and D (rho = -.43, P = .046) only in the ADP group. Comparing the ADP group versus the group without anxio-depression (ADO) and high or low BMI (P = .008), WHR (P = .026), and D (P = .012) showed blunted dexamethasone inhibition only in ADP men with high anthropometric measurements. These findings suggest there is a subgroup with elevated BMI, WHR, and D in whom a blunted dexamethasone response is found associated with traits of anxiety and depression, conditions characterized by such an abnormality. The reason for the association might be insufficient control of cortisol secretion, followed by visceral fat accumulation.
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PMID:Endocrine and metabolic aberrations in men with abdominal obesity in relation to anxio-depressive infirmity. 978 19

The effect of recombinant bovine somatotropin (bST) on the chemiluminescence, diapedesis, and expression of adhesion receptors (CD11a, CD11b, CD18) of isolated polymorphonuclear leukocytes was studied. The plasma concentrations of insulin-like growth factor-I (IGF-I), bST, cortisol, and alpha-lactalbumin were also monitored. In addition, general and local clinical symptoms and the differentiation of circulating leukocytes were also studied during experimentally induced Streptococcus uberis mastitis in cows. Ten cows were infected with 500 cfu of S. uberis O140J in both left quarters. Five cows were subcutaneously treated with 500 mg of recombinant bST 7 d before and after infection, and 5 control cows received the excipient. General (fever, tachycardia, inappetance, and depression) and local symptoms (swelling, pain, firmness, and flecks in milk) were more acute, severe, and longer-lasting in control cows. Treatment with bST had no effect on chemiluminescence and diapedesis of circulating polymorphonuclear leukocytes and no effect on the expression of adhesion receptors. Recombinant bST induced significantly higher IGF-I and bST concentrations in plasma. The leukopenia observed after infection was less pronounced in the bST-treated cows, and the number of circulating band neutrophils and metamyelocytes was significantly lower in the treated group. The concentration of cortisol did not differ between both groups, but the blood concentration of alpha-lactalbumin significantly increased in both groups from 6 d after infection. These results showed that treatment with recombinant bST improves animal welfare by protecting the cows from severe local and general clinical symptoms during subsequent S. uberis mastitis, but that it has no effect on chemiluminescence, diapedesis, and the expression of adhesion receptors of circulating polymorphonuclear leukocytes.
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PMID:Effect of bovine somatotropin on neutrophil functions and clinical symptoms during Streptococcus uberis mastitis. 1041 62

It has been hypothesized that the physiological basis of follicle selection is the differential expression of factors, which modulate the action of gonadotrophins on follicular cells, at key points during the process of follicle development. The aim of this research was to test this hypothesis by identifying factors that can enhance or attenuate the action of the gonadotrophins in stimulating follicle development using both in vivo and in vitro models. Experiments in vivo utilized sheep with an ovarian autotransplant to allow intra-arterial infusion of putative local factors and exposure of the ovary to high local concentrations. Experiments in vitro utilized physiological serum-free cell culture systems for both granulosa and theca cells that allow gonadotrophin-induced differentiation in vitro. The putative local factors tested included insulin-like growth factor-I (IGF-I LR3 analogue), transforming growth factor alpha (TGF alpha) or epidermal growth factor (EGF) and inhibin A. IGF-I stimulated both cellular proliferation and hormone production by both granulosa and theca cells in vitro and similarly stimulated ovarian follicle development and ovarian androgen and oestradiol secretion in vivo. Both TGF alpha and EGF stimulated granulosa and thecal cell proliferation in vitro in a dose-responsive manner and concomitantly inhibited hormone production, whereas intra-arterial infusion of TGF alpha in vivo resulted in induction of atresia in large antral follicles and an acute fall in ovarian hormone secretion. Inhibin A in vitro augmented gonadotrophin stimulated androgen and oestradiol production by thecal and granulosa cells, respectively, but had no effect on cell number. Paradoxically, intra-arterial infusion of inhibin A resulted in an acute depression in ovarian steroid secretion. This depression, however, was also associated with an acute depression in circulating FSH concentrations. In conclusion, these data provide strong support for the hypothesis that factors can modulate the action of gonadotrophins on follicular cells to augment (IGF-I, inhibin A) or inhibit (TGF alpha/EGF) granulosa and thecal cell differentiation. The challenge for the future in this area of research is to understand how these factors interact to enable one follicle to be selected from an ovulatory cohort.
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PMID:The modulation of gonadotrophic hormone action on the ovary by paracrine and autocrine factors. 1048 30

Growth depression is a side effect of high-dose glucocorticoid therapy in childhood. It is partially mediated by alterations of the somatotropic hormone axis and partially by direct local effects on growth plate chondrocytes. The mechanisms of interaction of corticosteroids and somatotropic and calciotropic hormones at the cellular level were recently investigated in more detail, using experimental models of primary cultures of growth plate chondrocytes. In proliferative chondrocytes, growth hormone (GH) and the calciotropic hormones parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1alpha,25(OH)2D3] increase cell proliferation via stimulation of paracrine insulin-like growth factor-I (IGF-I) secretion. Corticosteroids decreased GH, and PTH or 1alpha,25(OH)2D3 stimulated cell growth in a dose-dependent manner. Corticosteroids in high doses reduced the expression of the GH receptor and type 1 IGF receptor. But the main antiproliferative molecular effect of corticosteroid was the reduction in basal and hormone-stimulated IGF-I secretion. The in vitro results are in accordance with the observation in animal experiments and in children treated with corticosteroids, demonstrating that the growth-depressing effect of corticosteroids can be compensated for by supraphysiological doses of GH or IGF-I.
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PMID:Suppression of growth plate chondrocyte proliferation by corticosteroids. 1091 28


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