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PubMedDate not supplied

Effect of dietary protein deficiency on the performance of turkeys and chickens.

Two field occurrences of protein-deficiency disease were reported in turkeys and chickens. The disease caused unthriftiness, poor growth, and the exhibition of pica in flocks of 15-week-old pedigree large white turkeys, and it resulted in a sharp drop (18%) in egg production in a flock of 60-week-old white leghorn layers. In each case, the disease was cured by replacing the protein-deficient diet with a protein-sufficient one.

Animals↗
PubMed2000

Relative and combined effects of ethanol and protein deficiency on bone histology and mineral metabolism.

This study was performed to analyze the relative and combined effects of ethanol and protein deficiency on bone histology and mineral metabolism in 4 groups of 7 animals each which were pair-fed during 8 weeks with 1) a nutritionally adequate diet; 2) a 36% (as energy) ethanol containing isocaloric diet; 3) a 2% protein, isocaloric diet; and 4) a 36% ethanol 2% protein isocaloric diet, respectively, following the Lieber-DeCarli model. Another group of five rats were fed ad libitum the control diet. The first and second lumbar vertebrae were removed after sacrifice, and processed for histomorphometrical analysis of undecalcified bone samples. Blood and 24-h urine were also collected. Protein malnutrition, but not ethanol, leads to osteoporosis and reduced osteoid synthesis, whereas ethanol and protein malnutrition both lead to impaired bone mineral apposition and increased urinary hydroxyproline excretion. These changes are accompanied by an increase in serum parathormone and serum 1,25 dihydroxy vitamin D3, a slight hypomagnesemia, hypercalciuria and hyperphosphaturia; protein deficiency plays an independent role in these alterations, whereas both ethanol and protein deficiency exert independent effects on decreasing serum testosterone levels; this last alteration may contribute to the bone changes mentioned before.

Animals↗
PubMed2000

Maternal protein deficiency causes hypermethylation of DNA in the livers of rat fetuses.

Maternal protein deficiency during pregnancy is associated with changes in glucose tolerance and hypertension in the offspring of rats. In this study the growth of rat fetuses was examined when the dams were fed diets containing 18% casein, 9% casein or 8% casein supplemented with threonine. The extra threonine was added to reverse the decrease in circulating threonine concentrations that occurs when pregnant rats are fed protein-deficient diets. The fetuses of the group fed the low protein diet supplemented with threonine were significantly smaller than those of the control group and not significantly different from those fed low protein. Homogenates prepared from the livers of dams fed the diet containing 9% casein oxidized threonine at approximately twice the rate of homogenates prepared from dams fed the diet containing 18% casein. We conclude that circulating levels of threonine fall as a consequence of an increase in the activity of the pathway that metabolizes homocysteine produced by the transulfuration of methionine. Serum homocysteine was unaffected in the dams fed low protein diets compared with controls, but was significantly greater in dams fed the low protein diet supplemented with threonine. Elevated levels of homocysteine are associated with changes in the methylation of DNA. The endogenous methylation of DNA was greater than that of controls in the livers of fetuses from dams fed the 9% protein diets and increased further when the diet was supplemented with threonine. Our results suggest that changes in methionine metabolism increase homocysteine production, which leads to changes in DNA methylation in the fetus. An increase in maternal homocysteine may compromise fetal development, leading to the onset of glucose intolerance and hypertension in adult life.

Animals↗
PubMed1975

Cyclic AMP metabolism and nucleic acid content in the lymphocytes of the thymus, spleen, and lymph nodes of protein-deficient rats.

The concentration of cyclic AMP (cAMP) and its metabolites (5'-AMP and adenosine) as well as the adenyl cyclase, cAMP phosphodiesterase, and 5'-nucleotidase activities were determined in lymphocytes of thymus, spleen, and lymph nodes of control and protein-deficient rats. The values of these parameters, when expressed as per milligran DNA and as per 10-8 cells, but not always when expressed as per milligran protein, were much lower in the thymus as compared with the spleen and the lymph nodes in the control rats. The protein-deficient diet increased the nucleotide concentrations in the thymus and spleen lymphocytes on a per milligram DNA basis except those of thymic cAMP, which did not change. The same diet also increased the activities of the enzymes involved in the cAMP metabolism in thymic, splenic, and lymph node lymphocytes. Such a peculiarity could be related to the reduction of the mitotic activity of lymphocytes caused by protein deficiency since an inverse relationship has been reported between this activity and the synthesis of cAMP. On the other hand, it was noted that purified lymphocyte suspensions contained paradoxically higher amounts per cell of DNA, RNA, and protein in the thymus, spleen, and lymph nodes of protein-deficient rats as compared with those of the control rats. However, when the cell preparations were not purified, only the lymph node cells displayed a strong increase in their DNA content. Prolongation of the S phase of the cell cycle in these lymphocytes is suggested.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Rat small intestinal morphology with special reference to villi: effects of maternal protein deficiency and hydrocortisone.

The heights of villi were less in all the segments of mildly undernourished (by increasing litter size) pups at 21 days of age, in comparison with controls, while the heights of villi in the duodenum and jejunum, but not in the ileum, were less in severely undernourished (by maternal protein deficiency) pups. Administration of hydrocortisone during 18--21 days of age to normal pups and to pups undernourished by maternal protein deficiency during lactation showed a marked reduction of villi heights in the ileum but not in other segments of the intestine. When the pups of protein-deficient mothers (during lactation) were fed on a normal diet during the post-weaning period, the villi in the ileum were found to be longer than those of controls. Superimposition of post-weaning protein deficiency over pre-weaning undernutrition only left the heights of ileal villi unaltered, but in other segments deficits in heights of villi were observed. These studies suggest that the suggested 'villi-reducing factor' did not appear in the ileum of severely undernourished pups even after the availability of an adequate nutrition in the post-weaning period, probably due to hydrocortisone deficiency at about 21 days of age, and that the hormone has a role in maintaining ileal villi heights. In addition to the heights of villi, other morphological retardations and alterations of enterocyte structure were observed in the severely undernourished intestine. These effects differed in different parts of the intestine and with the degree of neonatal undernutrition. Most of the morphological abnormalities showed a trend for recovery when a normal diet was given in the post-weaning period.

Animals↗
PubMed1995

[Molecular biological analysis of hereditary thrombophilia--genetic characterization of protein S deficiency].

Protein S is a plasma glycoprotein, which functions as a cofactor for activated protein C in the protein C pathway and also directly inhibits factors Va and Xa, independently of protein C. In plasma, protein S circulates as a free molecule (40%) or in a complex with C4b-binding protein (60%). Only a free protein S acts as an anticoagulant and its activity is lost by binding to C4b-binding protein. The physiological importance of protein S has been established by observations in patients with hereditary protein S deficiency who have an increased risk of developing thrombosis. Several previous studies reported that hereditary protein S deficiency was as common as protein C deficiency and that approximately 5% of hereditary thrombophilia was caused by protein S deficiency. But molecular biological analysis of protein S deficiency is not as advanced as protein C deficiency because the genetic characterization of protein S deficiency is limited by the presence of the inactive pseudogene that is highly homologous to the active true gene. Only a few previous studies have examined the genetic features of hereditary protein S deficiency. Further investigation is needed to characterize the pathophysiology and molecular basis of hereditary protein S deficiency.

Humans↗
PubMed1976

The effects of nutritional rehabilitation on antibody production in protein-deficient mice.

The transfer of chronically protein-deficient mice to an optimal diet a few days before immunization with sheep erythrocytes, tetanus toxoid or Brucella abortus vaccine either failed to increase antibody production above the level produced by deficient mice, or suppressed the responses to below those produced by deficient mice or normally-fed controls. Transfer to high protein diet on the day of immunization or feeding deficient mice the normal diet for just 2 days at the time of injection produced higher titres than did transfer a few days before immunization. Secondary responses to TT were affected by transfer to the normal diet at priming, rather than at rechallenge. Some mechanisms which may explain these findings and their implications for immunization schedules in malnourished humans are discussed.

Agglutination Tests↗
PubMed1978

Responses to polyvinyl pyrrolidone and pneumococcal polysaccharide in protein-deficient mice.

Indirect haemagglutination titres induced by polyvinyl pyrrolidone (PVP) or pneumococcal polysaccharide Type III (S111) were determined in mice maintained on a 4% albumin diet from weaning and normally-fed littermates. Responses to PVP, given intravenously (i.v.) or intraperitoneally (i.p.), were elevated by protein-deficiency at low antigen doses and increasingly depressed at high doses. Increases in the duration of protein-deficiency generally improved these responses. The persistence of tolerance was reduced by protein-deficiency and priming was evident in both groups when tolerance was broken. The low protein diet depressed responses to moderate doses of S111 given i.p. to C57Bl mice, but such responses were normal in BALB/c mice and in C57Bl mice injected i.v. High doses of S111 (i.p., i.v.) elicited poor responses in deficient mice. These findings are discussed in relation to previous studies using other antigens, with a view to elucidating mechanisms responsible for the effects of protein-deficiency.

Animals↗
PubMed1986

Decreased hepatic retinyl palmitate hydrolase activity in protein-deficient rats.

28-day-old weanling rats were fed a diet containing 3% casein as the only source of protein for eight weeks to induce protein deficiency. When compared to control animals (fed a diet containing 25% casein), these rats had significantly lowered body (5.2-fold reduction) and liver (2.5-fold reduction) weights. The circulatory level of retinol (nmol per ml plasma) as well as retinol (nmol per g tissue) in the liver of these protein-deficient animals were also reduced significantly, although their liver concentration of retinyl palmitate (nmol per g tissue) was comparable to that of the control group. Assay of liver tissue for retinyl palmitate hydrolase activity revealed a 4-fold reduction (compared to that of control animals) of specific enzyme activity (nmol retinol formed per g protein per h). These findings suggest that severe protein deficiency results in a decreased hydrolysis of retinyl esters in the liver, which may be in part responsible for the reduced level of metabolically 'active' retinoids available for normal physiological functions.

Animals↗
PubMed1977

Effect of protein deficiency on absorption, transport and distribution of alpha-tocopherol in the rat.

The absorption, transport and distribution of alpha-[3H]tocopherol were greatly decreased in protein deficiency. This was reflected in the subcellular distribution of alpha-[3H]tocopherol in livers of protein-deficient rats. The ratio, bound:free for alpha-[3H]tocopherol, also decreased in both serum and liver cytosol. After protein refeeding, absorption, transport and distribution patterns of alpha-[3H]tocopherol for the protein-deficient rats were restored to patterns similar to those of control animals.

Animals↗
PubMed1979

Reversible modification of Escherichia coli ribosomes with 2,3-dimethylmaleic anhydride. A new method to obtain protein-deficient ribosomal particles.

Treatment of Escherichia coli ribosomes with the protein reagent 2,3-dimethylmaleic anhydride is accompanied by inactivation of polypeptide polymerization and by dissociation of ribosomal proteins. Regeneration of the modified amino groups at pH 6.0 is followed by reactivation and reconstitution of the ribosomes. Prior to regeneration of the amino groups, ribosomal particles and split proteins can be separated by centrifugation, which allows the preparation of new protein-deficient particles. The ribosomal particles obtained by three successive treatments with 2,3-dimethyl-maleic anhydride at a molar ratio of reagent to ribosome equal to 16,000 lack proteins S1, S2, S3, S5, S10, S13, S14, L7, L8, L10, L11, L12, and L20 and have lost part of proteins S4, L1, L6, L16, and L25. This new procedure to obtain protein-deficient ribosomal particles is mild and might be useful to dissociate other protein-containing structures in addition to ribosomes.

Escherichia coli↗
PubMed1991

Changes in rat plasma apolipoproteins and lipoproteins during moderate protein deficiency: potential use in the assessment of nutritional status.

To test apolipoprotein sensitivity as protein deficiency markers, concomitant evolution of plasma apolipoproteins (apo) and usual nutritional markers (transthyretin, albumin, transferrin) were followed during a 28-d protein restriction in young male Wistar rats. In addition, plasma lipids and chemical composition of lipoproteins were assayed by d 28. The control and the deficient groups were fed 18% and 6% casein diets, respectively. By d 28 the protein-deficient group exhibited hypotriglyceridemia resulting from the decrease in VLDL triacylglycerols; free cholesterol and phospholipids were increased, reflecting the increment in LDL-HLDL1. In plasma total lipoproteins, apo BH, AI and E were not different than controls in the deficient group. Apolipoprotein AIV decreased after d 14 and was significantly less than in controls at d 28. Apolipoprotein BI was considerably reduced by d 14 (43% less) and d 28 (52% less) compared with the control group. Apolipoproteins C + AII were significantly lower in the protein-deficient group by d 14 (43%). By d 28, VLDL apo C were decreased 60% by protein restriction. Transthyretin level was 20% lower in the protein-deficient group by d 7 but returned to control values by d 14. A moderately lower value was observed for albumin by d 7 and d 14 and for transferrin by d 28. These results indicate that, in this model, apo BI and C are more sensitive to protein depletion than usual nutritional markers.

Animals↗
PubMed1992

Additivity of protein deficiency and carbon monoxide on placental carboxyhemoglobin in mice.

OBJECTIVES: The purpose of the study was to estimate maternal and placental carboxyhemoglobin in protein-deficient and carbon monoxide-exposed mice. STUDY DESIGN: Pregnant CD-1 mice were placed on diets containing 27% (control), 16%, 8%, or 4% protein on gestation day 1. The dams were exposed to carbon monoxide concentrations of 0 (control), 65, 125, 250, or 500 ppm from gestation days 8 to 18. The dams were killed on gestation day 18, and blood samples were collected from the maternal hearts and placentas for carboxyhemoglobin determination. RESULTS: Maternal carboxyhemoglobin levels were related to the carbon monoxide exposure levels and were not affected by protein deficiency. Placental carboxyhemoglobin levels were higher than maternal carboxyhemoglobin levels, were related to carbon monoxide exposure levels, and were inversely related to dietary protein levels. CONCLUSION: The data suggest that maternal protein deficiency enhances the placental carboxyhemoglobin levels resulting from carbon monoxide exposure and exacerbates hypoxic conditions for the developing fetus. Special groups at risk may include drug abusers and cigarette or marijuana smokers.

Animals↗
PubMed1979

The effect of iron and protein deficiency on the development of acquired resistance to reinfection with Nippostrongylus brasiliensis in rats.

Iron and protein deficiency delays the immunological rejection of Nippostrongylus brasiliensis from the small intestine of rats undergoing a primary infection with the parasite. In the present study, iron and protein deficiency significantly reduced acquired resistance to reinfection with N. brasiliensis. Repletion of deficient animals with iron and protein restored their capacity to mount an effective immune response to a secondary infection with the parasite. These results suggest that chemotherapy of helminthiasis should be integrated with nutritional supplementation.

Animals↗
PubMed1981

The effect of iron and protein deficiency on plasma levels and parasite uptake of [14C] fenbendazole in rats infected with Nippostrongylus brasiliensis.

The Nippostrongylus brasiliensis-rat model was used to determine whether iron and protein deficiency, which are commonly associated with parasitic infections, affected the pharmacokinetic behaviour of fenbendazole as measured by plasma concentrations and uptake by worms. Plasma 14C concentrations after [14C] fenbendazole administration were higher in iron and protein-deficient rats than in sufficient rats. However, the uptake of 14C by N. brasiliensis in iron and protein-deficient rats was significantly less than in worms from diet-sufficient rats. The reduced anthelmintic uptake by worms in protein and iron-deficient hosts may account, in part, for reduced anthelmintic efficacy under these circumstances. These findings are relevant to understanding variations in response to chemotherapy in populations of parasitised hosts containing malnourished individuals.

Animals↗
PubMed1979

Metrical analysis of growth changes in the jaws and teeth of normal, protein deficient and calorie deficient pigs.

Weanling pigs were separated into three groups: control animals were allowed unlimited food; protein deficient animals were allowed unlimited carbohydrate or fat but restricted in protein intake; calorie deficient animals were restricted in total food intake. The skulls and teeth of animals killed at one year and at two years of age were measured from radiographs, and from the results were derived the following conclusions: (1) Pigs fed on protein and on calorie deficient diets all showed considerable retardation of the growth of jaws and teeth, consistently more severe in the calorie deficient than in the protein deficient animals. (2) The shape of the mandible was altered by both types of malnutrition, the height of the ascending ramus being reduced to a greater extent than either its anteroposterior width or the length of the body of the mandible. The labial alveolar process became more proclined with increasingly severe malnutrition. (3) The upper and lower jaws were retarded to a similar extent in both groups of experimentally malnourished animals. (4) Retardation of tooth growth was less severe than that of jaw growth. (5) Contralateral asymmetry of molar crown size in the protein deficient animals was initally quite marked, but when the teeth were approaching their final size the asymmetry was no greater than in control animals.

Animals↗
PubMed1986

The effect of methionine and protein deficiency in delaying expulsion of Nippostrongylus brasiliensis in the rat.

Three protein-deficient diets containing 5%, 6%, or 7% casein, with and without 0.3% methionine supplementation, were fed to Wistar rats from weaning for 6 wk. Animals were infected subcutaneously with 1500 larvae of Nippostrongylus brasiliensis and killed after 14 days when nutritionally normal animals have expelled more than 97% of the worm burden. There was a delay in worm expulsion that was related to both the protein content (p = 0.0006) and to methionine content (p less than 0.0001). Methionine supplementation significantly reduced the worm burden in animals fed the 7% protein diet from a geometric mean of 32.4 to 5.2 (p = 0.0408) and in rats fed the 6% protein diet from a mean of 162 to 8.1 (p = 0.0002) but had no effect in rats on the 5% casein diet. Thus, addition of methionine overcame the adverse effect of protein deficiency in these less severely affected groups.

Animals↗
PubMedDate not supplied

Relative and combined effects of ethanol and protein deficiency on gonadal function and histology.

The aim of the present study is to analyse the relative and combined effects of ethanol and protein deficiency on serum testosterone and LH, and on gonadal histology, in ethanol fed rats. The study was performed in 32 animals divided into four groups, fed with the Lieber & DeCarli control, 36% ethanol, 2% protein, and 36% ethanol 2% protein containing diets, respectively. Two months later, rats were anaesthetized with pentobarbital and sacrificed, and the right testes and epididymus were carefully removed. Both ethanol and protein deficiency independently lead to a decrease in serum testosterone levels, and to testicular atrophy, lowest testosterone levels and highest degrees of atrophy being observed in the rats receiving the 36% ethanol, 2% protein containing diet. Both serum testosterone and testicular size and weight significantly correlated with final weight and serum albumin. Hypospermia, atrophy of the seminiferous tubules, and reduced epididymal diameter were also observed in this last group of animals. Thus, protein deficiency may contribute to hypogonadism of alcoholics.

Animals↗