[Vitamin E deficiency (alpha-tocopherol transfer protein deficiency)].
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Biomarkers↗
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The influence of dietary protein deficiency on the performance of isolated muscle preparations from the rat left ventricle.
The contractile performance of isolated muscle preparations from the left ventricle of rats receiving a 3% casein protein deficient diet for two to three weeks was compared with the performance of muscle preparations from animals receiving a normal diet. The right and left ventricular weights from protein deficient animals were significantly decreased, but left ventricle/body weight and right ventricular/body weight ratios did not differ from control animals. The performance of the isolated muscle preparations revealed no differences in the following parameters measured at the apex of the length tension curve: peak active tension, resting tension, maximum rate of tension development and time to peak tension. RT1/2, an index of relaxation, and maximum rate of tension decline indicated relaxation rate was increased in preparations from protein deficient animals. We conclude that, while a protein deficient diet of two to three weeks duration results in proportionate decreases in body and cardiac chamber weight in comparison to control animals, no evidence for impaired contractile activity is seen.
Animals↗
Physiological effect of protein deficiency with special reference to evaluation of protein nutrition and protein requirement.
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Blood Proteins↗
Changes in fatty acid compositions of total serum and lipoprotein particles, in growing rats given protein-deficient diets with either hydrogenated coconut or salmon oils as fat sources.
The present study examines the effects of dietary saturated (hydrogenated coconut oil) and polyunsaturated (salmon oil) fats on the composition and metabolism of lipoproteins in growing rats fed on protein-deficient diets. Four groups of rats were fed on the following diets for 28 d: 200 g casein + 50 g coconut oil (COC)/kg, 20 g casein + 50 g coconut oil (COd)/kg, 200 g casein + 50 g salmon oil (SAC)/kg, 20 g casein + 50 g salmon oil (SAd)/kg. Both protein-deficient groups exhibited low concentrations of protein and triacylglycerol (in serum, very-low-density lipoprotein (VLDL), low-density lipoprotein-high-density lipoprotein, (LDL-HDL1) and HDL2-3), of cholesterol (in LDL-HDL1) and of phospholipids (in VLDL). Furthermore, serum and VLDL cholesterol concentrations were also reduced in the SAd group. Compared with rats given 200 g casein/kg diets, those fed on low-protein diets presented lower linoleic and arachidonic acid levels, in serum phospholipids and a dramatic decrease in the polyunsaturated: saturated fatty acid value. Relative amounts of linoleic and arachidonic acids in phospholipids of VLDL and HDL2-3 were also lowered in the COd group but not in the SAd group. However, proportions of 22:5n-6 and 22:6n-3 in VLDL and HDL2-3 phospholipid fractions were enhanced in the COd and SAd groups respectively. The most affected apolipoproteins (apo) were apo B100 and apo B48 in rats fed on protein-deficient diets, apo AI and apo E in the COd group, and apo AIV in the SAd group. Compared with rats fed hydrogenated coconut oil diets, those fed salmon oil diets had enhanced LDL-HDL1 and HDL2-3 but lower VLDL total apolipoproteins (mainly due to a fall in apo B100 and apo B48). Arachidonic and eicosapentaenoic acids, which are impaired by protein deficiency, are the precursors of prostaglandins, thromboxanes and leukotrienes which are implicated in a number of regulatory processes. Our results demonstrate that protein malnutrition is associated with impaired metabolism of arachidonic and eicosapentaenoic acids. Protein malnutrition and essential fatty acid (EFA) deficiency are characterized by many common clinical features and the link between the two may be an impaired production of eicosanoids, since arachidonic and eicosapentaenoic acids are the precursors of these important metabolic regulators. Because of the apparent involvement of EFA deficiency in the aetiology of protein malnutrition, it may be prudent to include adequate amounts of EFA in diets of infants suffering from kwashiorkor.
Animals↗
Effects of protein deficiency and food restriction during gestation in rats on maternal and fetal plasma and pituitary thyrotropin levels.
The effects of protein deficiency and food restriction during pregnancy on maternal and fetal plasma and pituitary thyrotropin (TSH) levels were investigated on day 20 of gestation. The same parameters were also determined following administration of exogenous thyrotropin-releasing hormone (TRH). Maternal plasma and pituitary basal TSH concentrations were significantly elevated in protein deficiency. TRH injection to protein-deficient dams caused a marked reduction in pituitary TSH concentration, suggesting that the elevated plasma TSH seen in uninjected dams might be due to decreased metabolic clearance rather than to hypersecretion by the pituitary. Food restriction resulted in significant lowering of plasma TSH, but did not alter pituitary TSH in comparison to that of control dams. TRH administration had no effect on pituitary TSH concentration in food-restricted and control dams. Pituitaries of fetal young of protein-deprived dams were significantly smaller and contained significantly less total TSH, accompanied by a slight reduction in circulating plasma TSH. These observations are suggestive of developmental and functional retardation of the fetal pituitary. Fetal pituitary TSH was unaffected by TRH administration to control and food-restricted dams whereas, in young of protein-deprived females, total gland TSH was reduced.
Animal Nutritional Physiological Phenomena↗
Dietary protein deficiency induces osteoporosis in aged male rats.
Low dietary intake is common in elderly males with low femoral neck areal bone mineral density (BMD). To evaluate the selective influence of a low-protein diet in the pathogenesis of osteoporosis in males and to uncover early and late adaptation of bone cells to protein deficiency, 8-month-old male rats were pair-fed a control (15% casein) or isocaloric low-protein (2.5% casein) diet for 1 or 7 months. BMD, bone ultimate strength, stiffness, and absorbed energy were measured in tibia proximal metaphysis and diaphysis. After double-labeling, histomorphometric analysis was performed at the same sites. Serum osteocalcin, insulin-like growth factor I (IGF-I), and urinary deoxypyridinoline excretion were measured. In proximal tibia, isocaloric low-protein diet significantly decreases BMD (12%), cancellous bone mass (71%), and trabecular thickness (Tb.Th; 30%), resulting in a significant reduction in ultimate strength (27%). In cortical middiaphysis, a low-protein diet decreases BMD (9%) and enlarges the medullary cavity (36%), leading to cortical thinning and lower mechanical strength (20%). In cancellous bone, protein deficiency transiently depresses the bone formation rate (BFR; 60%), osteoid seam thickness (15%), and mineral apposition rate (MAR; 20%), indicating a decrease in osteoblast recruitment and activity. Cortical loss (15%) results from an imbalance between endosteal modeling drifts with impaired BFR (70%). From the first week of protein deficiency, osteocalcin and IGF-I levels drop significantly. Bone resorption activity and urinary deoxypyridinoline remain unchanged throughout the experiment. Protein deficiency in aged male rats induces cortical and trabecular thinning, and decreases bone strength, in association with a remodeling imbalance with a bone formation impairment and a decrease in IGF-I levels.
Aging↗
Factors determining the effects of chronic protein-deficiency on antibody responses to sheep red blood cells and Brucella abortus vaccine in mice.
Chronic protein-deficiency in weanling mice caused variable suppression of the humoral plaque-forming cell (PFC) responses to sheep erythrocytes. This was most prominent at high antigen doses and did not increase when mice were maintained on the diets for longer periods. Antibody responses produced by deficient mice were often short-lived and involved high levels of IgM. Total PFC counts were depressed slightly more than were circulating antibodies. Antibody responses to Brucella abortus were slightly decreased by protein-deficiency at high antigen doses but were normal or elevated at lower doses, the proportion of IgM produced was increased and the splenomegaly response to B. abortus was severely depressed. These results suggest that the depression of antibody production by protein-deficiency is not simply due to an impairment of helper T cell function, but a reduction in the availability or effectiveness of macrophage and regulatory or suppressor T cells may be important.
Animals↗
Relative and combined effects of propylthiouracil, ethanol and protein deficiency on muscle.
A hypermetabolic state with increased oxygen consumption has been described in alcoholic hepatitis, playing a major role in ethanol-induced liver damage. Based on its ability to decrease oxygen consumption, propylthiouracil (PTU) has been proposed as a therapeutic agent in this context. On the other hand, several muscle changes have been described in hypothyroidism, including both atrophy and hypertrophy of muscle fibres. The aim of this experimental study was to analyse the effects of PTU on the alcohol-induced changes in muscle fibre size and proportion, also taking into account the presence or absence of protein deficiency. The study was performed on 64 male Wistar rats divided into eight groups, fed with: (1) Lieber-DeCarli control diet: (2) an isocaloric 36% ethanol-containing diet: (3) an isocaloric 2% protein-containing diet: (4) an isocaloric 36% ethanol 2% protein-containing diet, without and with PTU, respectively. Right gastrocnemius muscle was removed 2 months later and histochemical and morphometric studies were performed. Type IIb fibre atrophy was observed both in the alcoholic and protein-deficient animals, but not in the PTU-treated animals. The combination of protein deficiency and ethanol led to a more marked type IIb atrophy, with PTU reversing this effect. Malnutrition led to a decrease in type I fibre diameter: ethanol and PTU caused an increase in its size and PTU reversed the effect of protein deficiency. Proportion of type IIb fibres decreased in the three experimental groups without PTU with respect to the control, especially in the alcoholic protein-deficient animals. PTU-treated animals, especially those fed a low-protein diet, showed a more marked reduction in type IIb fibre proportion than that presented by the groups without PTU. However, an increase in type I fibre proportion was observed in the PTU-treated animals, especially marked in those fed a low-protein diet. Thus, PTU seems to ameliorate ethanol-induced changes on type IIb muscle fibres.
Animals↗
The effect of protein-deficient isoenergetic diets on the growth of rat jejunal mucosa.
1. Newly weaned 21-d-old male rats were given isoenergetic diets containing 200, 100 and 50 g protein/kg for 7, 14, 28 or 70 d. The mid-jejunum was removed from the rats and a micrometric analysis of the mucosa was made. The following measurements were made: number of villi/mm2, villus dimensions, villus surface area, crypt depth, crypt: villus, the number of cells/crypt in metaphase arrest per h. 2. Comparison were made between animals of the same age but on different diets, and animals on the same diet but of different ages. The latter comparison gave information on the effect of protein deficiency on the pattern of maturation of each feature of the villus or crypt studied. 3. The effect of protein deficiency was not consistent at each stage of maturation. For instance villus height was decreased when compared with the controls following 28 d on a protein-deficient diet but not after 7 or 70 d. 4. The only measurement to be unaffected by protein deficiency was the number of villi per unit area. 5. In general the 50 g protein/kg diet had a more pronounced effect than the 100 g protein/kg diet. Protein deficiency delayed maturation by either slowing or inhibiting changes seen in normal maturation. 6. In rats given 50 g protein/kg diet, although the villus surface area did not increase as the rats matured there were increases in epithelial cell production rate and number of crypts per villus.
Animals↗
Effects of protein deficiency on the rate of radioactivity loss from body constituents in adult rats given 14C-amino acids.
The effect of protein deficiency on the rate of loss of radioactivity from body constituents was studied in adult rats administered 14C-Chlorella protein hydrolysate or 14C-lysine. Rats were kept on a protein-free diet for 3 weeks and then injected with labelled amino acids and fed on a protein-free diet for 3 more days to allow 14C deposition in tissues. Then they were given experimental diets (protein-free diet, 1% and 10% wheat gluten diets pair-fed with the protein-free diet, and 10% wheat gluten diet ad libitum) for 7 days and sacrificed. The rates of loss of radioactivity from tissue proteins became low in general with the extent of protein deficiency. This increased capacity of tissues to retain 14C-amino acids may result from higher efficiency of protein utilization in protein deficiency. The reutilization of free amino acids and the rate of catabolism of tissue proteins are discussed on the basis of the results. The half-life of muscle protein was too long to observe the effects of experimental diets given for 7 days on the rate of loss of radioactivity.
Amino Acids↗
Protein deficiency in premature infants receiving parenteral nutrition.
A classical finding of protein deficiency is hair depigmentation, or the flag sign. To determine the clinical conditions that predispose ill premature infants to the development of protein deficiency, we compared the clinical courses and nutritional histories of premature infants receiving parenteral nutrition who developed the flag sign (group F), with those of a matched control group (Group C). Occurrences of necrotizing enterocolitis (NEC) and consequent surgery were significantly higher in group F than in group C (p less than 0.002 and p less than 0.005, respectively). No differences were found in the mean (+/- SD) administration of amino acids (group F, 2.5 +/- 0.2 g X kg X day vs group C, 2.4 +/- 0.4) and total energy (83.4 +/- 13.4 kcal X kg X day vs 83.6 +/- 11.1, respectively). Mean serum albumin levels (2.6 +/- 0.4 g/dL vs 2.6 +/- 0.5, respectively) also were similar. Because infants in both groups received recommended amounts of protein, results suggest that infants who have NEC, and surgery as a consequence of NEC, require more protein than is presently recommended.
Enteral Nutrition↗
[Effect of alimentary protein deficiency in the early postnatal period on the function of the immunocompetent system in rats].
The influence of protein deficiency in the early postnatal period on the functional and morphological characteristics of the immunocompetent system was studied in 76 test and 60 control rats, 4 and 12 months after the experiment commencement. It was shown that protein deficiency in the early postnatal period induced shifts in the cellular parameters of the immunologic responsiveness, mainly, producing no significant changes in the nonspecific factors of body defence. The impairing effect of protein deficiency was more manifest at the early steps of the body development.
Animals↗
The effect of severe protein deficiency on serum zinc concentration of mice fed a requirement level or a very high level of dietary zinc.
The objective of the present study was to determine the effect of severe dietary protein deficiency on serum zinc concentration in weanling animals fed either a requirement level or a very high level of dietary zinc. Weanling (21-day-old) male and female CBA/J mice were randomly assigned to be fed one of four diets containing either 1.7% or approximately 18.5% protein and either 7 micrograms (predetermined requirement level) or about 200 micrograms zinc per gram of formulation. Serum zinc levels were measured after a 14-day feeding period. Dietary zinc content, over the range tested, did not influence the serum zinc level of protein deficient mice, and these animals exhibited serum zinc concentrations which were much lower than the levels found in adequately nourished mice fed the requirement level of zinc (7 micrograms/g diet). These results indicate that dietary zinc supplementation is unable to restore to normal the zinc status of severely protein-deficient animals. This may be an important factor to consider when studying the effect of protein deficiency on zinc-sensitive physiological processes.
Animals↗
Effect of dietary protein deficiency on rat hepatic drug-metabolizing enzyme system.
We have examined the effect of dietary protein deficiency on rat hepatic drug-metabolizing enzyme system for a period of two months. Cytochrome P-450 and b5 contents in liver microsomes, which were plotted on semilogarithmic paper as a function of the time of deficiency, showed biphasical reductions during protein deficiency: rapid decreases in the first 3 weeks were followed by more gradual decreases. However, the three enzymatic activities examined, i.e. aminopyrine demethylase, aniline hydroxylase and p-nitroanisole demethylase, were not reduced at a uniform rate. In the earlier phase, activities of the former two enzymes were reduced more rapidly than that of the last phase. This biphasical and non-uniform reduction of enzymatic activities suggests the existence of two or more cytochrome P-450 subspecies in non-depleted male rats. Intraperitoneal administration of well-known environmental pollutants, polychlorinated dibenzofurans and biphenyls (100 micrograms and 100 mg/kg, respectively) to the depleted rats resulted in a marked induction of drug-metabolizing enzymes. However, as the deficiency became more severe (2 months), the induction declined to a considerable degree, especially in the case of polychlorinated biphenyl administration.
Aminopyrine N-Demethylase↗
[Effect of dietary protein deficiency in female rats on the function of the immunocompetent system of their progeny].
The influence of alimentary protein deficiency, during early ontogenesis, on the morphofunctional characteristics of the immunocompetent system was studied in 115 experimental and 60 control female rats, 4 and 12 months after the commencement of the experiment. It was shown that protein deficiency in the period of prenatal ontogenesis induced significant changes in the humoral and cellular values, characterizing immunologic responsiveness and nonspecific resistance of the body, and leads to alteration of the morphological structure of the lymphoid organs. Such changes were also observed in the rats of the second generation, which received full-value food, thus evidencing grave and stable immunologic disorders as the result of protein deficiency during prenatal ontogenesis.
Animals↗
The effect of medroxyprogesterone acetate on the hepatic drug-metabolizing enzymes in normal and protein-deficient female rats.
Effect of depot medroxyprogesterone acetate on the hepatic drug-metabolizing enzymes was studied in female protein-deficient and normal pair-fed rats. Treatment with this drug did not cause any change in organ weight, microsomal protein, and soluble protein yield per gram of tissue in both groups. MPA administration resulted in significant increases in the content of cytochrome P-450 and b5, and activities of benzo[a]pyrene hydroxylase, UDP-glucuronosyltransferase, and NADPH-Cyt c reductase in both pair-fed control and protein-deficient rats. However, the content of glutathione and activity of glutathione-S-transferase were not affected appreciably. The present study suggests that MPA treatment induces drug-metabolizing enzymes in liver to almost the same extent in both protein-deficient and normal pair-fed rats.
Animals↗
Glucose-induced insulin secretion is impaired and insulin-induced phosphorylation of the insulin receptor and insulin receptor substrate-1 are increased in protein-deficient rats.
Malnutrition is related to diabetes in tropical countries. In experimental animals, protein deficiency may affect insulin secretion. However, the effect of malnutrition on insulin receptor phosphorylation and further intracellular signaling events is not known. Therefore, we decided to evaluate the rate of insulin secretion and the early molecular steps of insulin action in insulin-sensitive tissues of an animal model of protein deficiency. Pancreatic islets isolated from rats fed a standard (17%) or a low (6%) protein diet were studied for their secretory response to increasing concentrations of glucose in the culture medium. Basal as well as maximal rates of insulin secretion were significantly lower in the islets isolated from rats fed a low protein diet. Moreover, the dose-response curve to glucose was significantly shifted to the right in the islets from malnourished rats compared with islets from control rats. During an oral glucose tolerance test, there were significantly lower circulating concentrations of insulin in the serum of rats fed a low protein diet in spite of no difference in serum glucose concentration between the groups, suggesting an increased peripheral insulin sensitivity. Immunoblotting and immunoprecipitation were used to study the phosphorylation of the insulin receptor and the insulin receptor substrate-1 as well as the insulin receptor substrate-1-p85 subunit of phosphatidylinositol 3-kinase association in response to insulin. Values were greater in hind-limb muscle from rats fed a low protein diet compared with controls. No differences were detected in the total amount of protein corresponding to the insulin receptor or insulin receptor substrate-1 between muscle from rats fed the two diets. Therefore, we conclude that a decreased glucose-induced insulin secretion in pancreatic islets from protein-malnourished rats is responsible, at least in part, for an increased phosphorylation of the insulin receptor, insulin receptor substrate-1 and its association with phosphatidylinositol 3-kinase. These might represent some of the factors influencing the equilibrium in glucose concentrations observed in animal models of malnutrition and undernourished subjects.
Animals↗
Effects of protein deficiency and food restriction on lung ascorbic acid and glutathione in rats exposed to ozone.
Weanling (52 +/- 4 g) or adult (259 +/- 16 g) male Sprague-Dawley rats were fed ad libitum casein-based diets containing 4 or 16% protein. A third group (food restricted) was fed daily the 16% protein diet, but at the food intake level of the 4% protein group. After 3 wk (weanling) or 5 wk (adults), half of the rats in each group were continuously exposed to 0.64 ppm ozone for 7 d. Ascorbic acid and reduced glutathione levels were then measured. In the heart and liver from weanling rats, ascorbic acid concentrations were lower in the protein-deficient group than in either control group. In the liver from weanling rats glutathione concentrations were also reduced in response to protein deficiency. Exposure to ozone produced no additional response. For adult rats the response for liver glutathione was similar to that of the weanlings. The liver ascorbate concentration, however, was consistently lower in adult rats compared to weanlings exposed to ozone. In lungs from adult rats, the ascorbic acid concentration was lower in the protein-deficient group than in either control group. On a whole-organ basis, both ascorbic acid and glutathione were usually higher in lungs from rats exposed to ozone than from those exposed to air. Interestingly, protein deficiency did not appear to compromise the lung's ability to maintain, in relative terms, the ascorbic acid or glutathione concentration in response to ozone.
Aging↗