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PubMed1984

Effect of protein deficiency on growth and plasma zinc concentration in genetically lean and obese swine.

Thirty-two genetically lean and 32 genetically obese weanling (4 to 5 wk old) pigs from inter se matings of crossbreds produced by within-line matings of Duroc and Yorkshire breeds, selected for low or high backfat, were fed the following four diets for 8 wk (eight lean and eight obese pigs/diet): 10% protein -- 100 ppm Zn, 10% protein -- 200 ppm Zn, 18% protein -- 100 ppm Zn, 18% protein -- 200 ppm Zn. After 8 wk, all pigs were fed a standard 16% protein corn-soybean meal-type growing diet to a slaughter weight of about 87 kg. Lean pigs were more severely affected than obese pigs by low protein diets as measured by weight gain, plasma total protein and plasma albumin. Plasma Zn concentration was reduced in lean and obese pigs fed low protein diets. Supplemental Zn failed to increase plasma Zn in protein-deficient pigs. During repletion, weight gain of lean and obese pigs previously fed the 10% protein -- 100 ppm Zn diet was less than that of pigs previously fed other diets. The lower level (100 ppm) of Zn fed during protein depletion appeared to be associated with a negative effect on repletion weight gain of lean and obese pigs. Lean and obese pigs responded similarly during the repletion phase to earlier protein restriction. We conclude that supplementary dietary Zn does not maintain plasma Zn concentration in growing pigs fed protein-deficient diets and that repletion from dietary protein restriction is not associated with compensatory growth in genetically lean pigs.

Adipose Tissue↗
PubMed1982

Reversible hepatotoxicity associated with hepatic vitamin A accumulation in a protein-deficient patient.

A 62-yr-old white male presented with edema, protein malnutrition, and abnormal liver function. He had ingested from 40,000-50,000 IU of vitamin A per day for 7 yr. Examination of liver tissue by light and electron microscopy revealed findings characteristic of an excessive accumulation of vitamin A. Liver tissue contained massive amounts of vitamin A (19,000 IU/g); however, both the serum concentration of vitamin A and retinol-binding protein were below normal, and serum RBP was not saturated. On a normal diet the patient was able to mobilize hepatic vitamin A, as indicated 71 days later by a repeat biopsy of the liver, which then contained 9000 IU of vitamin A/g. During this time his nutrition improved, serum vitamin A rose, and serum RBP became transiently saturated. The amount of vitamin A ingested by this patient was less than that usually producing recognizable hepatotoxicity, and he had no extra hepatic manifestations of vitamin toxicity, consistent with a low serum vitamin A concentration and a low vitamin A to retinol-binding protein ratio. At presentation he was apparently unable to normally mobilize vitamin A from his liver, which may have been due to an accompanying protein deficiency.

Biopsy↗
PubMed1987

Mesenteric vein thrombosis as presenting manifestation of hereditary protein S deficiency.

Protein S deficiency is inherited as an autosomal dominant trait. Heterozygotes with a reduction of 50% in the plasma protein S concentration are at risk for the development of venous thromboembolism, often occurring at an early age without an apparent cause. In the majority of the patients thrombosis is restricted to the superficial or deep venous system of the legs. In this case report we describe the presence of mesenteric vein thrombosis in a 30-yr-old man with hereditary protein S deficiency. In his family protein S deficiency was also recognized in his mother, brother, and niece. Both his mother and brother had a history of thrombotic disease.

Adult↗
PubMed2003

Effects of protein deficiency on liver trace elements and antioxidant activity in carbon tetrachloride-induced liver cirrhosis.

In liver cirrhosis, liver tissue becomes progressively substituted by fibrosis, ultimately leading to architectural distortion, liver circulatory changes, and liver failure. Some data support the hypothesis that protein undernutrition may play a role in the development and progression of nonalcoholic liver cirrhosis and that this progression is at least partially mediated by changes in glutathione peroxidase (GPX), superoxide dismutase (SOD), and other antioxidative systems, leading to an increase in lipid peroxidation. We analyzed the effects of protein deficiency on liver Cu, Fe, Zn, Mn, and Se in carbon tetrachloride (CCl4)-induced liver cirrhosis, the relation of protein undernutrition and these trace elements with the activity of some hepatic antioxidative enzymatic mechanisms, and the relation of all of them with morphological and biochemical changes in 40 male adult Sprague-Dawley rats divided in four groups. Liver cirrhosis was induced by intraperitoneal injection of CCl4 to 10 rats fed a 2% protein diet and another 10 fed a 18% protein control diet; two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. The study period lasted 6 wk. GPX, SOD, and lipid peroxidation products as well as Zn, Cu, Mn, Se, and Fe were determined in liver samples. We found that liver GPX and Se were reduced in the cirrhotic animals, especially in the low-protein-fed ones, protein deficiency, but not cirrhosis, exerting the main effects. A close correlation was found between liver GPX and serum albumin and weight loss and an inverse one among GPX and hepatocyte ballooning, liver fibrosis, and fat, histomorphometrically determined. These results suggest a pathogenetic role of decreased GPX in the progression of liver disease, which may become enhanced by concomitant protein undernutrition. In addition to iron, the levels of which were increased in the malnourished rats, no differences were found regarding the other trace elements, SOD activity, and lipid peroxidation products.

Animals↗
PubMed1998

Maternal dietary protein deficiency decreases nitric oxide synthase and ornithine decarboxylase activities in placenta and endometrium of pigs during early gestation.

Little is known about the mechanism responsible for retarded placental and fetal growth induced by maternal dietary protein malnutrition. On the basis of the recent finding that nitric oxide (NO) and polyamines (products of L-arginine) play an important role in embryonic and placental development, the present study was designed to determine whether protein deficiency decreases placental and endometrial activities of NO synthase (NOS) and ornithine decarboxylase (ODC) (the first and key regulatory enzyme in polyamine synthesis). Primiparous gilts selected genetically for low or high plasma total cholesterol concentrations (low line and high line, respectively) were mated and then fed 1.8 kg/d of isocaloric diets containing 13% or 0.5% crude protein. At d 40 or 60 of gestation, they were hysterectomized, and placenta and endometrium were obtained for incubations, NOS and ODC assays, and measurements of free amino acids and polyamines. Maternal dietary protein restriction decreased arginine and ornithine concentrations, constitutive and inducible NOS activities and NO production, as well as ODC activity and polyamine concentrations in placenta and endometrium of both lines of gilts. Placental NO synthase activity and NO generation were lower in high line gilts than in low line gilts. ODC activities and polyamine concentrations in placenta and endometrium were decreased at d 60 compared with d 40 of gestation. These changes in placental and endometrial synthesis of NO and polyamines during early gestation may be a mechanism responsible for reduced placental and fetal growth in protein-deficient gilts and for altered conceptus development in high line gilts.

Amino Acids↗
PubMed1982

Effect of a dietary protein deficiency on the development of hepatic drug-metabolizing enzymes in young rats.

The effect of protein deprivation on the activities of hepatic drug-metabolizing enzymes was studied in young rats whose mothers had previously been on a protein-restricted diet during pregnancy. Dietary protein deficiency (5% lactic casein as the protein source) lowered the amount of cytochrome P-450 and the activities of epoxide hydrolase and UDP-glucuronosyltransferase (UDPGT) (l-borneol as the substrate) by about 45, 63, and 48%, for the first 8 weeks, respectively. Interestingly, UDPGT estimated with p-nitrophenol as the substrate was far less affected than that estimated from l-borneol glucuronidation. This finding provides further evidence of the heterogeneity of UDPGT. Restoration of a balanced diet for 15 days following protein deprivation quickly restored cytochrome P-450 and enzyme activities to control values. Our experiments showed that the development of drug-metabolizing enzymes was changed more by the diet in young rats than in older rats. This could affect the toxicity of drugs that are normally metabolized by these pathways.

Animals↗
PubMed1989

[The lymphoid system and protein deficiency. Differentiation in the thymus and Peyer's patches].

A: Thymuses from protein deprived rats present: 1) a significant decrease in the absolute number of thymic cells bearing the CD5 phenotype (OX19+), as well as Thy 1.1 (OX7+). The predominant cell population was the one containing TdT (terminal deoxynucleotidyl transferase) as a sole marker: 2) in severely protein deprived rats followed by refeeding during 9 and 21 days, the existence of a small population of cells containing TdT as a sole marker. The TdT+W3/13+ cell population was restored but the CD4+ subpopulation (W3/25+) exists in lower numbers than in the age-matched controls. B: Severe protein deficiency at weaning, led to the presence in the Peyer's patches of very immature B-cells mostly c mu+OX7s mu-. Protein refeeding reinitiated the differentiation process as follows: 1) c mu+OX7+s mu- c mu-OX7-s mu+ as in the normal Peyer's patches; 2) however, switching of sIgM to sIgA-bearing cells was altered; 3) a low absolute number of W3/13+ and W3/25+ T-cells (CD4+) was found. C: Oral tolerance to dextrin evolved due to antigen specific CD8+ T-cells (found in Peyer's patches, mesenteric lymph nodes and spleen) and could be transferred to normal recipients.

Animals↗
PubMed1992

Hypothalamic failure as a sequela of heterozygous protein C deficiency?

Protein C deficiency can lead to cerebrovascular occlusive disease. We describe a patient in whom heterozygous protein C deficiency (type 1) is suspected on the grounds of reduced protein C activity and who suffered from multiple thrombo-embolic events involving the brain and peripheral organs. The patient developed hypothalamic failure with hypernatraemia, hypodipsia, hypersomnolence and hyperkapnia, obesity, hyperprolactinaemia, hypogonadotropic hypogonadism and growth hormone deficiency. We hypothesize that protein C deficiency caused cerebrovascular occlusions which eventually led to hypothalamic insufficiency in this patient. Disorders of the anticoagulant system should be looked for in patients with unexplained hypothalamic disease.

Adolescent↗
PubMed1998

Sensitive analysis of serum 3alpha, 7alpha, 12alpha,24-tetrahydroxy- 5beta-cholestan-26-oic acid diastereomers using gas chromatography-mass spectrometry and its application in peroxisomal D-bifunctional protein deficiency.

The final steps in bile acid biosynthesis take place in peroxisomes and involve oxidative cleavage of the side chain of C27-5beta-cholestanoic acids leading to the formation of the primary bile acids cholic acid and chenodeoxycholic acid. The enoyl-CoA hydratase and beta-hydroxy acyl-CoA dehydrogenase reactions involved in the chain shortening of C27-5beta-cholestanoic acids are catalyzed by the recently identified peroxisomal d-bifunctional protein. Deficiencies of d-bifunctional protein lead, among others, to an accumulation of 3alpha,7alpha,12alpha, 24-tetrahydroxy-5beta-cholest-26-oic acid (varanic acid). The ability to resolve the four C24, C25 diastereomers of varanic acid has, so far, only been carried out on biliary bile acids using p -bromophenacyl derivatives. Here, we describe a sensitive gas chromatography-mass spectrometry (GC/MS) method that enables good separation of the four varanic acid diastereomers by use of 2R-butylester-trimethylsilylether derivatives. This method showed the specific accumulation of (24R,25R)-varanic acid in the serum of a patient with isolated deficiency of the d-3-hydroxy acyl-CoA dehydrogenase part of peroxisomal d-bifunctional protein, whereas this diastereomer was absent in a serum sample from a patient suffering from complete d-bifunctional protein deficiency. In samples from both patients an accumulation of (24S,25S)-varanic acid was observed, most likely due to the action of l-bifunctional protein on Delta24E-THCA-CoA. This GC/MS method is applicable to serum samples, obviating the use of bile fluid, and is a helpful tool in the subclassification of patients with peroxisomal d-bifunctional protein deficiency.

17-Hydroxysteroid Dehydrogenases↗
PubMed1996

Effect of protein deficient cassava diet on Cercopithecus aethiops hearts and its possible role in the aetiology and pathogenesis of endomyocardial fibrosis in man.

Despite the current hypotheses for its causation, the exact cause of endmyocardial fibrosis is unknown. However, endomyocardial fibrosis being a disease of the low socio-economic groups who feed on low protein high carbohydrate diets consisting exclusively of cassava in Uganda and the demonstration by the author of a bimodal age distribution among the female patients and monomodal pattern in the male patients, led the author to suspect protein deficiency and cassava as aetiological factors thereby attributing the first mode to the increased but unmet protein needs for childhood growth and the second mode to the increased but unmet protein needs for pregnancies and lactation in the 20-40 year age groups. Consequently a new hypothesis that "prolonged ingestion of tuber (cassava/tapioca) crops associated with extreme deprivation of protein causes EMF" was formulated. In order to verify this hypothesis, three Cercopithecus aethiops were fed on uncooked banana diet while another three were fed on uncooked cassava and hearts harvested for histology whenever the animal health deteriorated. Changes in the endomyocardium included cell vacuolation, interstitial fibrosis and endocardial thickening by the 130th day in the animals on cassava but the animals on bananas were free from such changes. By the 160th day, the former exhibited marked thickening of the endocardium, interstitial fibrosis, fibrous septa formation, pappillary muscle fibrosis as well as apical fibrosis of the left ventricle, which findings occur in the human disease. Calcification and inflammatory cells were absent. A repeat of the experimental feeding with cassava using a batch of five animals, one of which survived up to seven months revealed cardiac findings similar to those seen at 160 days. Thus, the pathogenetic process, hitherto obscure, begins with cardiac cell necrosis followed by fibrosis consequent upon the failure of cardiac cell repair due to protein deficiency caused by the protein free cassava diets since the animals on bananas, which also lacked protein did not develop similar changes. The low plasma amino acid profiles in EMF prone subjects, the poor blood supply and the great apical mechanical stress are incriminated for the severe apical lesions. This study shows that the disease can be experimentally induced in the monkey thereby validating the postulated hypothesis.

Adolescent↗
PubMed2005

Myelin basic protein accumulation is impaired in a model of protein deficiency during development.

During the development of the central nervous system (CNS) there is a great possibility of permanent effects in consequence of environmental disturbances. Nutritional deficiency is one of the factors that impair the normal CNS formation. In general, the protein deficiency evokes, beyond the damages in the maturation of nervous system, several consequences in body growth, biochemical maturation, motor function and the major cognitive functions. These effects were observed in undernourished children all over the world. Even in a restricted period, the malnutrition status may evoke permanent impairments in feeding behavior and in metabolism. Rats submitted to malnutrition during development, showed a marked decrease in the number of myelinated fibers. This condition may reflect a failure in the beginning of the wrapping of axons by oligodendroglial processes and/or a delay in the myelin synthesis. Myelin basic protein (MBP) is an intracellular oligodendrocyte protein that is directly related to the formation of the myelin sheath. In this study we verified the temporal pattern of MBP expression, by immunohistochemical and immunoblotting analyses, in a model of protein malnutrition induced during the first half of the lactation period. We showed that MBP expression was impaired in our malnutrition model and that some of the effects were maintained in adulthood, with possible consequences in the maturation of myelin sheath.

Aging↗
PubMed1997

Bile acid profiles in a peroxisomal D-3-hydroxyacyl-CoA dehydratase/D-3-hydroxyacyl-CoA dehydrogenase bifunctional protein deficiency.

Bile acid profiles in serum, urine and bile from an infant with a peroxisomal D-3-hydroxyacyl-CoA dehydratase/D-3-hydroxyacyl-CoA dehydrogenase bifunctional protein (D-bifunctional protein) deficiency were analyzed by means of gas-liquid chromatography, gas-liquid chromatography-mass spectrometry, and high-performance liquid chromatography. As in such several peroxisomal disorders as Zellweger syndrome, neonatal adrenoleukodystrophy, and infantile Refsum disease, the accumulation of C27-bile acid intermediates was also demonstrated in the infant with D-bifunctional protein deficiency, accounting for 74% of the total bile acids in serum, 59% in urine, and 35% in bile. In addition, the major constituents of the C27-bile acids were (24R,25R)- and (24R,25S)-3alpha,7alpha,12alpha,24-tetrahydroxy-5be ta-cholestanoic acids along with small amounts of their 24S counterparts. Since immunoreactive acyl-CoA oxidase, L-bifunctional protein, and thiolase were all present in the liver, the impairment of the oxidative side-chain cleavage in bile acid biosynthesis is considered to be due to the defect of D-bifunctional protein.

17-Hydroxysteroid Dehydrogenases↗
PubMed1995

Protein deficiency and the growing rat lung. II. Morphometric analysis and morphology.

Effects of protein deficiency during the whole period of postnatal development and intensive growth were studied in the rat lung parenchyma. Dams received a low protein diet as follows: early restriction, 8% casein diet from parturition, and delayed restriction, 12% then 8% casein diet from lactation d 8. After weaning (d 21), early restriction and delayed restriction group rats were maintained on the 8% casein diet until d 49, wherefore they were returned to normal food (18% casein) for 11 wk. Lungs were processed for light and electron microscopic morphometry on d 21, 49, and 126. The diffusion capacity of the lung for O2 (DLO2) was also determined from the morphologic parameters. Volume and surface densities of the parenchymal components of malnourished rats did not consistently differ from controls. Because of lower lung volumes, absolute values, including DLO2, were all significantly decreased. Further, although lung volume growth was less impaired than body growth and thus deviated from the normal allometric relationship, most morphometric parameters paralleled body weight changes. Visually, we detected minor morphologic alterations at d 21 and 49, not necessarily reflected by morphometric data. But, importantly, lung parenchyma appeared mature at weaning despite the growth retardation. Normal refeeding resulted in a striking regrowth of the lung parenchyma. Although early restriction rats did not fully catch up in lung volume, most parenchymal parameters and DLO2 were largely restored in both refed groups.

Animals↗
PubMed1993

Impact of protein deficiency and exposure to hexachlorocyclohexane or malathion on lipid metabolism in pregnant rats.

Dietary intake of three oral doses of hexachlorocyclohexane (HCH) (60 mg/kg body wt) or malathion (500 mg/kg) by normal and protein-deficient diet fed pregnant rats on the 6th, 10th and 14th day of gestation resulted in the impairment of lipid metabolism, viz. hypercholesterolemia and hypertriglyceridemia. The cholesterol, triglyceride and phospholipid contents in serum, brain, liver, kidney and uterus were increased significantly by HCH and malathion exposure, irrespective of the protein content in the diet. The incorporation of [1,2-14C]acetate into the hepatic lipids was stimulated by both HCH and malathion, suggesting a higher rate of lipid synthesis in the liver of normal and protein-deficient diet fed dams. The low protein content in the diet intensified the pesticide-induced changes and more severe alterations were noticed in HCH exposed dams than in malathion exposed dams.

Animals↗
PubMed1996

Changes in protein distribution in normal and protein-deficient rats during an acute-phase 'injury' response.

The present study investigated the effect of the acute-phase 'injury' response, induced by subcutaneous injection of turpentine, on the hydration and protein content of organs and tissues of normally nourished rats receiving a diet containing 200 g protein/kg, and of protein-malnourished rats receiving a diet containing 30 g protein/kg. The measurements were carried out 48 h after turpentine injection, and were compared with both saline-injected animals, and pair-fed control animals. Circulating alpha 2-macroglobulin was also measured as an index of the acute-phase-protein response. In normally nourished rats turpentine injection caused a significant increase in the mean masses of the liver, kidney and lung (7-35% compared with saline-injected animals, and 20-44% compared with pair-fed controls), and a small reduction in the mass of extra-abdominal and extrathoracic tissues ('carcass'). In general the protein content of tissues changed in a similar way (for liver, kidney and lung a 16-33% increase compared with saline-injected animals, and 32-49% compared with pair-fed controls). Protein deficiency produced a significant attenuation in the response to turpentine. The change in the mass and protein content of several tissues was reduced (for lung, liver and kidney, the increase in protein content was only 5-15%), and the effects on anorexia (1 v. 41% reduction in food intake) and the alpha 2-macroglobulin response (1.28 v. 4.28 g/l; P < 0.001) were also reduced. It is concluded that the injury response spares most central thoracic and abdominal organs, but this effect as well as the anorexia and acute-phase-protein response to injury are attenuated by protein deficiency.

Acute-Phase Reaction↗