Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to examine the influence of an eight day starvation period on semen characteristics and some endocrine parameters of young bulls. The experiments were performed with 18 bulls in two trials showing the following set-up: pre-treatment period (7 or 20 days), starvation period (8 days), realimentation period (3 days) and control period (64 days). During the pre-treatment period and the control period the bulls obtained a well-balanced food-ration, during the period of starvation only 2 kg straw daily. During the starvation period the bulls lost 6% of their bodyweight. No influence on general health could be noticed. The concentrations of testosterone, LH, bovine growth hormone, insulin and insulin-like growth factor decreased significantly during or after the period of starvation. There was no clear influence in volume, sperm density and total number of sperm due to the metabolic stress during the hunger period. The initial progressive motility of sperm was not affected. The percentage of morphological abnormal spermatozoa increased 45-55 days after the hunger period. Simultaneously the semen freezability was decreased. An influence on the acrosomal morphology of frozen/thawed spermatozoa could not be obtained. The concentration of fructose, citric acid and glycerylphosphorylcholine (GPC) of the seminal plasma was insignificantly influenced during the period of starvation. The realimentation caused a stimulating effect on the secretion mainly of GPC.
 ...
PMID:[Effects of a metabolic endurance test developed for the constitution examination of young bulls on spermatologic and endocrine parameters]. 207 62

The present study examined whether different proteins have different effects on whole-body protein turnover in adult rats. The rats were either starved, given a protein-free but energy-sufficient diet (1 MJ/kg body weight (BW) per d) or a diet containing intact casein, hydrolysed casein, or hydrolysed soya-bean protein at a level of 9.1 g/kg BW per d. The diets, which were isoenergetic with the same carbohydrate: fat ratio, were given as a continuous intragastric infusion for at least 4 d. During the last 19 h 15N-glycine (a primed continuous infusion) was given intragastrically and 15N was recovered from urinary ammonia and urea during isotope steady state for measurement of protein synthesis and protein degradation. Compared with starvation the protein-free diet decreased N excretion by 75%, probably by increasing the rate of reutilization of amino acids from endogenous proteins for protein synthesis. The protein diets produced a positive N balance which was independent of the protein source. Intact and hydrolysed casein increased protein synthesis 2.6- and 2.0-fold respectively, compared with the protein-free diet. Protein degradation increased 1.4- and 1.2-fold respectively. Hydrolysed soya-bean protein did not increase protein synthesis but decreased protein degradation by 35% compared with the protein-free diet. Compared with the hydrolysed soya-bean protein, intact casein resulted in 2.2- and 2.8-fold higher rates of protein synthesis and degradation respectively. These results are not easily explained by known sources of misinterpretation associated with the 15N-glycine method. Hydrolysed casein and hydrolysed soya-bean protein produced similar concentrations of insulin-like growth factor-1, insulin, glucagon, and corticosterone. The difference in amino acid composition between the dietary proteins was reflected in plasma amino acid composition and this is suggested to be responsible for the different effect on protein turnover. Preliminary results from this study have previously been published in abstract form (Nielsen et al. 1991).
 ...
PMID:Casein and soya-bean protein have different effects on whole body protein turnover at the same nitrogen balance. 791 30

The intracellular effects of bradykinin are mediated through the recently cloned B2 kinin receptor which belongs to the superfamily of receptors with seven transmembrane domains. The molecular events which transduce the bradykinin signal on the post-receptor level are not understood in detail. We studied whether in human foreskin fibroblasts bradykinin treatment induces tyrosine phosphorylation of cellular proteins. Using phosphotyrosine antibodies we detected a bradykinin-dependent phosphorylation of a group of proteins of about 130 kDa and an additional signal around 70kDa after starvation of cells. The effect evoked by 10 nM bradykinin was rapid (2 min) and it was partially reduced by the B2-kinin-receptor antagonist Hoe 140 which was shown to be a weak inducer of tyrosine phosphorylation. The bradykinin-mediated tyrosine phosphorylation events were reproduced in human embryonal kidney 293 fibroblasts which were transiently transfected with the rat B2 kinin receptor, but they were not observed in untransfected 293 control cells. These data suggest that the B2 kinin-receptor subtype is involved. Upon fractionation of cells the 130kDa protein group was recovered both in the membrane and the cytosolic protein fraction. To assess the specificity of this bradykinin effect we stimulated human foreskin fibroblasts with epidermal growth factor (EGF), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF-I) and insulin. While IGF-I, insulin and EGF were almost ineffective, PDGF stimulated the tyrosine phosphorylation of 130-kDa bands with a similar pattern to that produced by bradykinin. Immunoprecipitation experiments with specific antibodies against potential candidate proteins in the molecular-mass range around 130kDa revealed positive results for the focal adhesion kinase FAK and the p130 Src substrate while negative results were obtained for the GTPase-activating protein GAP, the phospholipase C-gamma1, the Janus kinase JAK-1 and vinculin. The data suggest that the tyrosine phosphorylation of FAK and the pl30 Src substrate might be involved in the B2-kinin-receptor signalling cascade.
 ...
PMID:Bradykinin induces tyrosine phosphorylation in human foreskin fibroblasts and 293 cells transfected with rat B2 kinin receptor. 866 18

Substrate fluxes in response to growth hormone administration depend on both the calorie as well as acid-base balance. Growth hormone's acidogenic action as a consequence of promoting fatty acid utilization yields protons required for driving hepatic glutamate efflux; effective uncoupling of nitrogenous precursors from ureagenesis and recycling as glutamate bound for the periphery appears dependent upon this mechanism. Subsequent peripheral retrieval of the salvaged glutamate requires insulin-like growth factor-1 (IGF-1) activated uptake and acid-base homoeostasis. In addition to this nitrogen sparing acidogenic effect, growth hormone is also basogenic in combination with IGF-1 and acting on the kidney as a target organ. Therefore acid-base and nitrogen homoeostasis are normally attuned to one another through the co-ordinated action of growth hormone/IGF-1 on substrate fluxes. However during starvation ketoacid production as the consequence of incomplete fatty acid oxidation and ketone excretion swamps the basogenic limb and full-blown metabolic acidosis prevails; under this condition growth hormone's effectiveness in sparing nitrogen for anabolic processes is curtailed as glutamate (emanating from the liver) and glutamine (derived from muscle proteolysis) are directed to the kidneys, supporting ammoniogenesis: nitrogen balance is now sacrificed for acid-base homoeostasis. Underlying this state is an intracellular acidosis that may contribute to insulin resistance and developing hyperglycaemia in response to growth hormone. In acute injury, an additional acid load contributed from muscle proteolysis and cytokines reinforces an intracellular acidosis that further blunts growth hormone responsiveness and suppresses coupled IGF-1 production. From this perspective growth hormone's acidogenic and basogenic actions should balance for an effective anabolic response during hypermetabolic catabolic illnesses.
 ...
PMID:The role of growth hormone in substrate utilization. 958 78

In vivo, in the sheep ovary, the expression of insulin-like growth factor binding protein (IGFBP)-2 and particularly IGFBP-5 has been shown to increase dramatically in apoptotic granulosa cells from atretic follicles. The aim of this work was to study the relationship between apoptosis induced by serum starvation in vitro and expression of IGFBP-2 and -5 by ovine granulosa cells. For this purpose, granulosa cells from follicles 1-3 mm in diameter were cultured in the presence of serum for 2 days, then cultured in the presence or absence of serum for 24, 48, or 72 hr. At the end of the culture, cells were counted, cell viability was assessed by studying DNA fragmentation, and IGFBPs expression was studied by quantitative autoradiography, Western-ligand blotting, immunoblotting, and quantitative in situ hybridization. In vitro, IGFBP-2 and particularly IGFBP-5 were the main IGFBPs secreted by ovine granulosa cells. Serum starvation provoked (i) apoptosis of granulosa cells within 48 hr, (ii) a marked decrease in cell density, and (iii) a marked increase in the amount of IGFBP-5 associated with cell membranes and with the walls of culture wells, but no change in culture medium. The increase in the amount of cell- and wall-associated IGFBP-5 after serum starvation was essentially due to the consecutive decrease in cell density rather than to an increase in cell apoptosis. Indeed, irrespective of the presence or absence of serum, the amount of IGFBP-5 associated to cell membranes was inversely correlated to cell density. In contrast, the amount of IGFBP-5 present in culture medium was positively correlated to cell density. Furthermore, expression of IGFBP-5 mRNA was shown to increase with both cell density and cell death. Indeed, the expression of IGFBP-5 mRNA dramatically increased with cell density, irrespective of the presence or absence of serum, but at a similar cell density, expression was higher in serum-free than in serum conditions. Overall, these results indicate that, in vitro, the localization of IGFBP-5 on ovine granulosa cell membranes and in culture medium, respectively, was mainly dependent on cell density, whereas expression of IGFBP-5 mRNA was related to both cell density and cell death. These data suggest that IGFBP-5 is involved in both growth arrest and apoptosis of granulosa cells in the sheep.
 ...
PMID:Expression of insulin-like growth factor binding protein-5 by ovine granulosa cells is regulated by cell density and programmed cell death in vitro. 973 41

Multiple and complex mechanisms are likely to be involved in producing the growth retardation that occurs in children with chronic disease. The principal mechanisms in the pathway leading to growth arrest include too little substrate available to the child, excessive need for and over-consumption of substrate, and inefficient management of body components needed for growth. It is proposed that alterations in the growth hormone (GH)-insulin-like growth factor (IGF) system play a major role at each of the steps between insult from chronic disease and growth retardation. When substrate is insufficient, the production and action of IGF-I are attenuated at multiple points in the GH-IGF cascade. When over-consumption of substrate occurs, a situation of 'internal starvation' probably develops--leading to events similar to those that take place when substrate supply is inadequate. Finally, conditions that cause inefficient management of body components needed for growth, as characterized by increased proteolysis, appear to be attenuated by GH and IGF-I.
 ...
PMID:Growth retardation in chronic diseases: possible mechanisms. 1010 62

Both starvation and sepsis are characterized by growth hormone (GH) insensitivity, which leads to a reduction in circulating insulin-like growth factor (IGF)-I. Because of the anabolic properties of this growth factor, its decline may contribute to the growth arrest and the catabolic reaction observed in starvation and sepsis. This review focuses on the mechanisms responsible for the reduction in circulating IGF-I and impairment of GH responsiveness that occur during starvation and sepsis. A clearer understanding of the complex nature of GH resistance should lead to the development of new therapeutic strategies aimed at restoring the beneficial effects of anabolic agents such as GH and IGF-I.
 ...
PMID:Regulation of insulin-like growth factor-I in starvation and injury. 1043 29

We investigated the effects of acute starvation on mitogen-induced T-cell activation and Th1/Th2 cytokine responses in rheumatoid arthritis (RA) patients. Ten RA patients with active disease underwent a 7-day fast followed by a 2-week refeeding period. Immunological, hormonal, laboratory and clinical evaluations were carried out on days 0, 7 and 21. Using flow cytometry, mitogen-stimulated T-cell activation was assessed in fresh heparinised blood via analysis of CD69 expression. Production of Th1 (interferon-gamma) and Th2 (interleukin-4, IL-4) cytokines was also assessed by ELISA. The 7-day fast significantly decreased the erythrocyte sedimentation rate, C-reactive protein level, joint count, morning stiffness, body weight, CD4+ and CD8+ counts and CD69+ expression on mitogen stimulated CD4+ lymphocytes. A significant increase in mitogen-induced IL-4 production after fasting was found. The fast markedly reduced serum leptin and insulin-like growth factor-1 concentrations. No significant differences occurred in serum cortisol or prolactin before and after fasting. Decreases in CD4+ lymphocyte activation during fasting correlated with decreases in body weight. Our results suggest that the clinical and laboratory improvements in fasting RA patients may be attributed to decreased CD4+ T-cell activation and an increase in the number and/or function of IL-4-producing Th2 cells. Factors associated with loss of body weight during acute starvation appear to have an inhibitory effect on CD4+ lymphocyte activation.
 ...
PMID:Decreased CD4+ lymphocyte activation and increased interleukin-4 production in peripheral blood of rheumatoid arthritis patients after acute starvation. 1052 54

We have investigated the expression and secretion of insulin-like growth factor binding proteins (IGFBPs-1 to -6) in human vascular smooth muscle cells (hVSMCs) cultured from human renal arteries. Solution hybridization was used to determine IGFBP mRNA levels and Western immunoblot to detect the corresponding peptides. The hVSMCs expressed mRNAs for IGFBPs-2 to -6; IGFBP-1 mRNA was not detected. IGFBPs-3, -4 and -6 mRNAs were the most abundant, IGFBP-5 was also highly expressed, whereas the IGFBP-2 mRNA was just above the limit of detection. Serum starvation for 48 h significantly decreased the mRNA levels of IGFBPs-2 to -5 and tended to decrease IGFBP-6 mRNA also. IGFBPs-2, -4, -5 and -6 peptides could be detected in conditioned medium, but IGFBP-3 peptide was not detected. IGFBP-4 was the only peptide detected without any concentration step. Low-molecular-mass immunoreactive degradation products were found for IGFBPs-2 and -4. Exogenous IGFBPs-1, -3 and -4 in concentrations of 50 ng/ml inhibited DNA synthesis induced by 1 nM IGF-I, whereas IGFBPs-2, -5 and -6 had no significant inhibitory effects at this concentration. We conclude from these results that all IGFBPs except IGFBP-1 are expressed in hVSMC. Our results indicate that locally produced, in addition to circulating, IGFBPs may have an important role in the regulation of hVSMC.
 ...
PMID:Insulin-like growth factor binding proteins-2 to -6 are expressed by human vascular smooth muscle cells. 1055 78

Macrophage migration inhibitory factor (MIF) is a cytokine that mediates inflammatory processes in a variety of tissues. In this study, we examined the expression of MIF mRNA in the mouse osteoblastic cell line MC3T3-E1, whose proliferation is promoted by various growth factors. In the subconfluent state, transforming growth factor-beta, basic fibroblast growth factor, insulin-like growth factor-II, and fetal calf serum markedly upregulated MIF mRNA expression. The upregulation of MIF mRNA was less extensive when the cells were stimulated by the same growth factors in the overconfluent state. We also investigated the expression of MIF mRNA through a whole cell cycle from G0 phase when the osteoblastic cells were synchronized by serum starvation. The MIF mRNA expression, which gradually increased from the G0 and reached its maximum at the S phase, was nonperiodic. Moreover, human recombinant MIF upregulated the expression of urokinase plasminogen activator inhibitor-1 (PAI-1) precursor mRNA in human osteoblastic Saos-2 cells. Plasminogen activator (PA) is known to play an important role in bone metabolism, for example, in activation of procollagenase or growth factors indirectly via the formation of plasmin, and in mitogenic activity for osteoblastic cells. Our results suggest that MIF modulates the proliferation of osteoblasts and, moreover, bone tissue remodeling through the PA and plasmin system.
 ...
PMID:Growth factor-induced expression of macrophage migration inhibitory factor in osteoblasts: relevance to the plasminogen activator system. 1063 79


1 2 3 4 5 6 Next >>