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PubMed2000

Effect of feeding protein deficient diet on phospholipid turnover and protein kinase C mediated protein phosphorylation in rat brain.

Feeding of protein deficient diet is known to alter the transmembrane signalling in brain of rat by reducing total protein kinase C (PKC) activity. Phospholipid metabolism regulates the activation of PKC through generation of second messengers and the extent of PKC activation accordingly influences the magnitude of phosphorylation of its endogenous substrate proteins. Thus it was speculated that ingestion of protein deficient diet may modify the turnover rate of membrane phospholipids and magnitude of phosphorylation of endogenous substrate proteins of PKC. The experiments were conducted on rats fed on three different types of laboratory prepared diets viz. casein (20% casein), deficient (4% protein, rice flour as source of protein) and supplemented (deficient diet supplemented with L-lysine and DL-threonine) for 28 days. The metabolism of phosphoinositides (PIs) and phosphatidyl choline (PC) was studied by equilibrium labeling with [3H] myo inositol and [14C methyl] choline chloride respectively. The phosphorylation of endogenous substrate proteins of PKC was studied by using 32P-gamma-ATP followed by SDS-PAGE and autoradiography. The results suggest that in deficient group, there is an increased incorporation of [3H] myo inositol in PIs and inositol phosphate pool in comparison to the casein group. The phosphatidyl inositol (PI) turnover reduced, although there was a marginal increase in the phosphatidyl inositol monophosphate (PIP) and phosphatidyl inositol bis phosphate (PIP2). Supplementation of diet showed a reversal of the pattern towards control to a considerable extent. In the deficient group, PC metabolism showed an increased incorporation of [14C methyl] choline in choline phospholipids but decreased incorporation in phosphoryl choline in comparison with the casein group. The increase in total PC contents was significant but marginal in residue contents. The turnover rate of PC increased only marginally and that of residue declined. Supplementation of diet reduced the total contents of PC and residue, but the turnover rate of PC and residue remained still higher. Phosphorylation of endogenous proteins showed four different proteins of 78, 46, 33 and 16 kDa to be the substrates of PKC in casein group. In deficient group, phosphorylation of these proteins increased markedly while supplementation of diet had a reversing effect rendering the values to be intermediate between casein and the supplemented group. The changes in phospholipid metabolism and in phosphorylation of endogenous substrate proteins of PKC suggest that dietary protein deficiency causes alterations in transmembrane signalling mechanism in rat brain. These effects are partially reversed by improving the quality of proteins in the diet.

Animals↗
PubMed1978

Hair root diameter measurement as an indicator of protein deficiency in nonhospitalized alcoholics.

Protein status of alcoholics admitted to a detoxification center was investigated with a view to adapting a hair root test for use in screening for protein deficiency. Hair root volume and hair root diameter had previously been shown to correlate well with hair root protein and to be sensitive indicators of protein deficiency. Hair root volumes in this study correlated well with mean maximum hair root diameters (n = 35, r = 0.9), which were simpler to measure, so diameter measurements were used. Mean maximum hair root diameters (range 0.02 to 0.19 mm) correlated with plasma RNase concentrations (range 6000 to 14,000 units/ml; n = 17, r = -0.7). Mean hair diameters of 84 alcoholics averaged 0.0864 +/- 0.0366 mm; those of 25 nonalcoholics were significantly greater: 0.100 +/- 0.0254 mm (P less than 0.05). Frequency of occurrence of hair root diameters of 0.06 mm or less was significantly higher in 71 alcoholics (29.5%) than in 23 nonalcoholics (8.6%) matched by age. Mean hair root diameters of 0.06 mm or less therefore can be used to signify protein deficiency where more expensive or technically demanding tests are not feasible. Protein deficiency occurs extensively in non hospitalized alcoholics. This method enables staff to single out those clients most likely to be in need of nutritional counseling and therapy.

Alcoholism↗
PubMed1996

Hypoparathyroidism in mitochondrial trifunctional protein deficiency.

Mitochondrial trifunctional protein deficiency, a recently identified disorder of fatty-acid oxidation, may show characteristic features such as peripheral neuropathy, pigmentary retinopathy, and acute fatty liver degeneration in pregnant women with an affected fetus. We describe a patient with trifunctional protein deficiency whose clinical picture consisted of severe calcium and phosphate abnormalities caused by hypoparathyroidism.

Female↗
PubMed1983

Changes of alveolar macrophages in protein-deficient rats.

Protein malnutrition was achieved by feeding female F344 rats a 5% casein diet for 7 weeks. At appropriate times, animals were killed and their alveolar macrophages (AM) were obtained by broncho-pulmonary lavage of the lung. Functional changes of AM were determined by measuring phagocytosis of latex beads, yeast cells or opsonized sheep red blood cells (SRBC) and the ability to respond to a macrophage-activating factor (MAF) such as lymphokines. After 3 weeks on a low casein diet, the number of AM was much lower than in rats on control diet, but the abilities of the AM to phagocytose latex and yeast cells were the same as those of controls. Phagocytosis of opsonized SRBC was higher than in control rats but could not be enhanced by in vitro treatment with MAF. The most striking ultrastructural feature of these AM was the abundance of finger-like microvilli on the cell surface before phagocytosis; after ingestion of SRBC into phagocytic vacuoles there were only a few short microvilli on the surface. These data suggest that dietary protein malnutrition affects the number and phagocytic functions of AM responsible for host defense in the lung.

Animals↗
PubMed1980

Anti-inflammatory and ulcerogenic effects and pharmacokinetics of dexamethasone in protein-deficient rats.

Influence of dietary protein deficiency on the anti-inflammatory and ulcerogenic effects of dexamethasone (oral) and on its pharmacokinetics (i.v. and oral) was studied in male Sprague-Dawley rats fed ad libitum a 21% (normal) or a 5% (low) protein diet for 4 weeks. A low protein diet was associated with a decrease in the acute (inhibition of carrageenan-induced paw edema) and chronic (suppression of carragennan-induced granulomas) anti-inflammatory effects of dexamethasone. Also, the ulcerogenic effect of dexamethasone was greater in pyloric ligated control rats than in protein-deficient rats. Dietary protein deficiency was not associated with any significant change in plasma half-life, apparent volume of distribution, clearance, bioavailability and serum protein binding of dexamethasone. However, the concentration of dexamethasone in the inflamed as well as uninflamed subplantar soft tissues and granulomas of protein-deficient rats was greater than in the tissues of control rats. It is concluded that the observed decrease in the anti-inflammatory effects of dexamethasone in protein-deficient rats cannot be attributed to any changes in its pharmacokinetics; it may be due to alterations in cell-steroid interactions.

Animals↗
PubMed2003

IgE responses in mice fed moderate protein deficient and high protein diets.

While severe protein energy malnutrition (PEM) has been known to depress several immune functions, allergies are suppressed by decreasing IgE and impairing vascular permeability and mast cell functions. To address the effect of moderate protein malnutrition without growth arrest and protein hypernutrition on type I allergy, we examined the effect of various levels of protein nutrition on allergy at humoral immunity and the regulation of Th cell function levels. Mice fed 100 g/kg (moderate protein malnutrition; MPM), 200 g/kg (normal protein nutrition; PN) and 400 g/kg (protein hypernutrition; PH) protein diets were intraperitoneally sensitized to ovalbumin (OVA) in aluminum hydroxide. Higher elevations of OVA-specific IgE and total IgE in the serum were observed in the PH group as compared to the PN group. However, OVA-specific IgE in the MPM group was not significantly different from that in the PN group, although the former appeared higher than the latter. While CD3, CD4, CD8 and B220 expressions in the splenic lymphocytes were decreased in the MPM group, B220 expressions were increased in the PH group. Splenic lymphocyte proliferative responses to OVA were augmented in the PH group and depressed in the MPM group. IFN-gamma production from splenic lymphocytes was significantly decreased; however, IL-4 production was not affected significantly in the MPM group, and increased in the PH group. These findings suggest that immune functions to specific antigens in the MPM state are depressed at the cytokine level but not in terms of IgE responses. They also suggest that immune functions become Th2-predominant in the PH state, resulting in an increased risk of type I allergy.

Animals↗
PubMedDate not supplied

[Morphologic changes in the kidneys in experimental cholino-protein deficiency].

Experiments were made on male Wistar rats fed the cirrhosogenous diet deficient in protein and choline (group I), protein deficient diet with choline addition (group II), and the animal house diet (group III). Based on histological and electron microscopy studies of rat kidneys and liver made 10 months after the onset of experiments, the group I animals developed glomerulopathy with tubulointerstitial component in the presence of liver fibrosis and cirrhosis. The animals belonging to group II with fatty hepatosis had a similar liver lesion, which was less marked, however. The liver lesion in rats with liver cirrhosis was marked by depositions in the mesangial matrix and in the basal membrane of glomerular capillaries. The severity of the pathological process in the kidneys directly correlated with the morphofunctional status of the liver. Alterations in the liver of the group III animals (with the histological liver structure being normal) were regarded as age-associated.

Animals↗
PubMed1992

Effect of aseptic abscesses in protein-deficient rats on the relationship between interleukin-6 and the acute-phase protein, alpha 2-macroglobulin.

1. Rats established on a normal (20% protein) diet or a protein-deficient (3% protein) diet were given either a subcutaneous injection of turpentine (5 ml/kg), which induces formation of aseptic abscesses, or saline. Plasma samples were obtained at timed intervals (0-14 days) after the injection for determination of albumin, total protein, alpha 2-macroglobulin (a major acute-phase protein in the rat) and interleukin-6 concentrations. The magnitude and pattern of the acute-phase protein response was then compared with the local inflammatory reaction, assessed histologically, and with changes in the circulating concentration of interleukin-6, which is an important mediator of the acute-phase protein response. 2. After turpentine injection there was an early fall in the plasma albumin and total protein concentrations in both normal and protein-deficient rats. After 12 h the total protein concentration increased in both groups of animals reaching a peak at about 48 h, whereas the plasma albumin concentration continued to fall reaching a minimum at 48 h. The main alpha 2-macroglobulin response was delayed and attenuated in the protein-deficient rats (onset 9 versus 24 h, peak concentration 8.95 +/- 0.5 versus 5.33 +/- 0.75 g/l, P < 0.01, and area under the concentration-time curve 18.43 +/- 2.13 versus 7.96 +/- 1.48 g/l-1 days, P < 0.01, in the normal group and protein-deficient group, respectively). 3. The circulating interleukin-6 concentration showed a transient early rise at 1 h, and was followed by a larger more sustained peak at 6-48 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Abscess↗
PubMed1983

Protein synthesis in liver, skeletal muscle, and brown adipose tissue of rats fed a protein-deficient diet.

Feeding protein-deficient diets to rats is known to stimulate diet-induced thermogenesis and activate brown adipose tissue (BAT). The fact that BAT protein content, unlike that of other tissues, is unnaffected by protein deficiency prompted us to measure tissue protein synthesis in vivo in animals maintained on normal- (18.8%) and low- (7.6%) protein (LP) diets. Protein synthesis was depressed in the liver of the LP rats due to a fall in RNA activity, with no change in RNA content, and synthesis was also reduced in skeletal muscle from the LP group, but this was due to decreased RNA content with no change in RNA activity. Conversely, protein synthesis, RNA, DNA, and protein content of interscapular BAT were all unaltered in protein-restricted animals. These data indicate that, unlike liver, skeletal muscle, and whole carcass, BAT protein synthesis is not reduced in protein-restricted rats, and this may be related to activation of thermogenesis in the tissue.

Adipose Tissue, Brown↗
PubMed2000

[Histological structure of adult mouse brain in protein-deficient nutrition].

The effect of protein deficient nutrition on histostructure of different regions of brain of mature animals was studied in the experimental model of protein and energy deficiency. Protein deficient nutrition was shown to exert negative influence on structural and functional state of brain neurons which is manifested through increase of dystrophic changes in neurons of all brain regions, accumulation of lipofuscine in neurons and complex of structural changes in synaptic contacts.

Animal Nutritional Physiological Phenomena↗
PubMed2005

Phospholipid metabolism and protein kinase C mediated protein phosphorylation in dietary protein deficiency in rat lung.

Nutritional deprivation of proteins decreases the protein kinase C (PKC) activity in rat lung. The activity of (PKC) is influenced by lipid metabolism. Changes in PKC activity may influence phosphorylation of its substrate proteins in the tissues. Therefore, alterations in phospholipid metabolism and PKC mediated protein phosphorylation in dietary protein deficiency in rat lung were envisaged. The study was conducted on rats fed on three different types of diet viz., casein (20% protein), deficient (4% protein, rice flour as source of protein) and supplemented (deficient diet supplemented with L-lysine and DL-threoning). Feeding of protein deficient diet caused reduction in incorporation of [3H] myo-inositol in the total phosphoinositides in lungs and an increase in total inositol phosphate pool. There was a significant reduction in the contents and turnover rate of phosphatidyl inositol and phosphatidyl inositol monophosphate. Supplementation of diet with L-lysine and DL-threonine had a reversing effect on total pool of phosphoinositides and, the metabolism of phosphatidyl inositol bisphosphate and phosphatidyl inositol. In phosphatidyl choline metabolism, the dietary protein deficiency led to a decrease in incorporation of [14C-methyl] choline-chloride in total phospholipids. In contrast, its incorporation increased in phosphatidyl choline pool. The contents of phosphatidyl choline and residue, incorporation of [14C-methyl] choline-chloride in them and their turnover rate also increased. Supplementation of diet had a reversal effect on most of these parameters. Phosphorylation of proteins of 84, 47, 35 and 16 kDa was identified to be mediated by PKC. In dietary protein deficiency, phosphorylation of all these proteins, except that of 47 kDa, increased. Supplementation of diet reversed the pattern except that of 84 kDa. The findings suggest that changes in phospholipid metabolism in dietary protein deficiency may effect the activity of PKC thereby influencing the phosphorylation of its substrate proteins and hence associated functions that may lead to pathophysiology of lung.

Animals↗
PubMed1975

1. The effect of dietary fat on the host-parasite relations in cotton rat filariasis. 2. Host-parasite relations in the progeny of cotton rats fed protein deficient diets and infected with filariasis-a preliminary report. 3. Immunoglobulin levels in the early stages of infection with filariasis in cotton rats with and without dietary protein deficiency. 4. Action of aliphatic alcohols on aquatic stages of mosquitoes.

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Alcohols↗
PubMed1992

Meningococcaemia in an adult with hereditary C4b-binding protein deficiency: study of the variations of the protein S system.

Serial studies of the plasma protein C-protein S system were performed during the clinical course of a pregnant woman with meningococcaemia who recovered under therapy. The patient had limited purpura fulminans skin lesions and hereditary C4b-binding protein deficiency was suspected. This diagnosis was confirmed in the patient 1 year after delivery and also by family studies. During the meningococcaemia, an initial mild and transient acquired protein C deficiency was seen but no protein S deficiency was observed despite consumption of the latter protein. As C4b-binding protein partial deficiency is associated with high free protein S and protein S activity, this may have protected against acquired protein S deficiency during meningococcaemia.

Adult↗
PubMed1988

Alterations in synaptic membrane molecular order associated with alcoholization and protein deficiency in rats.

The effects of chronic alcoholization and protein deficiency on synaptic membrane characteristics were studied in rats fed the following four liquid diets for 4 weeks: a protein-deficient diet containing alcohol, a protein-deficient diet containing no alcohol, a non-protein-deficient diet containing alcohol and a non-protein-deficient diet containing no alcohol. A fluorescent probe, diphenylhexatriene (DPH), was used to estimate the fluidity of synaptic membranes and their sensitivity to the fluidizing effect of ethanol added in vitro, in concentrations ranging from 50 mM to 800 mM. Prior to in vitro addition of ethanol, the difference between the fluidity of synaptic membranes of alcoholized and non-alcoholized animals was significant for the two groups of protein-deficient animals but not for the two groups of non-protein-deficient animals. After in vitro addition of ethanol, the differences between the fluidity of synaptic membranes of the alcoholized and non-alcoholized animals were larger and more frequently significant for the protein-deficient animals than for the non-protein-deficient animals. In view of previous observations that rats fed a protein-deficient diet experience more severe withdrawal symptoms following alcoholization than rats fed a nutritionally adequate diet, the results of the present experiment lend additional support to the hypothesis that tolerance and dependence may be mediated by alterations in biomembrane characteristics.

Alcoholism↗
PubMed1985

Mycobacterium bovis BCG vaccine fails to protect protein-deficient guinea pigs against respiratory challenge with virulent Mycobacterium tuberculosis.

Specific-pathogen-free Hartley guinea pigs were maintained on isocaloric-purified diets either adequate (30%) or moderately deficient (10%) in protein. Half of each diet group was vaccinated with viable Mycobacterium bovis BCG. Six weeks later, all animals were challenged by the respiratory route with virulent Mycobacterium tuberculosis H37Rv. At intervals of 1, 2, and 3 weeks postchallenge, guinea pigs from each diet and vaccination group were skin tested with tuberculin and sacrificed. Protein deficiency resulted in loss of tuberculin hypersensitivity. Vaccination with M. bovis BCG protected control animals, as determined by significant reductions in the number of M. tuberculosis H37Rv organisms recovered from lungs, spleen, and bronchotracheal lymph nodes 2 and 3 weeks postchallenge. Based upon the same criteria, the degree of protection afforded protein-deficient animals by M. bovis BCG vaccine ranged from partial (spleen and lymph nodes) to none at all (lungs). Approximately the same numbers of tubercle bacilli were recovered from nonvaccinated guinea pigs in both diet groups. Protein deficiency appears to impair M. bovis BCG-induced immunity while not affecting primary pulmonary infection with virulent M. tuberculosis.

Animals↗
PubMed1992

The magnitude of the acute phase protein response is attenuated by protein deficiency in rats.

We assessed the growth rate and changes in plasma albumin, total protein and alpha 2-macroglobulin concentrations (a major acute phase protein in rats) before and after a subcutaneous injection of turpentine (0.5 mg/kg body wt) in groups of rats receiving one of a series of protein-deficient diets (protein concentrations of 0.5, 1.5, 3.0, 4.5 or 6.0 g/100 g) or a diet containing an adequate level of protein (20 g/100 g) for maximal growth. Increasing protein deficiency in the different groups of animals reduced the basal albumin and total protein concentrations and attenuated the total protein and alpha 2-macroglobulin responses to turpentine. Increasing protein deficiency delayed the time taken for alpha 2-macroglobulin to reach peak concentrations post-injection and its return to basal concentrations. The turpentine-induced hypoalbuminemia was similar in all groups of animals (approximately 10 g/L depression) but restoration to values that were present before turpentine injection was increasingly delayed with increasing protein deficiency. The magnitude of the acute phase response (peak alpha 2-macroglobulin concentration) was found to be directly related to growth rate (r = 0.70, P less than 0.001). We concluded that protein deficiency can alter the pattern and magnitude of the acute phase responses in circulating protein concentrations to an extent that is dependent on the severity of protein deficiency.

Acute-Phase Proteins↗