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PubMed1980

Effect of moderate chronic protein deficiency on rat salivary components.

Chronic protein insufficiency was achieved in rats with an 8% protein diet initiated at weaning. The total activity and activity per milliliter of the principal salivary protein, amylase, were significantly decreased at day 66. The amount of total protein per milliliter of saliva and total protein in stimulated saliva collected during 30 minutes was decreased in the malnourished rats. The levels of immunoglobulin G (IgG) and aminopeptidase in saliva were not affected by dietary status. Prolonged malnutrition on the low-protein, high-starch diet resulted in an apparent stimulation or induction of salivary amylase and protein secretion by day 110. Total protein collected and milligram of protein per milliliter of saliva were very similar in the malnourished and control rats at day 110. Salivary amylase activity in the malnourished rats was significantly greater than in the saliva of controls. The initial decrease in the principal salivary protein, amylase, and in total protein followed by a significant increase with prolonged stimulation by low-protein and high-starch diets suggests that early protein deficiency retards synthesis of amylase and that a high-starch diet may induce salivary amylase production.

Aging↗
PubMedDate not supplied

The combined effects of protein deficiency and chronic ethanol administration on rat ethanol metabolism.

This investigation was performed to examine the combined effects of protein deficiency and chronic ethanol consumption on ethanol clearance and hepatic ethanol metabolism of the rat. Protein deficiency alone was associated with reduced ethanol clearance and decreased activity of hepatic alcohol dehydrogenase and the microsomal ethanol-oxidizing system. However, when ethanol (as 36% of energy) was administered concurrently with protein-deficient diets, accelerated ethanol clearance and increased microsomal oxidation of ethanol was observed. Furthermore, in protein-deficient animals fed ethanol, liver alcohol dehydrogenase levels were less decreased when compared with values observed in animals fed protein-deficient diets without ethanol, and this effect was associated with markedly reduced serum testosterone levels in the former group.

Alcohol Oxidoreductases↗
PubMed1978

Effect of oral pancreatic enzymes on the course of cholera in protein-deficient vervet monkeys.

The effect of pancreatic extract on the course of cholera infection in protein-deficient vervet monkeys (Cercopithecus aethiops) was studied. Eleven animals were made protein deficient by diet. Thier intestinal pancreatic enzyme concentration decreased as they became protein depleted. These animals were then challenged with Vibrio cholerae. Four control animals given a standard diet were similarly challenged. Immediately after challenge, 6 of the protein-deficient monkeys were given a highly purified pancreatic extract at a dose of 500 mg per day, and the other 5 protein-deficient animals received heat-inactivated pancreatic extract. Pancreatic extract significantly reduced the severity and duration of diarrhea in the treated animals so that they resembled the controls. The period of fecal excretion of vibrios was prolonged in the group of monkeys which received inactivated pancreatic extract. In addition, the response of intestinal antibody titers to cholera toxin was also significantly lower in this latter group. These observations suggest that exocrine pancreatic secretion is involved in the local defense mechanism against cholera during prtein deficiency.

Animals↗
PubMed1987

The effect of protein deficiency on systemic release of rat mucosal mast cell protease II during Nippostrongylus brasiliensis infection and following systemic anaphylaxis.

Serum rat mucosal mast cell protease II (RMCPII) was measured in protein-deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis, and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the first study, serum RMCPII increased 4-fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein-deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein-deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein-deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein-deficient rats exhibited 3 to 7-fold less mucosal permeability of the small intestine to Evan's blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.

Anaphylaxis↗
PubMed1992

Defective mitochondrial cation transport during dietary protein deficiency in rats.

Mitochondria were isolated from the livers of male weanling and adult Wistar strain albino rats fed low-protein diet ad libitum for 30 and 84 days, respectively. Control animals consisted of adult and weanling rats fed purina chow for the same periods. Spectrophotometric estimations of mitochondrial passive transport of protons by following changes in matrix volume at 520 nm revealed that the mitochondria of protein-deficient rats are more permeable to protons than those of control rats; the mitochondria of protein-deficient weanling rats being more permeable than mitochondria of protein of malnourished adult rats. Similar results were obtained when a sensitive pH-glass electrode was used to monitor mitochondrial proton translocation. Although protons were slowly ejected from the mitochondrial matrix of protein-deficient rats, there was a significantly high rate of influx of the ion into the matrix of these mitochondria when compared with controls. Furthermore, FCCP, a classical protonophore carried protons less rapidly across the mitochondrial membrane of malnourished animals thus indicating that a small pH difference probably exists across the mitochondrial energy-coupling membrane of protein-deficient rats. Consequently, the rates of mitochondrial Ca(2+)-translocation were lower in protein-deficient animals than in normal rats. These defects are probably due to diet-induced looseness of mitochondrial bi-layer structure.

Age Factors↗
PubMed1997

Splenocyte glutathione and CD3-mediated cell proliferation are reduced in mice fed a protein-deficient diet.

Protein-energy malnutrition (PEM) is associated with decreased host immune defense. Glutathione (GSH) status is reported to be decreased in PEM, and GSH is important for lymphocyte function. The objective of the present study was to investigate the effects of PEM and dietary repletion (RP) on GSH status in various tissues and splenocytes and on CD3-mediated calcium mobilization and cell proliferation of splenic T-lymphocytes. For the PEM model, mice were fed a 0.5% protein diet (LP group) for 4 or 6 wk, and control mice were fed a 15% protein diet (CP group). In the RP study, LP mice were fed the 15% protein diet for 3 d, 1 wk, 2 wk or 3 wk (RP groups). Glutathione concentrations were significantly lower in liver, lung, heart and spleen of LP mice compared with CP mice at 4 and 6 wk. Splenocytes from LP mice were significantly lower in number and had a lower intracellular GSH concentration, depressed CD3-stimulated T-lymphocyte proliferation in culture media without thiol supplementation (2-mercaptoethanol), and enhanced CD3-stimulated proliferation in thiol-supplemented culture media compared with splenocytes from CP mice. CD3-stimulated calcium mobilization was significantly lower in CD8+, but not CD4+, splenocytes from LP mice. Within 1 wk of dietary repletion, splenocyte GSH concentration was normal and splenocyte numbers were greater, and in vitro sensitivity of CD3-stimulated T-lymphocyte proliferation to thiol was lower, compared with LP mice. Glutathione status in vivo and thiol supplementation in vitro seem to modulate the signal transduction pathway for T-lymphocyte proliferation in mice with PEM.

Animals↗
PubMed1995

Two alpha subunit donor splice site mutations cause human trifunctional protein deficiency.

Human trifunctional protein catalyzes three steps in mitochondrial beta-oxidation of fatty acids, including the long chain 3-hydroxyacyl-CoA dehydrogenase step. Deficiency of this heterocomplex, which contains 4 alpha and 4 beta subunits, causes sudden unexplained infant death, a Reye-like syndrome, cardiomyopathy, or skeletal myopathy. We determined the molecular basis of this deficiency in a patient with neonatal presentation and later sudden death using reverse transcription and PCR amplification of his alpha subunit mRNA. We demonstrated a universal deletion of exon 3 (71 bp) in his mRNA. This deletion causes a frameshift and very early premature termination. Amplification of genomic DNA demonstrated that the patient was a compound heterozygote with two different mutations in the 5' donor splice site following exon 3: a paternally inherited G to A transversion at the invariant position +1 and a maternally inherited A to G mutation at position +3. Both allelic mutations apparently cause exon 3 skipping, resulting in undetectable levels of alpha subunit protein, and complete loss of trifunctional protein. This is the initial molecular characterization of trifunctional protein deficiency.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1987

The effects of ozone on lung, heart, and liver superoxide dismutase and glutathione peroxidase activities in the protein-deficient rat.

The effects of protein deficiency or food restriction and ozone exposure on lung, heart and liver superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were studied in weanling and adult rats. Two groups of rats were fed diets containing 4 or 16% protein. A third group was fed the 16% protein diet, but at the level consumed by the rats fed the 4% protein diet. After 3 weeks (weanling) or 5 weeks (adult), one-half of the rats in each group were exposed continuously to 0.64 ppm ozone for 7 days. In adult rat lung, O3 exposure typically stimulated Cu,Zn-SOD and GPx activities in all groups, but in weanling rats only GPx activity was elevated and only in rats fed the 16% protein diet. Liver Cu,Zn-SOD activity was also influenced by diet; in adult rats, liver Mn-SOD and GPx activities were often depressed following O3 exposure. Heart SOD and GPx, however, were not affected by ozone or diet. The pulmonary and hepatic effects due to diet and O3 further illustrate the importance of nutritional status when assessing the health effects of O3 exposure.

Animals↗
PubMed1984

Protein deficiency in pregnant rats causes decreased levels of plasma somatomedin and its carrier protein associated with reduced plasma levels of placental lactogen and hepatic lactogenic receptor number.

Rats were fed either a 20% lactalbumin (control) or a 5% lactalbumin (low protein) diet for the last 2 weeks of pregnancy. At day 20 of gestation, rat serum placental lactogen levels, measured by radioreceptor assay, were significantly decreased by the low protein diet, thus confirming our earlier findings. The number of microsomal membrane lactogenic receptors, measured on the maternal livers at the end of pregnancy, was severely reduced in the livers of the low protein group, whereas protein deficiency did not affect binding affinity. Serum concentrations of somatomedin, measured by a competitive binding assay after acid treatment of the serum to remove endogenous carrier protein, were extensively reduced in the low protein group. The amounts of the somatomedin carrier proteins in the serum were assayed by separation on Sephacryl-S300 columns into higher- and lower-molecular-weight fractions peak 2 and peak 3, respectively. For the low protein diet group, both fractions showed a reduction in binding capacity, more marked in the case of peak 2. Since placental lactogen is known to influence output of somatomedin by the liver, we hypothesize that protein deficiency during pregnancy causes a fall in serum somatomedin level by reducing secretion of placental lactogen, which regulates its production by the liver.

Animals↗
PubMed2005

Biochemical, clinical and molecular findings in LCHAD and general mitochondrial trifunctional protein deficiency.

General mitochondrial trifunctional protein (TFP) deficiency leads to a wide clinical spectrum of disease ranging from severe neonatal/infantile cardiomyopathy and early death to mild chronic progressive sensorimotor poly-neuropathy with episodic rhabdomyolysis. Isolated long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency resulting from the common Glu510Gln mutation usually gives rise to a moderately severe phenotype with multiorgan involvement with high morbidity and mortality. However, isolated LCHAD deficiency can also be consistent with long-term survival in patients identified and treated from an early age. We present biochemical, clinical and mutation data in 9 patients spanning the full spectrum of disease. Fibroblast acylcarnitine profiling shows good correlation with clinical phenotype using the ratio C18(OH)/(C14(OH)+C12(OH)). This ratio shows a gradation of values, from high in four patients with severe neonatal disease (2.5+/-0.8), to low in two neuromyopathic patients (0.35, 0.2). Fibroblast fatty acid oxidation flux assays also show correlation with the patient phenotype, when expressed either as percentage residual activity with palmitate or as a ratio of percentage activity of myristate/oleate (M/O ratio). Fibroblasts from four patients with severe neonatal disease gave an M/O ratio of 4.0+/-0.6 compared to 1.97 and 1.62 in two neuromyopathic patients. Specific enzyme assay of LCHAD and long-chain 3-ketothiolase activity in patient cells shows lack of correlation with phenotype. These results show that measurements in intact cells, which allow all determinative and modifying cellular factors to be present, better reflect patient phenotype. Mutation analysis reveals a number of alpha- and beta-subunit mutations. Peripheral sensorimotor polyneuropathy, often as the initial major presenting feature but usually later accompanied by episodic rhabdomyolysis, is a manifestation of mild TFP protein deficiency. The mild clinical presentation and relative difficulty in diagnosis suggest that this form of TFP is probably underdiagnosed.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed2005

Protein deficiency balance as a predictor of clinical outcome in hereditary spherocytosis.

Vertical and horizontal interactions between membrane constituents account for integrity, strength and deformability of the erythrocyte. Disruption of vertical interactions caused by membrane protein deficiencies in hereditary spherocytosis (HS), favor membrane vesiculation with development of spherocytic cells. Our aim was to evaluate the hematological and clinical presentation of HS according to the type and amount of protein deficiency. We studied 81 Portuguese individuals, 71 belonging to 21 families plus 10 unrelated subjects, and found that 51 of them were HS patients. Patients were classified as presenting mild, typical or severe HS, according to laboratory results and clinical follow-up. We performed screening tests and the standardized electrophoretic membrane protein analysis to identify and quantify protein deficiencies. We found band 3 and ankyrin deficiencies as the major causes for HS. The ratios between the value of the primary and/or secondary protein deficiencies showed significantly different values according to the severity of HS, and a significant inverse correlation with the severity of HS was observed. In mild HS, the ratios between protein deficiencies reflected equivalent protein deficiencies, while an unbalance was observed in typical HS, which was enhanced in severe HS. Our data suggest that the relative quantification of each major membrane protein and of the ratios between the values of protein deficiencies may be helpful in providing additional data about the clinical outcome of HS.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1995

Synthesis and phosphorylation of macrophage membrane proteins in protein deficient rat.

Changes in the biosynthesis and phosphorylation of rat peritoneal macrophage membrane proteins induced by protein malnutrition have been studied. The results clearly indicate that the biosynthesis of high molecular weight proteins (45-200 kDa) and their phosphorylation are significantly reduced in the macrophages isolated from protein deficient (4% protein-fed) rats compared to the control group fed 20% protein diet. Lipopolysaccharide (LPS) treatment both in vivo and in vitro enhanced the synthesis and phosphorylation of these proteins in both control and protein deficient groups; however, the extent of enhancement was much less in the deficient group. These results indicate that besides the down regulation of these membrane proteins, protein malnutrition seems to make these macrophages less responsive to potent immuno stimulants like LPS.

Animals↗
PubMed1975

[Blood serum and liver phospholipids in rats with chronic choline-protein deficiency].

Serum and liver phospholipids were studied in rats at different stages of pathological processes induced by a diet with a high fat content, but deficient in protein and choline. Such cirrhosogenic diet caused fatty infiltration, fibrosis and nodular liver cirrhosis in rats, depending on the period of its administration. This diet resulted in a considerable decrease of the phospholipid content in the liver and the serum of experimental rats. Addition of choline to the cirrhosogenic diet prevented formation of fatty infilitration in rats, but failed to protect completely from a fall of phospholipids in the liver.

Animals↗
PubMed1991

A study on the B cell activity in protein deficient rats exposed to methyl isocyanate vapour.

The effect of MIC on the humoral immunity of the malnourished (protein deficient) subjects has been investigated. A single exposure of MIC (1.60 mg/l) on protein deficient rats showed no significant change in the body weight and mortality rate compared with the normal but the serum protein levels were found significantly low (P less than 0.01) in the protein deficient diet fed control (PDC) ones. Both PDC and protein deficient MIC exposed (PDMIC) rat showed diminished B-cell proliferation with the optimal dose of LPS, compared to the NDC and normal diet fed MIC exposed (NDMIC) group. Furthermore significant suppression (P less than 0.01) in the B-cell activation by LPS was observed in the PDMIC compared to PDC. The total IgM level in PDMIC was 43% less while 26% higher in NDMIC compared to NDC. The total IgG level in PDMIC and NDMIC was higher (20%) compared to NDC, while 25% less in PDC. The antigen specific B-cell immunity was affected in PDMIC, PDC and NDMIC. As the terminal differentiation process of B-cells were found equally affected in both PDC and NDMIC, it appears that MIC has no synergistic effect on the humoral immunity of the protein malnourished host.

Animals↗
PubMed1985

Comparative effects of protein, protein hydrolysate and amino acid diets on nitrogen metabolism of normal, protein-deficient, gastrectomized or hepatectomized rats.

The effects of diets containing protein, protein hydrolysate or an amino acid mixture on nitrogen metabolism of normal and severely protein-deficient rats and on rats after gastrectomy and hepatectomy were compared. In experiment 1, rats weighing about 80 g were fed one of three experimental diets containing casein, protein hydrolysate or an amino acid mixture for 28 d. In experiment 2, rats weighing about 270 g were fed a protein-free diet for 40 d, and then one of the above three experimental diets for 14 d. In experiment 3, rats weighing about 220 g were totally gastrectomized and fed one of the three experimental diets for 21 d. In experiment 4, rats weighing about 210 g had about 70% of the liver resected, and then were fed one of the three experimental diets for 15 d. In all four experiments, daily food intake, daily body weight gain, nitrogen balance, urinary nitrogen compounds, body composition and hematologic values were measured. In normal, protein-deficient and hepatectomized rats, most results were similar for the groups fed protein, protein hydrolysate or amino acid diets, except that urinary ammonia was higher in the group fed the amino acid diet than in the other two groups. For about 10 d after total gastrectomy, food intake and growth of the animals fed the protein diet were lower than in the other two groups.

Amino Acids↗
PubMed1974

[The influence of a protein deficient diet on the activity of the hypothalamus-neurohypophysial system].

In mature as well as in prebuberal rats protein deficient diets activate the hypothalamo-neurohypophysial system, which is morphologically characterised by the decrease of neurosecret in the posterior pituitary and the increase of the cell nuclear volume of the supraoptic and paraventricular nuclei. The neuronal activity is stimulated significantly stronger by a protein deficient diet with addition of some essential amino acids (lysine, tryptophane, threonine and isoleucine) than by an extremely deficient protein diet in so far as it occurs in the cell nuclear volume of both neurosecretoric hypothalamic nuclei.

Age Factors↗
PubMed2000

Effects of protein-deficient nutrition during rat pregnancy and development on developmental hindlimb crossing due to methylmercury intoxication.

Pregnant rats were fed either a control (20% protein) or low (3.5%) protein diet during gestation and lactation. The pups were separated from their mothers on postnatal day 21, and were given the same diet as their corresponding mothers. The groups of pups from each diet group were treated on either postnatal day 21 or postnatal day 60 with 7.5 mg methylmercury chloride (MeHgCl) per kg b.w. once daily by gavage for 10 consecutive days, and the development of ataxia (hind-limb crossing) was monitored. The offspring from mothers on the protein-deficient diet were found to be more sensitive to MeHg-induced ataxia than those on the protein-sufficient diet. The former accumulated more mercury in different brain regions than the latter. The rates of protein synthesis in different brain regions of the offspring fed the protein-deficient diet were significantly reduced compared with the rates in those fed the protein-sufficient diet. However, MeHg treatment did not significantly modify the rates of such protein synthesis further in protein-deficient rats. Thus, a significantly much higher inhibition of the intrinsic rates of protein synthesis in different brain regions due to severe protein deficiency, as observed in this study, may be partly responsible for the increased susceptibility of developing rats fed a protein-deficient diet to MeHg-induced ataxia, or hindlimb crossing, although other factor(s) might also be involved.

Animals↗
PubMed1991

Protein deficiency suppresses bone resorption in sheep based on a short-term in vivo bone model.

Six sheep were fed protein-deficient and control diets for 40 d for each diet in a crossover design. Each sheep was intramuscularly injected with 120 pmol.d-1.kg body wt-1 of 1,25-dihydroxycholecalciferol during the last 7 d of each dietary period. Approximately 100 mg of bone powder was implanted on the abdominal muscle on d 21 and d 28 of each dietary period. Plaques induced by the bone powder were harvested 12 d after the implantation. Tartrate-resistant acid phosphatase (TR-ACP) activity was lower and the number of multinucleated cells was smaller in plaques of animals during the protein-deficient period than during the control period. The administration of 1,25-dihydroxycholecalciferol increased the activity of TR-ACP and the number of multinucleated cells during both dietary treatments. However, TR-ACP activity was still lower and the cell number was still smaller during the protein-deficient period than during the control period when they were injected with 1,25-dihydroxycholecalciferol. These results suggest that protein deficiency reduces the activity of osteoclastic cell induction. The suppressive effect of protein deficiency on the induction and the activity of osteoclastic cells is not related to the action of 1,25-dihydroxycholecalciferol.

Animals↗