Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROTEIN DEFICIENCY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1980

The effect of iron deficiency, protein deficiency and dexamethasone on infection, re-infection and treatment of Giardia muris in the mouse.

The association between nutrient deficiencies, steroid administration, anti-flagellate therapy and giardiasis was examined using the Giardia muris/mouse model. Administration of steroids to BALB/c mice resulted in persisting high levels of infection with G. muris, whereas untreated animals were able to eliminate this parasite. In addition, steroid treatment significantly reduced the efficacy of anti-flagellate therapy. Protein-deficient mice eliminated the parasite at the same rate as mice on an optimum diet and also developed strong acquired resistance to re-infection. A similar pattern was observed in iron-deficient mice, except that the number of parasites that became established during the first 2 weeks of infection was significantly reduced. Thus, there was no evidence of synergism between iron and protein deficiency and infection in this model.

Animals↗
PubMed1989

Expression of liver-specific genes coding for plasma proteins in protein deficiency.

Protein deficiency leads to a decreased concentration of plasma proteins, although it is not clear whether this response is caused by alterations in gene transcription or in post-transcriptional events. The aim of this study was to investigate the expression of some liver-specific genes coding for plasma proteins in rats kept on a protein-free diet for 30 days. Cloned cDNA probes for the albumin, transthyretin, retinol-binding protein and prothrombin genes were used in Northern hybridizations to total liver RNA to compare their transcript levels in protein-deficient and control animals. Liver polysomes were also isolated and fractionated from the two groups of animals to examine the possible effects of protein deficiency on translation of the mRNAs. The results indicate that the albumin and transthyretin mRNAs are present in lower amounts in protein deficiency. The distribution profile along sucrose gradients shows that all mRNAs are undergoing translation, but in protein-deficient animals a small but consistent fraction of each mRNA is also present in the non-polysomal, low molecular weight fractions.

Actins↗
PubMed1982

Rat cornea in experimental protein deficiency.

Protein deficiency is one of the major morbid nutritional disorders of the developing world. Increased incidence of infection in a protein-deficient state is well documented in the literature. Structural alterations produced by isolated protein deficiency on the cornea are not clear hitherto. In this investigation, it has been shown that protein deficiency in rats results in thinning of the corneal epithelial cell layers and oedema of the epithelial, stromal and endothelial cells. The pathomechanisms are discussed.

Animals↗
PubMedDate not supplied

[Nucleic acid and protein metabolism in vitamin D and dietary protein deficiency].

Protein deficiency and D-hypovitaminosis lead to marked disturbances of the RNA and protein metabolism in different organs, tissues and subcellular fractions. With a complex action of the food protein and vitamin D deficiency, changes in most organs and tissues became more intensive. The nature of the discovered shifts is largely determined by the kind of the tissue, and the degree of its metabolic activity.

Animals↗
PubMed1980

Lacrimal lysozyme alterations in experimental protein deficiency.

Protein deficiency increases the susceptibility of the host to infection. Depressed phagocytic function, fall in non-specific protective substances of the serum, and poor immune response have all been recorded in the literature. The malnourished population exhibit recurrent ocular infections. The role of local defence mechanisms, principally lysozyme, is not known hitherto. In the present report, protein-deprived weaning Wistar rats showed a significant reduction in lysozyme against Staphylococcus aftermentas.

Animals↗
PubMed1999

Inherited protein C deficiency, protein S deficiency and hyperhomocysteinaemia in a patient with hereditary spherocytosis.

We report a family with hereditary spherocytosis in whom there is, in addition, a cluster of genetic predispositions to thrombosis. Although inherited prothrombotic abnormalities are prevalent in the general population, the likelihood of this combination of abnormalities being found in a single family is extremely low. The management of such high risk individuals is discussed.

Adult↗
PubMed1980

Effect of calorie restriction and protein deficiency on protein metabolism in rats.

The changes induced by the deficiency of calories or nitrogen on the protein metabolism in rats were investigated. Animals were fed either a restricted normal diet, a protein-deficient diet or control diet ad libitum. Rats receiving protein-free diet failed to grow, while the growth of animals given restricted diet was less than those fed ad libitum. Despite that, the dietary deficiency of either calories or proteins caused the loss of protein and increased the incorporation of 1-C14 glycine into liver proteins. The contents of liver-free amino acids and urea were significantly increased only in the protein-deficient rats.

Amino Acids↗
PubMed2006

[Effect of diarrhea on nutrient utilization in protein deficient or protein-calorie deficient rats].

Diarrhea increases the effects of malnutrition. Accordingly, the effect of diarrhea on two types of malnutrition (protein deficiency and protein-calorie deficiency) was studied. The experiment included 42 young Sprague Dawley rats. The rats were distributed into three groups with 14 rats per group. During the first 16 of the experiment, the first group was fed a control diet ad libitum, the second received the same diet but with food intake reduced in 50% whereas the third group was offered a protein deficient diet. Thus, at the end of this period there were well-fed rats (control), as well as protein and protein-calorie malnourished rats. Then one half of the rats in each group were given lactose to produce diarrhea and all rats continued with their previously assigned diet and feeding regime during one more week. Therefore, during this period there were control rats, protein deficient rats and protein-calorie deficient rats with and without diarrhea. The results showed that diarrhea caused a substantial reduction in food intake and growth in the well-fed rats and also in the group fed the protein deficient diet. However, the protein-calorie deficient group did not reduce its intake nor its growth rate. As a result, diarrhea caused malnutrition in the control group and increased malnutrition in the protein deficient but it did not have an additional effect in the protein-calorie deficient rats. The apparent absorption of lipids and nitrogen measured in these rats showed that the absorption reduction caused by diarrhea was more pronounced in the protein deficient group. This group also had the lowest activities of intestinal disaccharidases. These results showed that diarrhea had a more detrimental effect in protein deficient than in protein-calorie deficient rats.

Animals↗
PubMedDate not supplied

[Toxic effect of methanol under conditions of complete and deficient protein nutrition].

In experiments with albino rats receiving complete and protein-deficient nutrition the effect of different doses of methanol (10,100 and 500 mg/kg) administered daily per os for a month was studied. Methanol was shown to display toxic hepatotropic action, producing in the liver a focal proteinic degeneration of the hepatocytic cytoplasm, causing changes in the activity of some microsomal enzymes and enlarging the average size of hepatic cells (early age-specific changes). The damaging action of methanol manifested itself in a particularly distinct fashion by depressing the synthesis of DNA, when used in large doses and against the background of a protein-deficient ration.

Animals↗
PubMed1997

Dietary protein deficiency induced changes in protein kinase C activity and phospholipid metabolism in rat hepatocytes.

Dietary protein deficiency is known to alter the protein kinase C activity in various tissues of rats. Protein kinase C activity is influenced by the metabolism of membrane phosphoinositides and phosphatidyl choline (PC). For metabolic studies, hepatocytes have been the cells of choice of various workers. Therefore, studies on protein kinase C and these phospholipids were conducted in hepatocytes of rats maintained on three different diets viz. casein (20% protein) deficient (4% protein, rice flour as source of protein) and supplemented (deficient diet supplemented with L-lysine and DL-threonine) diet for 28 days. The protein deficiency in diet led to a decline in protein kinase C activity (P < 0.01) without effecting its translocation, an increase in phosphatidyl inositol 4,5-bisphosphate (P < 0.001) and a decrease in phosphatidyl inositol 4-monophosphate and phosphatidyl inositol (P < 0.01) but did not alter the PC contents, as compared to the casein group. Supplementation of deficient diet with L-lysine and DL-threonine could considerably reverse the effect of deficiency of protein in diet. The results suggest that quality of dietary protein is mainly relevant for maintaining phospholipid metabolism and physiology of hepatocytes and thus the signalling mechanism in these cells.

Animals↗
PubMed2002

Sleep deprivation in prion protein deficient mice sleep deprivation in prion protein deficient mice and control mice: genotype dependent regional rebound.

We have previously reported a larger and more prolonged increase of slow wave activity (SWA) in NREM sleep after sleep deprivation (SD) in prion protein deficient mice (PrP) compared to wild-type mice. Regional differences in the SWA increase were investigated by comparing the effect of 6 h SD on a frontal and occipital derivation in PrP deficient mice and wild-type mice. The larger increase of SWA after SD in PrP deficient mice was restricted to the occipital derivation. The difference appeared after the waking-NREM sleep transitions, making it unlikely that PrP is involved in the mechanisms enabling the transition to sleep. Our findings may reflect differences between the genotypes in the need for recovery in this particular brain region.

Animals↗
PubMed1997

Effect of lithium on hepatic drug-metabolizing enzymes of protein-deficient rats.

Protein deficiency was produced by feeding synthetic 8%-protein diet. Lithium carbonate at the dose level of 1.1g/kg diet was administered to normal and protein-deficient rats for a period of one mo. A significant inhibition in the levels of cytochrome (cyt) P450, cyt b5, glutathione (GSH), glutathione S-transferase (GST) and glutathione peroxidase (GPx), but an increase in gamma-glutamyl transpeptidase (gamma-GT), was observed in low-protein LP-fed rats. Lithium treatment to normal rats caused no significant change in the activities of cyt P450, cyt b5, GST, and GSH levels, whereas there was elevation in the activities of gamma-GT and GPx and suppression in glutathione reductase (GRd) activity. Lithium administration to LP-fed rats resulted in significant increases in the hepatic gamma-GT and GPx activities.

Animals↗
PubMed2006

Activator protein 1-mediated transcriptional regulation strategy sustains long-term expression of a xenogeneic gene product in vivo: an implication for gene therapy targeting congenital protein deficiencies.

Maintenance of high-level transgene expression is the main challenge in current gene therapy. Although the cytomegalovirus (CMV) promoter/enhancer or its derivative the CAG promoter has been harnessed in current gene therapy vectors, transgene expression by these vectors is often transient and remains at suboptimal levels due to undefined mechanisms, possibly including the shortage of transcriptional machinery. To overcome this drawback, we designed a novel transcriptional control system, designated here as transcription factor-supercharging promoter system, in which transgene expression is regulated by the positive feedback circuit consisting of cis- and trans-acting elements of gene expression machinery. Among combinations of these elements, a plasmid composed of a target gene expression cassette driven by the chimeric CMV promoter containing repetitive 12-O-tetradecanoylphorbol-13-acetate-responsive elements as cis-acting elements (CMV-TTT) and expression cassettes for c-Fos and c-Jun genes as trans-acting elements facilitated high and long-term (>10 months) expression of a transgene after its intramuscular electroporation-mediated delivery in mice. Since human secretory alkaline phosphatase was used as a reporter, it was suggested that the immune evasion mechanism elicited by the CMV-TTT and/or c-Fos/ c-Jun expression also contributed to the sustained expression in mice. Our strategy may open a new avenue for a gene therapy that involves lifelong supplementation of a deficient protein that could be targeted by the host's immune system.

Animals↗