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PubMed1980

Myocardial effects and pharmacokinetics of digoxin and ouabain in protein-deficient guinea pigs.

Myocardial effects and pharmacokinetics of digoxin and ouabain were studied in male albino guinea pigs fed ad libitum either a 21% (control) or a 5% (low) protein diet for 4 weeks. Dietary protein deficiency was associated with a decrease in body weight gain, ventricular weight, total plasma proteins and plasma albumin, hepatic total and microsomal proteins, cytochrome P-450, and protein:DNA ratios; serum potassium was slightly but insignificantly decreased. No significant differences were found in the following experiments with digoxin and ouabain in control and protein-deficient animals: inotropic effects of ouabain on isolated papillary muscles and left atria; uptake of [3H]ouabain by isolated papillary muscles; ventricular fibrillatory doses of digoxin and ouabain in anesthetized animals and the concentrations of digoxin in plasma and papillary muscles at the onset of ventricular fibrillation in these animals; plasma half-life of digoxin in unanesthetized guinea pigs. It is concluded that although dietary protein deficiency influences several physiological and biochemical parameters it does not alter the myocardial effects and pharmacokinetics of digoxin and ouabain in guinea pigs.

Animals↗
PubMed1990

Lipid peroxidation of rat liver microsomes membranes related to a protein deficiency and/or a PCB treatment.

In this study, we investigated the influence of protein deficiency on lipid peroxidation (LP) and cellular defense systems against oxidative damage in control or polychlorinated biphenyl (PCB) treated rats. Rats were fed either a standard diet (22% casein) or a low protein diet (3.5% casein) for 1, 2 and 6 weeks. Five days prior to killing, one half of the animals were given a single i.p. injection of Phenoclor DP6 (50 mg/kg body weight). In protein deficient rats, liver vitamin E was depressed and ascorbate level was lowered. Total and selenium-dependent glutathione peroxidases (GSH-Px) activities were decreased whereas glutathione reductase (GSH-red) was enhanced. Enzymatic and non enzymatic LP ('spontaneous' or with ADP-Fe2+) were increased. Phenoclor DP6 treatment enhanced liver ascorbate concentration. Microsomal LP was increased. Total and selenium-GSHPx remained unmodified while GSH-red was increased. Liver glutathione and alpha-tocopherol contents appeared to be independent of the PCB injection. Our data suggest that low protein intake and PCB exposure may reduce liver defensive protection against electrophilic species.

Animals↗
PubMed1981

The effect of protein deficiency on the development of chronic antigen-antibody complex disease in mice.

Mice genetically selected to produce antibodies of either high or low affinity to protein antigens injected in saline were fed either a normal protein diet or a protein-deficient diet and were given daily injections of HSA for up to 73 days to induce chronic antigen-antibody complex disease. In low-affinity mice fed the normal protein diet, this resulted in impairment of renal function, deposition of immunoglobulin, C3 and HSA in the glomeruli, high levels of circulating antigen-antibody complexes and death from apparent renal failure in 50% of the animals. High-affinity mice on either diet had no impairment of renal function, fewer deposits in the glomeruli, lower levels of circulating complexes and no deaths. Low-affinity mice fed the protein-deficient diet had less impairment of renal function and less glomerular deposition of complexes than did low-affinity mice fed the normal diet. In addition, none of these mice died from renal failure. These results demonstrate that the protein-deficient diet reduced the severity of the experimental chronic antigen-antibody complex disease in low affinity mice but did not increase the susceptibility of high-affinity mice to the disease.

Animals↗
PubMed1981

Intestinal transport of amino acids in protein-deficient rats and the effect of rehabilitation using a casein diet.

The effects of protein deprivation and subsequent rehabilitation on the intestinal absorption of a mixture of amino acids were studied in albino rats. The absolute amounts of amino acids transported across the intestine were greater in rats fed for 28 days 17% casein diet than those fed 3% maize protein or no-protein diets. The absorption per unit intestinal DNA (termed as absorptive capacity) of amino acids, except L-arginine in males, was more in rats fed the 3% maize protein diet than those fed the casein diet. The changes in the absorptive capacity of two sexes, when fed the protein-free diet, were not similar. The males absorbed L-arginine and L-methionine, and females L-histidine and L-tryptophan at rates faster in the protein-free group than their counterparts in the casein group. The differences between protein-free and casein groups in the absorption of L-tryptophan and L-histidine in males and L-arginine and L-methionine in females were not significant. The augmentation in absorptive capacity of intestinal cells in protein-deficient rats was a temporary adaptation to the condition that resulted in reduced intestinal cell population. Rehabilitation of protein-deficient rats for 32 days on the casein diet, resulted in an increase in intestinal cell population, return of absorptive capacity of intestinal cells to normal, and improvement in net absorption rates.

Amino Acids↗
PubMed1981

Effects of rehabilitation on the jaws and teeth of protein-deficient and calorie-deficient pigs.

The growth of the jaws and teeth was examined in pigs which had been fed protein-deficient and calorie-deficient diets for the first year of life and thereafter allowed unlimited food. After 2 years of rehabilitation, jaw size had almost reached that of well-fed controls, although in the mandible the labial alveolar process remained abnormally proclined and in both jaws the crowns of third permanent molars were smaller than in control animals. Calorie-deficient pigs did not recover as well as did protein-deficient animals. Pigs fed a calorie-deficient diet for the first 2 years of life before rehabilitation also made a good recovery and were only slightly smaller in most dimensions than those undernourished for 1 year and then rehabilitated. Despite the excellent recovery in jaw dimensions, some malposition of teeth persisted after rehabilitation, especially in animals which had been undernourished for 2 years.

Animals↗
PubMedDate not supplied

Micro- and macrovesicular steatotic liver model for transplantation induced by ethanol and protein-deficient diet.

Steatotic liver grafts are associated with a high incidence of primary nonfunction and initial poor function. Due to the increasing number of liver transplant candidates, centers are inclined to accept marginal donors more frequently. For a lack of a reliable fatty liver model, preservation concepts for fatty livers have hardly been evaluated. Moreover, there is an ongoing debate on the relevance and impact of micro- versus macrovesicular steatotic organs. We therefore intended to establish a steatotic liver model in pigs comprising both micro- and macrovesicular steatotic livers. Five groups of pigs received daily 1 to 6 g ethanol/kg body weight and/or a protein-deficient diet for up to 72 days. Liver biopsy was carried out at days 24, 48, and 72. With an increasing amount and duration of ethanol intake, higher levels of microvesicular steatosis were induced. Ethanol and protein deficient diet resulted in more than 60% microvesicular steatosis after 72 days. Exclusively protein-deficient diet without ethanol induced macrovesicular steatosis of more than 70% after 72 days. For the first time, we established a porcine model of hepatic steatosis that comprises both histologic types of fatty liver: micro- and macrovesicular steatosis induced by ethanol and a protein-deficient diet. We would like to conclude that our model is particularly qualified to study new concepts of preservation for steatotic livers to improve on the posttransplant outcome.

Animals↗
PubMed2006

Protein deficiency impairs DNA vaccine-induced antigen-specific T cell but not B cell response in C57BL/6 mice.

DNA vaccination is a simple method to induce antigen (Ag)-specific immunoresponse and has many potential advantages over other vaccines. Although people who need to receive vaccines often suffer undernutrition, there has been no study on a how nutritional status affects the immunoresponse induced by DNA vaccination. The aim of this study was to determine the relationship between protein deficiency and DNA vaccine-induced immunoresponses. C57BL/6 mice were fed a 5% or 20% casein diet for 30 d. The mice were immunized with an ovalubumin (OVA)-expression plasmid by the gene gun-based method three times at 10-d intervals. Body weight and serum albumin concentration in protein-deficient mice were significantly lower than those in mice fed the 20% casein diet (p<0.01, p<0.05). The percentage of OVA-specific CD8+ T cells was significantly decreased in the 5% casein group compared to that in the 20% casein group (p<0.05). Furthermore, CD4+ T cells from mice fed the low-protein diet showed lower interleukin (IL)-2 production than did those from the 20% group. In contrast to the T-cell function, protein deficiency did not affect OVA-specific Ab responses (p>0.05). These results suggest that protein deficiency impairs the induction of Ag-specific T-cell but not B-cell response in DNA-immunized mice. Our observation indicates that, in addition to development of an effective of DNA vaccine, the management of nutritional state is important for the prevention of infectious disease by DNA vaccination.

Animals↗
PubMed1994

Dietary protein deficiency affects n-3 and n-6 polyunsaturated fatty acids hepatic storage and very low density lipoprotein transport in rats on different diets.

Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition. The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, or hydrogenated coconut oil poor in EFA. Animals were divided into six groups, SOC (20% casein + 5% soybean oil), SOd (2% casein + 5% soybean oil), COC (20% casein + 5% hydrogenated coconut oil), COd (2% casein + 5% hydrogenated coconut oil), SAC (20% casein + 5% salmon oil) and SAd (2% casein + 5% salmon oil). After 28 d, liver steatosis and reduced VLDL-phospholipid contents (P < 0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein levels, DHA levels remained higher in rats fed salmon oil diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Protein deficiency potentiates oxygen toxicity.

Male rats (Charles River COBS-CD derived) fed protein-deficient diets showed enhanced toxicity with failure of elevation of lung glutathione levels with exposure to greater than 98% O2. Replenishment of S-containing amino acids in the protein-deficient diets allowed elevation of lung glutathione and prevention of enhanced toxicity. Studies with endothelial cell cultures exposed to hyperoxia showed elevation of cellular glutathione coupled with enhanced uptake of amino acid precursors of glutathione. We postulate that hyperoxia causes an enhancement of uptake of S-containing amino acids necessary for glutathione synthesis, overriding glutathione feedback of its own synthesis. Limitation of available S-containing amino acids prevents elevation of glutathione synthesis and is detrimental to the cell exposed to hyperoxia.

Amino Acids↗
PubMed1986

Kinetics of lymphocyte subpopulation in intestinal mucosa of protein deficient Giardia lamblia infected mice.

Kinetics of gut lymphocyte subpopulations were studied in normal and malnourished groups of mice infected with Giardia lamblia. The maximum parasite load was observed at second, third, and first week of postinfection in normal controls, moderate (8%) and severe (3%) protein deficient groups respectively. The number of G lamblia trophozoite in 3% protein deficient group was low compared with control groups. A significant increase in T cell population of intraepithelial lymphocytes and lamina propria in normal and moderate protein deficient groups was observed with the development of infection. It was less marked, however, in the severely malnourished group. Interplay of mucosal immune status with nutrition and G lamblia infection is discussed.

Animals↗
PubMed1986

Thymosin fraction 5: effects on T cell functions in mice immunosuppressed by severe dietary protein deficiency.

The present studies were performed to determine the effects of severe protein deficiency and subsequent injection of thymosin fraction 5 (TF5) on T and B cell functions. BALB/c mice, 4 weeks old, were fed a normal protein (21%), a low protein (4%) or a protein free (0%) diet and then injected with TF5 or buffer (PBS). A significant increase was observed in the PHA (phytohemagglutinin) and LPS (lipopolysaccharide) induced mitogenesis with increasing age of the well-nourished, PBS injected animals. The severely protein malnourished mice, PBS injected and the well nourished mice, injected with TF5 had smaller increases in both B and T cell mitogenesis with increasing age. TF5 injection of the malnourished mice increased PHA and LPS mitogenesis nearly to the levels of the well-nourished mice. The protein malnourished mice consistently had higher serum corticosteroid levels than controls. No changes in serum corticosteroids were observed with TF5 injection of controls, but there was a significant decrease in the corticosteroid levels of the severely malnourished with TF5 injection. Cytoxicity assays of T cell function, antibody dependent cellular cytoxicity and cytoxicity to mouse thymona tumor cells, in mice fed moderately protein deficient diets showed suppression compared to controls fed 20% protein. TF5 injection partially and temporarily increased these functions in the malnourished mice.

Animals↗
PubMed1982

Reversible modification of 50S ribosomal subunits with dimethylmaleic anhydride: protein-deficient particles.

The reversible modification of protein amino groups with dimethylmaleic anhydride, which had already been used to dissociate proteins from the 70S ribosomes of Escherichia coli (Pintor-Toro, J. A., et al. (1979) Biochemistry 18, 3219) was applied to the preparation of protein-deficient particles from the 50S subunits. Three successive cycles of treatment with dimethylmaleic anhydride, separation of dissociated proteins and regeneration of the modified amino groups produce partially inactivated ribosomal 'cores' lacking proteins L7, L11 and L12, and having very small amounts of L1, L6 and L10. Incubation of these 'cores' with the corresponding split proteins is accompanied by complete reactivation of the polypeptide synthesizing activity as compared with control 50S subunits.

Bacterial Proteins↗
PubMed1978

Body collagen nitrogen in protein-deficient adult rats.

Four groups of 10 young adult male rats of the Wistar strain were fed on a protein-free diet ad libitium for periods of 7, 28, 56, and 84 days. Control groups were fed a purified 20% casein diet. Food intake and body weights of rats were measured. Hemoglobin and plasma protein levels, weight, total nitrogen, and collagen nitrogen of skin, carcass, muscle, and liver were determined. Protein-deficient rats lost body weight and had low plasma protein concentrations, but hemoglobin levels remained normal until day 56 of deficiency. The liver lost weight and nitrogen more rapidly than the other organs; the severity of nitrogen depletion in the organs increased with time fed the protein-deficient diet. When protein deficiency was severe, collagen nitrogen concentration increased in organs and carcass. This was not due to an actual increase of collagen nitrogen content; comparisons among malnourished groups showed that the total amount of collagen nitrogen in carcass, liver, and muscle was maintained and that the amount in skin diminished as periods of protein deprivation increased. In control rats, results indicated that the amount of collagen nitrogen in skin, muscle, and carcass increased during growth. These results indicate that protein restriction in adult rats affects collagen metabolism, with skin collagen being more markedly affected than that of other tissues.

Aging↗
PubMed1996

Beta-adrenergic receptors in porcine adipocyte membranes: modification by animal age, depot site, and dietary protein deficiency.

Adipocyte lipid metabolism is primarily regulated by insulin and the catecholamines norepinephrine and epinephrine. Stimulation of the beta-adrenergic receptors (beta-AR) by catecholamines causes an increase in the rates of adipocyte lipid degradation and a decrease in the rates of lipid synthesis. These catabolic effects are in opposition to insulin, which causes net anabolic effects. Because most of the postnatal development of adipose tissue mass in pigs results from hypertrophy of adipocytes (rapid in first few weeks of life) caused by increased net synthesis of triacylglycerol, there is interest in the modulation of beta-AR in adipocytes of growing pigs. The beta-AR are characterized by measuring ligand binding to the receptor to ascertain the affinity of the ligand for the receptor and the receptor number. We found the affinity of the receptor did not vary with animal age (10, 28, and 75 d), with adipose tissue depot site, or in adipocytes of protein-deficient pigs. The beta-AR in obese pigs tended to have greater affinity than those in crossbred pigs of the same age and weight. The beta-AR number was not different when expressed per milligram of adipocyte membrane protein in pigs of different age, in obesity, in different adipose tissue depots, or during protein deficiency. The number expressed per cell or per unit adipocyte surface area did not differ between depots or during protein deficiency. The number per cell tended to be greater in the larger cells from 75-d-old pigs than in the smaller cells from 10- and 28-d pigs. It was greatest in obese pigs with the largest adipocytes. Under the various experimental conditions (age, obesity, depot, protein deficiency), the membrane fatty acid composition was greatly different, but in most cases there was no modulation of beta-AR affinity.

Adipocytes↗
PubMed1991

Cardiovascular effects in bonnet monkeys (Macaca radiata) of a cassava-based protein-deficient diet.

Bonnet Monkeys (Macaca radiata) were maintained for up to 5 mo on protein-deficient diets that contained tapioca starch (cassava starch) as the source of carbohydrate. The animals developed mucopolysaccharidosis of blood vessels and cardiomyopathic changes in the heart. These changes were similar to the mucoid vasculopathy and cardiomyopathy seen in Kerala where tapioca is consumed as a staple diet by a large proportion of the people. The lesions were enhanced by longer duration of feeling the diet and in protein-deficient animals given additional amounts of tapioca starch. This indicates that protein-carbohydrate malnutrition does play a role in the induction of such cardiovascular disorders.

Animals↗
PubMed1990

Reconstitution of protein translocation from detergent-solubilized Escherichia coli inverted vesicles: PrlA protein-deficient vesicles efficiently translocate precursor proteins.

Proteoliposomes were reconstituted by detergent dialysis of a sodium cholate extract of inverted vesicles derived from Escherichia coli plasma membrane. The translocation of precursor proteins into reconstituted vesicles occurred at high efficiency and was SecB dependent. The protein composition of the reconstituted vesicles differed markedly from that of native vesicles. Immunoblot analysis of the sodium cholate extract and of the reconstituted vesicles indicated that PrlA (SecY) protein remained largely unsolubilized under the described conditions and was virtually absent from the reconstituted vesicles, suggesting that PrlA may not be required for in vitro translocation.

ATP-Binding Cassette Transporters↗