[Interesting aspects of the study on deficient protein nutrition].
Explore the source record for details and available documents.
Humans↗
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.
Responses of the protein-deficient rabbit to staphylococcal bacteremia.
Staphylococcal bacteremia was induced in two groups of rabbits that were pairfed high protein and protein deficient diets. Marked deviations in response were observed as a result of protein deficiency: a) blood clearance of S aureus was delayed; b) persistence and multiplication of bacteria in blood and tissues were pronounced; c) neutrophilic response was poor and transitory; d) mortality was very high and occurred very early and e) focal necrotizing lesions, rather than well-formed abscesses, were found in organs.
Animals↗
The effect of dietary energy and protein deficiency on drug metabolism.
The influence of a diet deficient in energy or protein on hepatic oxidation (Phase I reactions) and glucuronidation (Phase II reactions) in man has been examined. Nine healthy volunteers were fed an energy deficient diet (daily energy intake 4.3 MJ; daily protein intake 0.94 g/kg) and a protein deficient diet (daily energy intake 11.4 MJ; daily protein intake 0.31 g/kg) in random order. The control energy and protein intakes were 12.0 MJ and 1.52 g/kg, respectively. Each test diet period lasted 12 days. On Day 10, antipyrine 1000 mg and metronidazole 500 mg were given and elimination in saliva was determined. The metabolism of neither drugs was changed during the two dietary interventions, nor was their clearance to metabolites. On Day 12, the metabolism of oxazepam 15 mg was studied. The energy deficient and the protein deficient diet reduced the clearance rate of oxazepam by 20.3%, and 14.1% respectively. The elimination half-life was prolonged by 17.4% after the former and by 11.4% after the latter diet. Thus, both a low energy and a low protein intake decreased the glucuronidation of oxazepam, whereas no effect was observed on the rate of oxidation, expressed as the metabolism of antipyrine and metronidazole.
Adult↗
Pyridoxine (vitamin B6) neurotoxicity: enhancement by protein-deficient diet.
Large doses of pyridoxine cause injury to the primary sensory neurons in trigeminal and dorsal root ganglia of animals and patients subjected to megavitamin therapy. The increased hazard to subjects with reduced renal excretory function has been explored previously. In the present work, the neurotoxicity of pyridoxine for rats was found to be increased by dietary protein deficiency. A mere 3 or 7 days of pretreatment with either of two protein-deficient diets were sufficient to accelerate and intensify the clinical neurological signs and histological lesions from pyridoxine injections. These results are caused, at least in part, by loss of body weight, decreased protein binding in serum and decreased consumption of water and decreased volume of urine, which reduce the urinary losses of the toxicant. The vitamers related to pyridoxine (pyridoxal, pyridoxamine) and the coenzyme (pyridoxal 5-phosphate) did not cause clinical signs or lesions similar to those produced by pyridoxine even when injected in maximum tolerated doses. Neither a protein-deficient diet nor bilateral nephrectomy changed the results with the vitamers.
Animals↗
The effect of dietary protein deficiency on albumin synthesis and on the concentration of active albumin messenger ribonucleic acid in rat liver.
In rats fed on a protein-deficient diet, albumin synthesis as a percentage of total liver protein synthesis falls from the normal value of approx. 15% to about 8%. We have extracted total cytoplasmic RNA from individual rat livers and measured the concentration of active albumin mRNA by translation in a reticulocyte lysate system from which the endogenous mRNA had been removed [Pelham & Jackson (1976) Eur. J. Biochem. 67, 247-256]. In this messenger-dependent system it is possible to measure the synthesis of albumin as a proportion of the overall protein synthesis promoted by the addition of the hepatic RNA. The results show that the concentration of translatable albumin mRNA in samples of total cytoplasmic RNA from livers of protein-deficient rats is decreased markedly. These findings suggest that dietary protein supply affects selectively the synthesis and/or functional stability of albumin mRNA in rat liver.
Albumins↗
Nucleoside-nucleotide mixture increases bone marrow cell number and small intestinal RNA content in protein-deficient mice after an acute bacterial infection.
The aim of this study was to determine if intraperitoneal administration of a nucleoside-nucleotide mixture would affect small intestinal morphology, bone marrow cell number, and DNA content in protein-deficient mice subjected to acute bacterial infection. Mice were randomized into two groups and orally fed protein-free diet or nucleotide-free 20% casein diet for 10 d. The mice in each group were divided into two subgroups and intraperitoneally administered 0.35 mL saline or nucleoside-nucleotide mixture (17.5 mL/kg body weight) for 10 d. On day 10, one subgroup from each major dietary group was either inoculated intravenously with methicillin-resistant Staphylococcus aureus or saline. Three days later, small intestinal morphology, bone marrow cell number, and DNA content were evaluated in infected and noninfected mice. Protein-deficiency in association with infection significantly (P < 0.05) reduced body weight, small intestinal weight, crypt depth, villous height, and wall thickness. All dietary groups exhibited similar small intestinal DNA and protein contents (protein:DNA ratio, RNA:DNA ratio) at 3 d postinfection. However, small intestinal RNA content in the infected protein-free dietary group administered nucleoside-nucleotide mixture was higher (P < 0.05) and tended to be higher relative to the infected nucleotide-free 20% casein group administered nucleoside-nucleotide mixture compared with the rest of the groups. In the infected protein-free dietary group administered nucleoside-nucleotide mixture, bone marrow cell number and bone marrow DNA content were higher (P < 0.05) relative to the infected protein-free dietary group, nucleotide-free 20% casein diet administered saline, or nucleoside-nucleotide mixture, respectively. We conclude that intraperitoneal administration of nucleoside-nucleotide mixture may stimulate bone marrow cell proliferation, DNA content, and small intestinal RNA content during periods of relative deficiency such as protein-deficiency in combination with infection.
Animals↗
Immune responses of the protein-deficient guinea pig to BCG vaccination.
Two groups of guinea pigs were maintained on high-protein and low-protein diets and immunized with intradermal BCG. Protein deficiency was accompanied by marked inhibition of local and systemic immune responses: a) The BCG nodule was poorly formed. There was marked delay and deficiency in the mobilization of macrophages. b) The draining lymph node was atrophic and showed little or no proliferation of lymphoid cells in the paracortical area. Macrophage accumulation occurred late but became diffuse and marked, in contrast to its consistent scarcity in the BCG nodule. c) In either location epithelioid cell transformation was retarded. Well-formed mature epithelioid cell granulomas were not seen. d) Bacilli persisted for a long time in the skin and lymph node lesions, e) Tuberculin sensitivity was greatly impaired in one-fifth of animals and absent in others. These findings were suggestive of macrophage dysfunction and depression of cell-mediated immunity to BCG in the protein-deficient guinea pig.
Animal Nutritional Physiological Phenomena↗
Reversible nutritional myopathy with myotonia in the protein-deficient rat given methionine.
Rats fed a protein-deficient synthetic diet developed hind limb weakness caused by a myopathy with myotonic features on electromyography. Deficiency of vitamin E and selenium, known causes of nutritional myopathy, were excluded. Methionine supplementation of the diet reversed the clinical signs of weakness within 12 h.
Amino Acids↗
The elevation of adoptive responses to sheep erythrocytes in protein-deficient mice.
Plaque-forming cell responses and antibody titres to sheep red cells (SRC) were elevated in normally-fed irradiated adult mice reconstituted with spleen cells from young mice which had received a 4% albumin diet, compared with those given cells from normally-fed littermates. This was independent of the dose of cells transferred (5 x 10(6)--4 x 10(7)), the day of assay (3--10) and the duration of protein-deficiency (1 or 3 weeks). It suggests that the depressed responses produced by protein-deficient (donor) mice reported in earlier papers resulted from an impairment of reticuloendothelial function or a shortage of protein reserves, not directly associated with the spleen. As protein-deficiency (of the donor) accelerated the initiation of the adoptive response and increased the cell yields of the recipients it is considered likely that an enhancement of cell proliferation during the first 3--5 days after transfer was responsible for the elevated responses.
Animals↗
Intestinal permeability to large particles in normal and protein-deficient adult rats.
Intestinal absorption of ferritin and virus particles was assessed in control and protein-deficient rats using light and electron microscopic procedures. Rats weighing 100 to 130 grams were divided into two groups and fed either a 0.5% of 18% lactalbumin diet. At monthly intervals following diet initiation, three rats from each group were administered ferritin (MW-650,000) or adenovirus Type 5 (MW is greater than 1,000,000) via ligated jejunal loops either 15 or 30 minutes prior to loop excision and processing for electron microscopy. Morphological evaluation of jejunal tissues revealed that both control and protein-deficient rats absorbed ferritin and virus particles via pinocytosis and in both situations the exogenous particles were believed to be present in lysosmal bodies of typical absorptive cells. Neither ferritin molecules nor virus particles were identified elsewhere in the jejunal mucosa of control rats. Rats deprived of sufficient dietary protein for four months or longer, however, demonstrated exogenous tracer materials in intercellular spaces of the epithelium and lamina propria. Since these severely protein-deprived rats also demonstrated deterioration of apical intercellular junctions, the possibility exists that large particles moved directly between cells of the epithelial lining and subsequently into underlying connective tissue and vascular compartments for conveyance (as antigens) to other body regions.
Adenoviridae↗
Protein deficiency and energy restriction in young cebus monkeys.
Infant cebus monkeys (Cebus albifrons) were fed liquid formulas that were limited in protein, energy, or a combination of the two restrictions. Weight gain, food intake, hematological development, and plasma protein and cholesterol levels were monitored over a 20-week period. The animals restricted in protein developed the classical signs of protein deficiency--reductions in plasma albumin, a mild anemia, accumulation of fat in the liver, and, in a few cases, facial edema. These animals maintained a relatively high energy intake, and apparently wasted energy when compared to similarly non-growing energy-restricted animals. Energy-restricted animals did not exhibit these symptoms, even when their daily protein intake was reduced to match that of protein-restricted monkeys. It is concluded that an energy restriction superimposed upon a limited protein intake did not increase protein requirements or precipitate protein deficiency.
Amino Acids↗
Histobiochemical changes in lung of protein deficient rats following repeated exposures of MIC vapour.
Adult male albino rats, maintained on normal or protein deficient diets from weanling, were exposed to repeated doses of MIC vapour (0.32 mg/L for 8 min for 5 consecutive days) under static conditions. Histopathology and the activities of alkaline and acid phosphatases and GSH content of lung were studied upto day 14 after exposure. Mild but repeated exposures of MIC vapour caused severe pulmonary lesions like denudation of bronchiolar epithelial lining tissue, cellular infiltration, edema, emphysema followed by hyperplasia, hypertrophy, fibrosis and intraluminal fibroplasia. The activities of alkaline and acid phosphatases were increased at earlier intervals while GSH content decreased significantly and remained low throughout the experimental duration. Protein deficiency was found to aggravate the toxic potentials of MIC in present condition.
Acid Phosphatase↗
Regulatory T cells in the humoral response of protein deficient mice.
Cell suspensions from the spleen or thymus of mice fed normally or mice that were protein deficient were injected into mice from each dietary group and also syngeneic nudes. Antigen, polyvinyl pyrrolidone (PVP), was injected at the stage of cell transfer and the antibody titres of the recipient animals were compared with those of control animals given only antigen. The regime was repeated using cell suspensions from donor animals which had been primed with antigen. These experiments showed that spleen cells were suppressive only when transferred from deficient to normal mice. Thymocytes generally lacked suppressive effects, except when given to irradiated mice also injected with "normal" spleen cells. However, thymocytes from deficient mice were marginally enhancing in nude mice, deficient mice and older "normals". To explain these results, it is suggested that responses to PVP are determined by distinct "suppressor-inducing" and "suppressor" T cells which act via helper T cells. The latter probably affect B cells directly and largely influence IgG production. It also appears likely that the ratio of helper to suppressor (inducer and effector) T cells is increased by protein deficiency.
Animals↗
[Study of protein-deficient anemias. Ideas on the importance of protein metabolism in erythropoietic processes].
Explore the source record for details and available documents.
Anemia↗
[Protein deficiency in hospital food. Possibilities of using protein preparations].
During a twenty days period, the daily supply of protein with the normal diet was investigated for thirty patients of an emergency station. The system of food distribution allowed precise weighing of each patient's portion. According to the calculation by the "kleine Nährwerttabelle" an average daily protein allowance of 12.4 kcal% at an average daily energy allowance of 2100 kcal with an average worth of material of 20 öS was found. The nitrogen loss accounted in the literature for different stress situations enables to calculate a far higher protein need. The use of protein preparations is discussed for satisfying the need. The possibility to use milk-protein for food preparations was tested. In a trial was found that 46.2% of the patients accepted the given protein-enriched soup. Thus the share of protein in total daily calories should be lifted from 12.4 kcal% to 14.6 kcal% spending only 4.44 öS more than before. Elevating the protein portion with normal food is possible only by spending multiple costs.
Energy Metabolism↗
Protein deficiency, energy deficiency, and the oedema of malnutrition.
The role of dietary protein deficiency in kwashiorkor is uncertain, although it has been shown not to be involved in the famine oedema of adults. A study of six different diets given to 103 children with oedematous malnutrition showed that the rate of loss of oedema was strongly correlated with the dietary energy intake (r = 0.75) but not with the protein intake (r = 0.03). 66 patients given a very-low protein diet (2.5% protein energy) lost oedema as fast as those given five times as much protein. The energy intake above which oedema resolved and below which oedema accumulated was 245-270 KJ/kg/day. Because energy deficiency is not invariably associated with oedema it cannot be the only factor involved, and the necessary dietary component(s) must therefore have been present in surfeit in all the therapeutic diets. This could be potassium together with factors necessary for its retention. The accessory ingredients must be low in foods associated with human and experimental nutritional oedema. It is suggested that protein deficiency is not the cause of the oedema of kwashiorkor and that there is no need to postulate a different pathogenesis for this oedema from starvation oedema of adults.
Adult↗
Genomic and mutational analysis of the mitochondrial trifunctional protein beta-subunit (HADHB) gene in patients with trifunctional protein deficiency.
Mitochondrial trifunctional protein (TP), an enzyme of beta-oxidation, is a multienzyme complex composed of four molecules of the alpha-subunit (HADHA) containing the enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase domains and four molecules of the beta-subunit (HADHB) containing the 3-ketoacyl-CoA thiolase domain. An inborn error of this enzyme complex can cause sudden infant death syndrome, acute hepatic encephalopathy or liver failure, skeletal myopathy, or hypertrophic cardiomyopathy. TP deficiency is classified into two different biochemical phenotypes: one represents the existence of both subunits and the lack of only the 3-hydroxyacyl-CoA dehydrogenase activity and the other represents the absence of both subunits and the lack of all three TP activities, although their clinical features are similar. We have identified two Japanese patients with this disorder. Three enzyme activities of TP were undetectable in fibroblasts from these two patients. We detected two mutations in the HADHB gene from two Japanese patients, an exonic single T insertion which created a new cryptic 5' splice site and a G1331A transition (R411 K). Patient 1 was a compound heterozygote, while patient 2 was a homozygote of a G1331A transition.
Animals↗
Production of IL2 and IL3 in syngeneic mixed lymphocyte reactions of BALB/c mice are elevated during a period of moderate dietary protein deficiency.
The mixed lymphocyte reaction (MLR) is a model of T cell responsiveness to antigenic peptides complexed with major histocompatibility (MHC) proteins on antigen presenting cells (APC). Since dietary protein deficiencies alter T cell development, syngeneic and allogeneic MLR were investigated in mice fed a low protein 4% casein (4Ca) or control 20% casein (20Ca) diet. Proliferation of splenic lymphocyte populations from BALB/c mice fed 4Ca was increased during syngeneic and allogeneic MLR compared with lymphocytes from mice fed 20Ca. Increased proliferation was accompanied by significantly higher production of IL2 and IL3 during syngeneic, but not allogeneic MLR. To determine the influence of autologous B cells on IL2 and IL3 production during MLR, lymphocyte populations of mice fed 4Ca or 20Ca were depleted of B cells. Splenic lymphocyte populations of mice fed 4Ca that were depleted of B cells did not exhibit increased IL2 or IL3 production during syngeneic or allogeneic MLR. Splenic APc of mice given 4Ca caused greater proliferation during MLR. However, APC of 4Ca mice did not cause greater IL2 or IL3 production. Similarly neither IgM-B cells nor macrophage from mice fed 4Ca induced elevated IL2 or IL3 production during syngeneic or allogeneic MLR. A dichotomy appeared in that 4Ca-APC were able to induce higher T cell proliferation but not cytokine production compared with 20Ca-APC. The enhancement of T cell responsiveness to Class II MHC determinants on APC during moderate protein deficiency appears to require both T and B cells from mice fed the deficient diet.
Animals↗