[Effect of protein deficiency in rats on the activity of selected enzymes participating in protein and carbohydrate metabolism].
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Animals↗
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Protein deficiency and endogenous pyrogen fever.
Blood monocytes have been shown to be a major source of endogenous pyrogen (EP), the protein mediator of fever. This study describes the effects of chronic dietary protein deficiency in rabbits on the in vitro production of EP by monocytes, the time course for the dietary effects on EP production, and the possible role for serum factors in the modification of EP production and (or) development of fever. EP harvested from rabbits on a protein-free diet for 4 weeks induced normal fevers when injected i.v. into recipient animals; EP produced from the protein-deprived rabbits after 6 and 8 weeks did not elicit fevers when bioassayed. Injection of EP supernatants derived from protein-deprived rabbits and containing standard protein serum resulted in less aberrant temperature responses than injection of EP supernatants containing sera from protein-deprived rabbits. These results suggest that: (i) the production of EP by rabbit blood monocytes is sensitive to dietary protein status, (ii) the effect of protein deficiency on EP production is a threshold phenomenon, and (iii) factors present in sera of protein-deprived rabbits may modify EP-induced fever.
Animals↗
Effects of protein deficiency on plasma levels of 25-hydroxyvitamin and 24,25-dihydroxyvitamin D in the rat.
The effect of protein deficiency on plasma 25-hydroxyvitamin and 24,25-dihydroxyvitamin D concentrations was determined in weanling rats. The concentrations of these metabolites did not differ in rats fed diet providing either 0.5 or 21% casein for 4 weeks postweaning. Also, no change was observed in plasma levels of these metabolites in rats fed the 21% casein diet in amounts restricted to those consumed by the 0.5% casein animals for the same period of time. The results indicate that the synthesis and transport of 25-hydroxyvitamin and 24,25-dihydroxyvitamin D are not significantly affected by either a protein deficiency or a total food striction during the early postweaning period. This finding may be relevant to the vitamin D status of children with kwashiorkor.
24,25-Dihydroxyvitamin D 3↗
Dissociation of immune capacity from nutritional status by triiodothyronine supplements in severe protein deficiency.
Weanling mice were fed ad libitum from age 23 to 37 days either an 18 or an 0.6% protein diet. Half the animals in each dietary group received supplemental triiodothyronine (T3, 0.2 mg/kg diet). T3 increased the primary in vivo antibody response of protein-deficient mice to sheep red blood cells, as measured by both splenic plaque-forming cells (PFC) per 10(6) nucleated spleen cells and serum hemagglutinin titers. T3 also increased PFC/spleen in well-nourished mice. The effect on protein-deficient animals was achieved although nutritional status in these animals, as estimated by weight loss and carcass composition, was further impaired by T3 supplementation. These results support the hypothesis that immune functions can be improved independently of nutritional status in severe (wasting) malnutrition. Insofar as T3 was effective in a model of malnutrition that does not reduce serum total or free T3 levels, the phenomenon appears to represent a pharmacological action of the hormone.
Animals↗
Effect of medroxyprogesterone acetate on the intestinal absorptive functions in protein-deficient rat.
Effect of Medroxyprogesterone acetate (MPA) at a dose level of 35mg/Kg body weight per week for four weeks on the intestinal uptake of nutrients viz glucose, amino acids, (alanine and leucine), calcium and zinc has been investigated in protein-deficient female rats. The administration of MPA was found to enhance significantly the uptake of glucose and amino acids in both the pair-fed and the protein-deficient rats. In contrast, calcium uptake was depressed as a result of treatment with the drug as well as protein-deficiency. The uptake of zinc was not affected on drug administration. This steroidal contraceptive caused elevation in sodium-dependent glucose uptake, while the sodium-independent uptake remained unaltered. The kinetic parameters of glucose and leucine uptake indicate that MPA might be inducing the transport carrier protein of these nutrients as elevation in Vmax of these nutrients transport system was observed following its administration.
Amino Acids↗
Relative and combined effects of ethanol and protein deficiency on zinc, iron, copper, and manganese contents in different organs and urinary and fecal excretion.
The relative contribution of protein deficiency to the altered metabolism of certain trace elements in chronic alcoholics is not well defined, so this study was performed to analyse the relative and combined effects of ethanol and protein deficiency on liver, bone, muscle, and blood cell content of copper, zinc, iron, and manganese, and also on serum levels and urinary and fecal excretion of these elements in four groups of eight animals each that were pair-fed during 8 weeks with a nutritionally adequate diet, a 36% (as energy) ethanol-containing isocaloric diet, a 2% protein isocaloric diet, and a 36% ethanol 2% protein isocaloric diet, respectively, following the Lieber-DeCarli model. Five additional rats were fed ad lib the control diet. Protein malnutrition, but not ethanol, leads to liver zinc depletion. Both ethanol and protein malnutrition cause muscle zinc depletion and increase urinary zinc and manganese excretion, whereas ethanol also increases urinary iron excretion and liver manganese content. No differences were observed regarding copper metabolism.
Animals↗
Analytical considerations for free protein S assays in protein S deficiency.
Protein S is an anticoagulant protein that circulates in plasma in complex with C4b-binding protein (C4BP) or in free form. Deficiency of protein S increases the risk of venous thrombosis. Measurement of free protein S, as compared to total levels, has been shown to be superior for prediction of protein S deficiency. We studied the effects of different handling protocols for an immuno- and a ligand (C4BP)-based assay for free protein S. When the assay was performed at 37 degrees C, the levels of free protein S in plasma from protein S deficient patients were approximately twice those obtained at room temperature. The reason for this phenomenon was that plasmas from protein S deficient patients exhibited a time-, temperature-, and dilution-dependent increase in free protein S, which was more pronounced than corresponding dilution of the normal plasma that was used to create the standard curve. These findings demonstrate the importance of assay procedure and sample handling in assays for free protein S.
Aged↗
Combined effects of ethanol and protein deficiency on hepatic iron, zinc, manganese, and copper contents.
The present study has been performed in order to establish the relative and combined roles of ethanol and malnutrition on liver Fe, Zn, Cu, and Mn alterations in alcoholic male adult Wistar rats, and also the relationships between these alterations and histomorphometrically determined hepatocyte and nuclear areas, perivenular fibrotic rim area, and total amount of fat present in the liver. Four groups of 8 animals each were fed: (1) a nutritionally adequate diet (C); (2) a 36% ethanol-containing (as percent of energy), isocaloric diet (A); (3) a 2% protein-containing, isocaloric diet (PD); and (4) a 36% ethanol, 2% protein-containing, isocaloric diet (A-PD), respectively, following the Lieber-DeCarli model. Ethanol-fed, protein-deficient animals showed the highest liver Fe, and the lowest Zn and Cu values, although differences in liver Zn, Mn, and Cu values were not significantly different between PD and A-PD groups. Statistically significant differences of these parameters were observed between the A and the A-PD groups, and between the A and PD groups, except for liver iron. Except for liver Mn, differences between C and A groups were statistically significant. These alterations correlated with liver fibrosis and steatosis, serum albumin, and weight loss, except for liver Mn, which was not correlated with fibrosis or steatosis. Thus, protein deficiency seems to enhance ethanol-induced liver Fe, Zn, and Cu alterations, whereas protein deficiency, but not ethanol, seems to play a major role on liver Mn alterations.
Animals↗
Zinc supplementation to protein-deficient diet in CO-exposed mice decreased fetal mortality and malformation.
In developing countries, diet during pregnancy is frequently low in both protein and zinc contents and exposure to CO is common because of environmental pollution and smoking. This study was conducted to evaluate whether zinc supplementation ameliorates fetal mortality and malformations in protein-deficient, CO-exposed mice. Pregnant mice of the CD-1 strain were maintained on 17% (reference) or 9% protein diets mixed with deficient, normal, or supplemental zinc throughout gestation. The dams in each dietary group were exposed to air (control) or 500 ppm CO in air in environmental chambers from gestation days 7-18. As compared to the control group (normal protein, normal zinc), the incidence of fetal mortality was 66.8% and 57.2% higher, respectively, and malformation incidence was 74.4% and 72.4% higher (0 and 500 ppm CO, respectively) in mice fed both deficient protein-zinc diets. However, the highest malformation rate was observed in the group with normal protein, deficient zinc (96% mortality in both 500 and 0 ppm CO, as compared to the reference group, p < 0.0001). The fetal mortality rate was -3.5% (0 ppm CO) and 25.4% (500 ppm CO) lower in zinc-supplemented, protein-deficient groups compared to the control group. There was a significant negative association between fetal zinc concentrations and fetal malformations (p < or = 0.001). The result of this study might be relevant to populations that are exposed to CO and or consume marginal zinc and protein diets during gestation.
Animals↗
Protein deficiency magnifies social influence on the food choices of Norway rats (Rattus norvegicus).
The food choices of protein-deprived juvenile rats were more profoundly affected by interaction with conspecifics than were the food choices of protein-replete juvenile rats. When choosing among four different-flavored, protein-deficient diets, protein-deprived rats ate significantly more of the diet eaten by a conspecific demonstrator than did protein-replete rats. These data suggest that the food choices of the relatively less successful members of a population are most affected by social interaction. Consequently, the mean effect of social interaction on diet selection in a population of Norway rats is likely to be positive.
Animals↗
Ultrastructural changes of alveolar macrophages of protein-deficient rats.
Enhancement of phagocytosis of alveolar macrophages (AM) was examined by cytochemical and electron microscopic studies on macrophages from protein-deficient rats. The macrophages from rats fed on 5% casein diet had longer microvilli, more phagocytic vacuoles and more lysosomes with acid phosphatase activity than those from control rats. Many phagocytic vacuoles were seen close to the site of attachment of opsonized sheep red blood cells (SRBC) and were mainly located in the subplasmalemmal layer which was rich in microfilaments but contained few cytoplasmic organelles. After attachment, opsonized SRBC were engulfed through a hemispherical crater into the phagocytic vacuoles. The phagocytic vacuoles seemed to be formed by invagination of the cell surface because they had membrane ATPase activity continuous with that of the outer surface of the plasma membrane. In the cell, the vacuoles fused with the numerous preexisting lysosomes in the interior of the cell receiving the contents of the latter. The mechanism of enhancement of phagocytosis in protein-deficiency is discussed.
Animals↗
Ozone exposure, food restriction and protein deficiency: changes in collagen and elastin in rodent lung.
Two groups of weanling or young adult rats were fed ad lib casein-based diets containing 4 or 16% protein. Food was restricted in a third group (fed the 16% protein diet) to the amount consumed daily by rats (adult or weanlings) fed the 4% diet. After 3 weeks (weanlings) or 1, 3 or 5 weeks (adults), one-half of the rats in each group were exposed to 0.64 ppm (1.28 mg/m3) of ozone for 7 days (23.5 h each day). Several parameters were then evaluated related to lung connective tissue metabolism including: (1) total lung hydroxyproline, (2) total lung elastin, (3) apparent rates for lung collagen synthesis and elastin accumulation and (4) lung and body weights. In general, the response to protein deficiency and food restriction was more pronounced than to ozone exposure. Protein deficiency and food restriction resulted in decreased lung size and collagen content. However, the ability of lung to respond to ozone (in relative terms) was not altered by changes in diet as assessed by changes in lung weight or the collagen synthetic rate.
Animals↗
METABOLISM OF ALBUMIN AND GAMMA-GLOBULIN IN PROTEIN DEFICIENT RATS.
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Albumins↗
Molecular analysis of genomic DNA allows rapid, and accurate, prenatal diagnosis of peroxisomal D-bifunctional protein deficiency.
Prenatal diagnosis was requested for a couple with a previous child affected by the peroxisomal disorder D-bifunctional protein deficiency. Prior analysis of the D-bifunctional protein cDNA sequence from the propositus had shown that it was missing 22 bp. This was subsequently attributed to a point mutation in the intron 5 donor site (IVS5 + 1G>C) of the D-bifunctional protein gene. Consistent with parental consanguinity, the patient was shown to be homozygous for this mutation, which is associated with loss of a Hph 1 restriction site in the genomic sequence. Prenatal testing of the fetus using genomic DNA isolated from uncultured amniocytes indicated that both alleles of the D-bifunctional protein had the IVS5 + 1G>C substitution. The peroxisomal defect was later confirmed biochemically using cultured amniocytes, which were found to have elevated levels of very long chain fatty acids (VLCFA). This is the first report of prenatal diagnosis of D-bifunctional protein deficiency using molecular analysis of genomic DNA.
17-Hydroxysteroid Dehydrogenases↗
The effect of protein deficiency on some rat liver lipid metabolic enzymes and CoA.
Two groups of male Wistar rats were fed normal (i.e., 18%) and protein-free diets, respectively, for 7 weeks. In vivo incorporation of [1-14C] acetate into palmitic, stearic, oleic, and arachidonic acids by the liver was reduced in the protein-deficient rats. In vitro incubation of liver microsomes with labeled palmitate or linoleate revealed no change in the specific activities of chain elongating or desaturating enzymes. Protein deficiency resulted in a decrease in specific activity of short chain acyl-CoA synthetase and in total CoA, accompanied by the virtual disappearance of acyl-CoA and an increase in free CoA. Furthermore, there was less microsomal fatty acid synthetase and mitochondrial beta-hydroxybutyrate dehydrogenase activity. These results are discussed in relation to fatty acid synthesis and the changes in liver fatty acid composition.
Animals↗
Prosaposin deficiency: further characterization of the sphingolipid activator protein-deficient sibs. Multiple glycolipid elevations (including lactosylceramidosis), partial enzyme deficiencies and ultrastructure of the skin in this generalized sphingolipid storage disease.
Sphingolipid activator protein (SAP) deficiency, previously described in two sibs and shown to be caused by the absence of the common saposin precursor (prosaposin), was further characterized by biochemical lipid and enzyme studies and by ultrastructural analysis. The 20-week-old fetal sib had increased concentrations of neutral glycolipids, including mono-, di-, tri- and tetrahexosylceramide, in liver, kidney and cultured skin fibroblasts compared with the controls. Glucosylceramide and lactosylceramide were particularly elevated. The kidney of the affected fetus showed additional increases in the concentration of sulphatide, galactosylceramide and digalactosylceramide. Free ceramide was stored in the liver and kidney, and GM3 and GM2 gangliosides were elevated in the liver, but not the brain, of the fetus. Phospholipids, however, were normal in the affected fetus. In the liver biopsy of the propositus, who later died at 16 weeks of age, only a few lipids could be studied. Glucosylceramide, dihexosylceramide and ceramide were elevated in agreement with our previous study. Enzyme studies were undertaken using detergent-free liposomal substrate preparations and fibroblast extracts. The sibs' beta-glucocerebrosidase and beta-galactocerebrosidase activities were clearly reduced, but their sphingomyelinase activities were normal. The normal activity of the latter enzyme and the almost normal tissue concentration of sphingomyelin in prosaposin deficiency suggest that the prosaposin-derived SAPs are not required for sphingomyelinase activity in vivo. In keeping with the biochemical findings, skin biopsies from the sibs showed massive lysosomal storage with a vesicular and membranous ultrastructure. The function of SAPs in sphingolipid degradation and the role of SAPs for enzyme activity in vitro are discussed. In addition, the similarity in neutral glycolipid accumulations in Niemann-Pick disease type C and in prosaposin deficiency are noted. The phenotype of the prosaposin deficient sibs resembled acute neuronopathic (type 2) Gaucher disease more than Farber disease in several aspects, but their genotype was unique.
Brain Chemistry↗
Peroxisomal D-hydroxyacyl-CoA dehydrogenase deficiency: resolution of the enzyme defect and its molecular basis in bifunctional protein deficiency.
Peroxisomes play an essential role in a number of different metabolic pathways, including the beta-oxidation of a distinct set of fatty acids and fatty acid derivatives. The importance of the peroxisomal beta-oxidation system in humans is made apparent by the existence of a group of inherited diseases in which peroxisomal beta-oxidation is impaired. This includes X-linked adrenoleukodystrophy and other disorders with a defined defect. On the other hand, many patients have been described with a defect in peroxisomal beta-oxidation of unknown etiology. Resolution of the defects in these patients requires the elucidation of the enzymatic organization of the peroxisomal beta-oxidation system. Importantly, a new peroxisomal beta-oxidation enzyme was recently described called D-bifunctional protein with enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase activity primarily reacting with alpha-methyl fatty acids like pristanic acid and di- and trihydroxycholestanoic acid. In this patient we describe the first case of D-bifunctional protein deficiency as resolved by enzyme activity measurements and mutation analysis. The mutation found (Gly16Ser) is in the dehydrogenase coding part of the gene in an important loop of the Rossman fold forming the NAD+-binding site. The results show that the newly identified D-bifunctional protein plays an essential role in the peroxisomal beta-oxidation pathway that cannot be compensated for by the L-specific bifunctional protein.
17-Hydroxysteroid Dehydrogenases↗
A young adult with coronary artery and jugular vein thrombosis: a case report of combined protein S and protein C deficiency.
Protein C and protein S deficiencies increase the risk of thromboembolic events. We report a case of combined protein C and S deficiency in a young woman, with resulted in acute myocardial infarction and asymptomatic jugular vein thrombosis. The patient was treated successfully with coronary artery bypass graft surgery and systemic anticoagulation. Our report emphasizes that a combined deficiency of protein C and S may be a high risk factor for arterial thromboembolic events in young adults.
Adult↗