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PubMed1988

Combined effects of protein deficiency and chronic ethanol consumption on rat pancreas.

This study was performed in order to delineate the combined effects of protein deficiency and chronic ethanol ingestion on the rat pancreas. Rats fed ethanol in combination with protein-deficient diets developed marked steatosis, whereas alcohol ingestion with nutritionally adequate diets and protein deficiency alone each were associated with a more moderate degree of pancreatic lipid accumulation. On biochemical analysis, it was found that protein deficiency decreased pancreatic phospholipid content. Furthermore, both protein deficiency and chronic ethanol consumption increased pancreatic cholesteryl ester content, and their effects were additive. Functional changes were studied using isolated pancreative acini. Protein deficiency depressed the tissue content of lipase and the ability of pancreatic acini to secrete lipase. Chronic ethanol feeding increased lipase levels in the acini and also their secretory capacity. Thus, to the extent that enzyme accumulation in the pancreas plays a role in the pathogenesis of alcoholic pancreatitis, these results may explain the higher incidence of pancreatitis in well-nourished alcoholics that has been documented in dietary surveys.

Alcoholism↗
PubMed1988

Effect of dietary protein deficiency and L-2-oxothiazolidine-4-carboxylate on the diurnal rhythm of hepatic glutathione in the rat.

Maximizing hepatic glutathione (GSH) concentration may provide greater protection against toxic compounds. A dietary supplement of L-2-oxothiazolidine-4-carboxylate (OTC), a stable derivative of cysteine, increased hepatic GSH in rats fed for 2 wk a diet deficient in protein (7.5%) but not in rats fed a diet adequate in protein (15%). Experiment 2 determined whether a dietary supplement of OTC could maintain the maximum GSH concentration over 24 h. Rats acclimatized for 5 d to a 7.5% protein diet and then fed a 7.5% protein diet supplemented with either 2.5 mmol OTC or cysteine-HCl (CYS)/100 g diet had a more rapid increase in hepatic GSH (4 and 8 h after beginning of feeding, P less than 0.05) than did rats fed an unsupplemented 7.5% protein diet. This response was not due simply to the greater supply of cysteine for GSH synthesis because supplementing the 15% protein diet with OTC or CYS had no effect on the hepatic GSH of rats acclimatized to a 15% protein diet. In experiment 3, rats acclimatized to the 7.5% protein diet had a more rapid rate of increase in hepatic GSH concentration in response to feeding than did rats acclimatized to a 15% protein diet, regardless of which diet they were fed during the 24-h period. It was concluded that in addition to cysteine availability, previous dietary protein status plays a key role in the regulation of the feeding-induced diurnal rhythm of hepatic GSH concentration in rats.

Analysis of Variance↗
PubMed1990

[Lupus and protein deficiencies of the classical complement pathway].

Deficiencies in proteins of the classic complement pathway are particularly frequent in patients with autoimmune diseases, notably systemic lupus erythematosus (SLE). The C4 component is a polymorphous glucoprotein coded by two closely linked genes, C4A and C4B, located within the HLA complex. C4, and in particular the C4A isotype plays a major role in maintaining immune complexes in solution. Fifty percent of patients with SLE are homozygous or heterozygous to the silent allele C4 AQO. Hereditary CE deficiency is often complicated by lupus-related diseases which may be associated with repeated infections. The biological particularity of SLE associated with complement protein deficiencies is the frequency of anti-SSA (Ro) antibodies.

Complement C2↗
PubMed1991

The effects of moderate protein deficiency on beta-adrenoceptor density in rat parotid and submandibular salivary glands.

The effects of moderate protein deficiency on the number and dissociation constant of beta-adrenergic receptors were investigated. One group of adult rats was fed a protein-deficient diet (5% protein), a control group was given a similar diet with 20% protein, and a third group was fed a standard pellet diet. After 21 days, the salivary glands were removed and the cell membranes were isolated. The binding of [3H]-dihydroalprenolol to cell membranes was measured, with or without the presence of timolol, a potent beta-adrenoceptor antagonist. The rats fed the 5% protein diet had fewer beta-adrenoceptors in both the parotid and the submandibular glands than did the 20% protein group, which did not differ from the standard pellet group. The dissociation constant was not affected by protein deficiency. The rats fed the 5% protein diet had a significantly lower gain in body weight, less heavy submandibular glands but heavier parotids than the rats fed 20% protein. Thus the cellular conditions for protein secretion in the salivary glands are impaired during moderate protein deficiency in the adult rat.

Animals↗
PubMed1979

Nippostrongylus brasiliensis infection in the rat: effect of iron and protein deficiency on the anthelmintic efficacy of mebendazole, pyrantel, piperazine, and levamisole.

The benzimidazole anthelmintics mebendazole and fenbendazole have been shown to be much less effective against Nippostrongylus brasiliensis infections in the rat on a combined iron and protein deficient diet. In the present experiments it was shown that the anthelmintic efficacy of mebendazole was significantly impaired in the rat on either an iron deficient or a protein deficient diet. Furthermore, iron and protein deficiency reduced the efficacy of the anthelmintics pyrantel and piperazine but not levamisole. The finding that nutritional deficiencies reduce anthelmintic efficacy may well be relevant to worm eradication programmes in iron deficient and protein calorie malnourished populations.

Anemia, Hypochromic↗
PubMed2005

Time dependent study to evaluate the efficacy of zinc on hepatic marker enzymes and elemental profile in serum and liver of protein deficient rats.

This study was designed to determine the time dependent protective effects of zinc sulfate on the serum and liver marker enzymes along with elemental profile in protein deficient Sprague Dawley (S.D.) female rats. Zinc sulfate in the dose of 227 mg/l in drinking water was administered to normal control as well as protein deficient rats for a total duration of 8 weeks. The effects of different treatments were studied on enzymes like alkaline phosphatase (ALP), aspartate aminotransferases (AST) and alanine aminotransferases (ALT) in rat serum at different time intervals of 1, 2, 4 and 8 weeks and in the rat liver at the end of study. The status of different essential elements in liver was also studied. The serum ALP activity got significantly depressed when estimated at the intervals of 4 and 8 weeks. Activity of serum ALT was significantly increased after 4 weeks interval in protein deficient rats and the increasing trend continued upto 8 weeks of protein deficiency. On the other hand, activity of AST showed a significant increase just after 2 weeks and activity continued to be increased up to 8 weeks. Moreover activities of all the hepato marker enzymes showed a significant increase in liver of protein deficient rats. Interestingly, supplementation of Zn to protein deficient rats helped in regulating the altered activities of ALP, AST and ALT both in serum and liver. However, zinc treatment alone to normal rats did not indicate any significant change in the activities of all the enzymes in liver as well serum except at the interval of 2 weeks where a marginal increase in the activity of AST was seen. It has also been observed that concentrations of zinc, copper, iron and selenium were found to be decreased significantly in protein deficient animals. However, the levels of these elements came back to within normal limits when zinc was administered to protein deficient rats.

Alanine Transaminase↗
PubMedDate not supplied

Protective effects of zinc on oxidative stress enzymes in liver of protein deficient rats.

This study was designed to evaluate the protective effects of zinc on the liver activities of antioxidant enzymes in protein-deficient rats. Zinc sulfate at a dose level of 227 mg/l in drinking water was administrated to Sprague Dawley normal control as well as to protein-deficient rats for a total duration of eight weeks. The effects of zinc treatment and protein deficiency alone as well as combined were studied on rat liver antioxidant enzymes which included catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), and glutathione S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic lipid peroxidation and in catalase, Gpx, GR and GST activity. A significant inhibition in the levels of SOD activity and reduced glutathione (GSH) was observed following protein deficiency in normal rats. Zn treatment to protein deficient animals lowered lipid peroxidation and catalase, Gpx and GST activities, and also resulted in a significant elevation in the levels of GSH and SOD activity. The concentration of zinc decreased significantly in protein deficient animals but returned to normal levels when zinc was administered.

Animals↗
PubMed2003

Protein deficiency and muscle damage in carbon tetrachloride induced liver cirrhosis.

Protein undernutrition, alterations of hormones such as IGF-1, testosterone and cortisol, and increased lipid peroxidation-which may be related with deranged metabolism of some elements such as iron (Fe), zinc (Zn), manganese (Mn), selenium (Se) or copper (Cu)-may contribute to muscle damage in non alcoholic cirrhosis. Here, we analyse the effect of protein deficiency on muscle Cu, Fe, Zn, Mn and Se in carbon-tetrachloride (CCl(4)) induced liver cirrhosis. We also study the association between protein undernutrition and these trace elements with the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD) and lipid peroxidation products, and how all these are related with muscle morphological changes in 40 male adult Sprague-Dawley rats. Liver cirrhosis was induced by intraperitoneal injection of CCl(4) to 10 rats fed a 2% protein diet, and to another 10 fed a 18% protein control diet. Two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. After sacrifice (6 weeks later), we found type IIa fibre atrophy in the cirrhotic animals, especially in the low-protein fed ones and this was due to protein deficiency. Muscle Fe increased in low protein fed cirrhotic rats. No relationship was found between muscle changes and any of the hormones, enzymes and trace elements analysed, or with liver fibrosis. These results suggest that muscle atrophy observed in CCl(4)-induced cirrhosis is related with protein deficiency, but not with cirrhosis itself.

Adenosine Triphosphatases↗
PubMed1994

Enumeration of macrophage carbohydrates in protein-deficient rats: relation to cell surface properties.

In order to study the effect of protein malnutrition on macrophage glycoproteins the carbohydrate composition of peritoneal macrophages from protein-deficient rats has been studied by paper chromatography and HPLC. The results show that the carbohydrate content of resident cells recovered from protein-deficient group was significantly greater than control and decreased on prolonged incubation. In the protein-deficient samples there was a significant decrease in the content of galactose, fucose and galactosamine known to be binding to specific ligands and increase in glucose and mannosamine. In both control and deficient groups, thioglycollate (TG) elicitation resulted in higher total sialic acid content. Prolonged incubation (18 hr) caused an elevation of sialic acid levels in the resident cells, whereas a drastic reduction was observed in the TG elicited cells. In the protein-fed (20%) group, the cell surface sialic acid which contributes to the negative charge of the cells, reduced significantly on culturing the TG cells but not the resident cells. In the protein-deficient group, this effect was seen in the resident cells also; in the TG cells the cell surface sialic acid was significantly low at the isolation stage suggesting that these cells had become comparatively more positively charged in vivo itself. This observed reduction could be correlated to the enhanced sialidase levels in these cells. These protein deficiency related changes in the carbohydrate composition of macrophages could lead to modification of their receptor activity and charge related functions.

Animals↗
PubMed1996

Severe protein deficiency and repletion alter body and brain composition and organ weights in infant pigs.

Three-wk-old genetically lean or obese pigs were used in two experiments to determine the changes in body composition, visceral organs and brain in response to severe protein deficiency. In Experiment 1, 16 obese pigs were fed an adequate (A, 21% protein, 3% fat) or a protein-deficient (D, 5% protein, 23% fat) diet for 7 wk. One-half of each group was killed at 7 wk, and the remainder of each group was fed the A diet for an additional 8 wk. At 7 wk, pigs fed D contained a higher percentage of fat than those fed A (P < 0.01); after 8-wk of repletion, body composition of the two groups was similar. Duodenum, jejunum, and ileum of the protein-deficient pigs had severely atrophic villi, submucosal edema, and atrophic muscle layers; after 8 wk of repletion, however, microscopic architecture of the gastrointestinal tract was restored to normal. Absolute cerebrum weight at 7 wk, but not after 8 wk repletion, in the pigs fed D were significantly less than in pigs fed A, indicating reduced brain cellularity after 7 wk of protein restriction, but not after 8 wk repletion. In Experiment 2, genetically obese (O, n = 8) and lean (L, n = 8) pigs consumed the A or D diet ad libitum for 10 wk. L and O pigs responded similarly to protein deficiency; D pigs were fatter than A pigs and plasma constituents, bone mineral content, bone mineral density and most organ weights revealed no interactions between diet and genotype. The pig model system used in these experiments enabled the isolation of protein deficiency from infectious disease, parasites and social environmental stimulation that may confound interpretation of human infant malnutrition experiments. The data suggest that genetically controlled body fatness is not a major determinant in the response of the infant pig to severe protein deficiency.

Animals↗
PubMed1993

Influence of protein deficiency on hexachlorocyclohexane and malathion toxicity in pregnant rats.

The effects of protein deprivation and 60 mg hexachlorocyclohexane (HCH)/kg or 500 mg malathion/kg body weight were studied in pregnant rats fed a diet containing 16% (control) or 5% (protein-deficient) casein throughout gestation. Three po doses of HCH or malathion on the 6th, 10th and 14th day of gestation resulted in maternal toxicity and fetal growth retardation. No skeletal anomalies were noted except for poor ossification in the protein-deficient dams, which was further exaggerated on exposure to HCH or malathion. Malathion caused more severe maternal and fetal toxicity compared to the HCH-dosed rats. Depletion in glutathione (GSH) and decreased activities of GSH peroxidase, GSH reductase and glucose-6-phosphate dehydrogenase were observed from the protein deficiency and pesticide exposure. Impairment of GSH-dependent routes of detoxification was noticed from exposure to HCH or malathion during pregnancy. The lipid peroxide content was elevated from protein deficiency and was magnified with pesticide exposure.

Animals↗
PubMed1983

Effects of protein deficiency on the metabolism of arachidonic acid by rat pleural polymorphonuclear leukocytes.

The effects of protein deficiency on the biosynthesis of metabolites of arachidonic acid by rat pleural polymorphonuclear leukocytes stimulated with calcium ionophore were investigated. The major products of metabolism by lipoxygenase in these cells were leukotriene B4 and 5-hydroxy-6,8,11,14-eicosatetraenoic acid, whereas the major cyclooxygenase products were thromboxane B2 and 12-hydroxy-5,8,10-heptadecatrienoic acid. At high substrate concentrations (100 microM), the formation of all products by polymorphonuclear leukocytes was lower for protein-deficient rats than for controls. Similar results were obtained when products synthesized from endogenous substrate were measured, except that there was no change in the amount of 5-hydroxy-6,8,11,14-eicosatetraenoic acid formed. The biosynthesis of prostaglandins E2 and F2 alpha by homogenates of rat kidney medulla was reduced as a result of protein deficiency. Acetylsalicylic acid inhibited the formation of cyclooxygenase products and stimulated the formation of lipoxygenase products by polymorphonuclear leukocytes. Protein deficiency did not alter the effects of acetylsalicylic acid on the biosynthesis of these products, although at any given concentration the amounts of products formed were less with protein-deficient rats than with rats fed control diets.

Animals↗
PubMed1993

Teratogenicity and developmental toxicity of carbon monoxide in protein-deficient mice.

Experiments were carried out to determine the teratogenicity and developmental toxicity of carbon monoxide (CO) in mice fed protein-deficient diets. Pregnant CD-1 mice were fed 27 (control), 16, 8, or 4% protein diets throughout gestation and each group was exposed to 0 (control), 65, 125, 250, or 500 ppm of CO from gestation days 8-18. The CO exposure was continuous except for daily watering, feeding or cage changing. The animals were killed on gestation day 18. Pregnancy status of the dams was examined. Fetuses were examined for gross and skeletal malformations. The percentages of dead or resorbed fetuses and of grossly malformed fetuses per litter were related to the CO exposure levels and inversely related to the dietary protein levels. All levels of CO and 8 or 4% protein diets significantly decreased the fetal weight of normal fetuses. The most commonly seen gross malformations were brachygnathia accompanied by protruding tongue, microstomia, microcephaly, open mouth, or open eyes. Most of the grossly malformed fetuses also had dry, bleached and wrinkled skin. An increased incidence of skull (interparietal or supraoccipital), and jaw (mandible or premaxilla) malformation; wavy ribs and scoliosis of spine; and limb unossifications were observed in the litters of dams fed protein-deficient diet and all levels of CO exposure. Malformed litters in each protein diet were related to CO exposure levels. The data suggest that CO is teratogenic under protein-deficient conditions. Protein deficiency had additive effect on CO teratogenicity and synergistic effect on fetal mortality. Special groups at risk may include cigarette or marijuana smokers and malnourished or undernourished populations.

Abnormalities, Drug-Induced↗
PubMed2004

Effects of protein deficiency induced by raw soy with and without sucrose on dentine formation and dentinal caries in young rats.

OBJECTIVES: The effects of protein deficiency and sucrose on formation and mineralization of dentine and dental caries in the molars of young rats were investigated. MATERIALS AND METHODS: Two groups of weaning Wistar rats received raw soy flour to induce protein deficiency with sucrose or starch as the carbohydrate source; the other two groups received skim milk powder as the protein source with sucrose or starch as the carbohydrate source. At the onset, tetracycline was injected to mark the dentine formed at that moment. After 6 weeks, lower molars were sectioned sagittally, and the areas of dentine formation and dentinal caries developed during the experiment were quantified separately in the first and second molars. Dental caries was also classified according to Schiff's reaction. Calcium (Ca), phosphorus (P) and total mineral elements were analyzed using an electron probe microanalyzer. RESULTS: Rats in both protein-deficient groups and normal protein sucrose group had significantly larger areas of dentine formed compared with rats fed with normal protein starch diet. Ca, P and total mineral elements in dentine were significantly reduced by normal protein sucrose diet. P content was significantly reduced in dentine of rats in protein-deficient sucrose group. Rats in normal protein sucrose group had significantly more and larger dentinal caries lesions than in any other group. CONCLUSION: This study suggests that protein deficiency induced by soy prevents the progression of dental caries even in highly cariogenic environment.

Animals↗