Effect Of Protein Deficiency Research Articles

The effect of protein deficiency on the small intestinal carbobidrase system after the transition to the definitive nutrition in rats

The effect of protein deficiency on enteral carbohydrases during post-lactotrophic feeding of rat pups was studied. During this period, low protein intake (8% of the energy value of the diet versus 27% in the norm) negatively affects the growth of body weight and pancreas of rats, leads to the disruption of the activity of intestinal enzymes without changing the morphological development of the small intestine.

Effect of protein deficiency on luteinizing hormone releasing hormone (LHRH), gonadotropin releasing hormone associated peptide (GAP) and luteinizing hormone (LH) immunocytochemistry in the hypothalamus and pituitary gland of prepubertal ewes.

Growing female lambs were fed diets containing 14.2% (standard) or 8.1% (protein restricted) of proteins to determine their effects on puberty and luteinizing hormone releasing hormone (LHRH), gonadotropin hormone associated peptide (GAP), luteinizing hormone (LH) hormonal system. At the end of the experiment (30-34 weeks of age), hypothalamic LHRH, GAP and pituitary LH were analysed by immunocytochemical methods using specific antibodies. Plasma LH were determined by radioimmunoassay at 21 weeks of age. It was found that lowering of the dietary proteins content decreased the concentration of basal plasma LH significantly in lambs of 21 weeks of age. None of the sheep of this group reached sexual maturity at the same time as the animals of the standard group. However, immunoreactive (ir) LHRH neuronal system of protein restricted lambs was normally developed: Numerous irLHRH perikarya, dense network of axons and abundant material stored in the nerve terminals were well visualized in the typical sites of the preoptico-septal area, hypothalamus and the median eminence (ME). Gonadotropin associated peptide (GAP) of the LHRH precursor was present in the same populations of neurons that contained LHRH in the sheep brain. The proportion of pituitary LH-cells was three fold higher in pituitaries of the nutritionally restricted group. They displayed hypertrophy and very strong immunoreaction. These results show that protein deficiency in diets of growing female sheep delays their puberty but does not impair the synthesis and processing of LHRH in the brain neurons and synthesis of LH in pituitary cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of protein deficiency during pregnancy on tissue mitochondrial cytochromes and protein concentration

Effect of protein deficiency during pregnancy on tissue mitochondrial cytochromes and protein concentration

Effect of Protein Deficiency on Macroelement and Trace Element Levels of Weanling Rats' Small Intestine and Liver Tissues

Protein energy malnutrition has become a major health issue in developing countries. In the present study, the effect of protein deficiency on the small intestine and liver tissue content of macroelements and trace elements was investigated in weanling rats. Forty-five male weanling Wistar albino rats were divided into three groups. The control group (C) was fed a standard diet containing 25% casein, whereas the two experimental groups E1 and E2 consumed 12% and 3% casein, respectively, over a period of 45 d. The tissue samples were analyzed for zinc, copper, iron, manganese, calcium, and magnesium by atomic absorption spectroscopy. The protein-deficient groups showed increased levels of iron in both tissues and decreased manganese in small intestine tissue from the E1 group. No other differences were found for the other elements. These results suggest that protein deficiency might cause iron accumulation in the liver and intestine and decreases of manganese in the small intestine.

Effects of protein deficiency on liver trace elements and antioxidant activity in carbon tetrachloride-induced liver cirrhosis.

In liver cirrhosis, liver tissue becomes progressively substituted by fibrosis, ultimately leading to architectural distortion, liver circulatory changes, and liver failure. Some data support the hypothesis that protein undernutrition may play a role in the development and progression of nonalcoholic liver cirrhosis and that this progression is at least partially mediated by changes in glutathione peroxidase (GPX), superoxide dismutase (SOD), and other antioxidative systems, leading to an increase in lipid peroxidation. We analyzed the effects of protein deficiency on liver Cu, Fe, Zn, Mn, and Se in carbon tetrachloride (CCl4)-induced liver cirrhosis, the relation of protein undernutrition and these trace elements with the activity of some hepatic antioxidative enzymatic mechanisms, and the relation of all of them with morphological and biochemical changes in 40 male adult Sprague-Dawley rats divided in four groups. Liver cirrhosis was induced by intraperitoneal injection of CCl4 to 10 rats fed a 2% protein diet and another 10 fed a 18% protein control diet; two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. The study period lasted 6 wk. GPX, SOD, and lipid peroxidation products as well as Zn, Cu, Mn, Se, and Fe were determined in liver samples. We found that liver GPX and Se were reduced in the cirrhotic animals, especially in the low-protein-fed ones, protein deficiency, but not cirrhosis, exerting the main effects. A close correlation was found between liver GPX and serum albumin and weight loss and an inverse one among GPX and hepatocyte ballooning, liver fibrosis, and fat, histomorphometrically determined. These results suggest a pathogenetic role of decreased GPX in the progression of liver disease, which may become enhanced by concomitant protein undernutrition. In addition to iron, the levels of which were increased in the malnourished rats, no differences were found regarding the other trace elements, SOD activity, and lipid peroxidation products.

Effects of dietary protein and L-2-oxothiazolidine-4-carboxylate on rat brain glutathione concentration

The objectives were to investigate the effects of protein deficiency on rat brain glutathione (GSH) concentration and oxidative stress. Supplementation of L-2-oxothiazolidine-4-carboxylate (OTC), a precursor of cysteine, the limiting amino acid for GSH synthesis, was also investigated. Male Long-Evans weanling rats were assigned to groups fed: 1) protein-deficient diet, 2) protein-deficient diet supplemented with 0.45% OTC, or 3) protein-adequate (control) diet. After 6 weeks of feeding, liver, neocortex, striatum, hippocampus, thalamus, cerebellum, and brain stem were analyzed for GSH concentration by reverse-phase high performance liquid chromatography. Carbonyl groups were reacted with 2,4-dinitrophenylhydrazine, and the adduct was measured at 365 nm as a marker of oxidative modification of proteins. Hepatic GSH concentration declined and protein carbonyl content increased with mild protein deficiency, but there were no effects in any brain region. OTC supplementation restored hepatic GSH but did not influence GSH concentration in brain. Mild protein deficiency appears not to disturb brain GSH metabolism.

Differential effects of protein deficiency on the expression of rat placental lactogen and prolactin-like proteins

Differential effects of protein deficiency on the expression of rat placental lactogen and prolactin-like proteins

Increased NaCl preference of rats fed low-protein diet.

Four studies were conducted to assess the effect of a low-protein diet on NaCl intake. Young rats fed either control (20% casein) or low-protein (5% casein) high-carbohydrate (CHO) diet were allowed to drink either water alone or water and 300 mM NaCl. Relative to rats fed control diet, rats fed the low-protein diet progressively increased NaCl intake so that, despite lower food and water intakes, they drank 180% more NaCl during the last 3 days of the 21-day test. Additional studies found that rats fed low-protein diet always maintained positive sodium balance, were neither sodium depleted nor hypovolemic, and had normal plasma renin activity and aldosterone concentrations. The elevated NaCl intake was not secondary to calcium deficiency and was unaffected by mineral supplementation of the protein-deficient diet. Increases in the diet's CH and/or fat content incidental to decreases in its protein content influenced, but could not completely account for, the effect of protein deficiency on NaCl intake. We conclude that protein deficiency is the primary cause of the elevated NaCl preference produced by being fed a low-protein diet and that a novel physiological mechanism underlies this behavior.

Effect of protein deficiency on plasma insulin-like growth factor-1 (IGF-I) level and protein and proteoglycan synthesis rates in skeletal muscle and bone

Although protein deficiency in young children or young animals is frequently associated with growth retardation, the mechanism for impaired growth has not been established. In this article studies on rats investigate changes in plasma concentration of IGF-I in relation to the inhibition of bone and muscle growth are reported. This article also examines protein and proteoglycan synthesis through protein deficiency and recovery afterwards. A marked reduction in weight, food intake, muscle and bone growth was detected in the protein-deficient rats. The decrease of protein and proteoglycan synthesis in the tissues was also observed. The concentration of IGF-I plasma correlated with both protein and tibial proteoglycan synthesis rates and with the increase of protein content in the diet. However, in the 7.5% casein group these parameters were well maintained due to the increase of food intake. The recovered groups showed an increase in the protein and proteoglycan synthesis and this change correlated with the concentration of IGF-I. Thus protein deficiency impaired growth by a combination of reduced food intake and a reduced anabolic response to food due to a reduced protein and proteoglycan synthesis possibly reflecting impaired IGF-I secretion.

Effects of protein deficiency and diet consistency on the parotid gland and parotid saliva of rats.

Protein deficiency results in an increased susceptibility to dental caries, suggesting that oral host-defense properties are compromised. An important component of oral host defense is salivary gland function, which is affected by both protein deficiency and diet consistency. This study describes the effects on rat parotid gland growth and secretory function induced by feeding rats diets of normal (20%) or moderately low (7%) protein content, provided in either a powdered or solid form. In addition, since protein deficiency may result in a secondary zinc deficiency which, in turn, may affect salivary gland function, the effects of these diets on liver zinc concentration were also measured. From 22 to 47 days of age, rats (18/group) were fed the following diets: normal protein, powdered; normal protein, solid; low protein, powdered; and low protein, solid. With each diet consistency, liver zinc was higher for the normal protein group. Within each protein level, liver zinc was higher for the solid diet. This latter observation suggests that food mastication and the resultant stimulation of salivary gland function may also play a role in zinc metabolism. With the normal-protein diet, parotid gland weight was higher for the solid diet; with the low-protein diet, parotid gland weight was similar for both consistencies and did not differ from that of the group fed the "normal protein, powdered" diet. For both consistencies, parotid saliva protein concentration was greater for malnourished rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Protein Deficiency and the Growing Rat Lung. II. Morphometric Analysis and Morphology

Effects of protein deficiency during the whole period of postnatal development and intensive growth were studied in the rat lung parenchyma. Dams received a low protein diet as follows: early restriction, 8% casein diet from parturition, and delayed restriction, 12% then 8% casein diet from lactation d 8. After weaning (d 21), early restriction and delayed restriction group rats were maintained on the 8% casein diet until d 49, wherefore they were returned to normal food (18% casein) for 11 wk. Lungs were processed for light and electron microscopic morphometry on d 21, 49, and 126. The diffusion capacity of the lung for O2 (DLO2) was also determined from the morphologic parameters. Volume and surface densities of the parenchymal components of malnourished rats did not consistently differ from controls. Because of lower lung volumes, absolute values, including DLO2, were all significantly decreased. Further, although lung volume growth was less impaired than body growth and thus deviated from the normal allometric relationship, most morphometric parameters paralleled body weight changes. Visually, we detected minor morphologic alterations at d 21 and 49, not necessarily reflected by morphometric data. But, importantly, lung parenchyma appeared mature at weaning despite the growth retardation. Normal refeeding resulted in a striking regrowth of the lung parenchyma. Although early restriction rats did not fully catch up in lung volume, most parenchymal parameters and DLO2 were largely restored in both refed groups.

Effect of hexachlorocyclohexane on biochemical parameters of rats on a protein deficient diet

Male albino weanling rats were fed diets containing 5% (group I) and 21% (group II) protein as casein for 28 days. At the end of the dietary period Hexachlorocyclohexane (HCH) was administered daily for 30 days to investigate the effect of protein deficiency on the toxicity of HCH. The results indicated that rats fed a low protein diet and HCH had a higher mortality, lower rate of growth and increased liver weight. An increased glycogen and decreased glutathione level was also observed in their livers. A significant decrease in blood glucose, erythrocyte enzyme G6PD and LDH of animals exposed to low protein diet is suggestive of the disruption of the energy provision of the cell.

The effects of protein deficiency and fluoride on bone mineral content of rat tibia.

This study examined the effects of chronic protein deficiency and fluoride administration (10 mg/kg/day), separately or in combination, on rat tibia properties. Protein deficiency increased the bone fluoride concentration and reduced the bone mineral content (BMC) especially at the proximal or growing end which contains mainly cancellous bone. Fluoride administration also reduced BMC, but to a lesser extent, and it resulted in proximal tibia fluoride concentrations that were nearly twice those of the distal tibia. The interaction between fluoride administration and the protein content of the diet on BMC was nonsignificant, suggesting that the effects were additive, not multiplicative or synergistic. Fluoride administration, but not protein deficiency, increased bone magnesium levels. It is hypothesized that the reduction in BMC in the areas where the fluoride concentrations were the highest was due to a localized toxic effect of fluoride.

Liver response to low-hexachlorobenzene exposure in protein- or energy-restricted rats

The individual effects of protein deficiency and energy restriction on liver response to low-hexachlorobenzene (HCB) exposure were investigated in adult male Wistar rats. In rats fed either the low-protein or control diet, the only effect caused by HCB was a decrease in paralysis time following an ip injection of zoxazolamine. This decrease was similar for both groups. In the animals subjected to energy restriction, HCB induced a greater decrease in paralysis time, an increase in the size of centrilobular hepatocytes, a lower liver DNA content and an increased concentration of HCB in the adipose tissue, compared with the control and protein-deficient groups. Our data suggest that energy restriction increases liver response to HCB, while protein deficiency does not impair the hepatic reaction to small doses of HCB exposure.

Effect of protein deficiency on the IL6 and acute phase protein response (APPR) in rats injected with turpentine

Effect of protein deficiency on the IL6 and acute phase protein response (APPR) in rats injected with turpentine

Expression of liver-specific genes coding for plasma proteins in protein deficiency

Protein deficiency leads to a decreased concentration of plasma proteins, although it is not clear whether this response is caused by alterations in gene transcription or in post-transcriptional events. The aim of this study was to investigate the expression of some liver-specific genes coding for plasma proteins in rats kept on a protein-free diet for 30 days. Cloned cDNA probes for the albumin, transthyretin, retinol-binding protein and prothrombin genes were used in Northern hybridizations to total liver RNA to compare their transcript levels in protein-deficient and control animals. Liver polysomes were also isolated and fractionated from the two groups of animals to examine the possible effects of protein deficiency on translation of the mRNAs. The results indicate that the albumin and transthyretin mRNAs are present in lower amounts in protein deficiency. The distribution profile along sucrose gradients shows that all mRNAs are undergoing translation, but in protein-deficient animals a small but consistent fraction of each mRNA is also present in the non-polysomal, low molecular weight fractions.

Effect of protein deficiency on some hypothalamic and pituitary hormones in growing male lambs. An immunohistochemical study

Growing male lambs were fed with diets containing 14.0, 10.8 and 7.6% protein for 3 months to determine their effects on the content of hypothalamic LHRH and SRIH and pituitary LH and GH, using immunohistochemical methods. Lowering the concentration of dietary proteins caused marked changes in the immunoreactivity of these hormones. The immunoreactive (IR) content of LHRH stored in the median eminence was enhanced, and the proportion of LH cells and their IR content increased. Opposite effects were observed in the SRIH/GH system; IR SRIH content stored in the median eminence markedly diminished, and, although hyperplasia of GH cells was observed, their IR content was diminished. This study indicates that prolonged restrictions of protein in the diet of growing male sheep affects the immunoreactive content of the investigated hormones. It seems that they suppress LHRH/LH release and augment GH release, possibly via suppression of hypothalamic somatostatin.

The Cafeteria Diet as a Tool for Studies of Thermogenesis

The cafeteria diet involves feeding experimental animals a choice of palatable human food items to stimulate energy intake, and has been used extensively to study diet-induced thermogenesis. In a recent commentary Moore has argued that this feeding regime is inappropriate for such studies because the nutrient composition cannot be controlled, many of the effects seen are due to protein or nutrient deficiency and accurate measurements of energy intake are difficult to achieve. We argue that all of these criticisms can be overcome by careful use of the feeding regime and well-controlled experiments. Gross nutrient composition of cafeteria diets can be modified over a wide range, and such studies demonstrate that the effects of protein deficiency can be clearly dissociated from those of hyperphagia. There is no experimental evidence for nutritional deficiency in cafeteria-fed animals even over very long periods of time. Furthermore, the alternatives suggested by Moore, i.e., presenting sucrose solutions to drink or high fat diets, suffer the same drawbacks of altered and often uncontrolled nutrient intake and yet produce little or no increase in energy intake. Criticism of the cafeteria diet is not justified simply because of its misuse by nutritionally naive experimenters. The value and validity of this feeding regime is further supported by the enormous impact it has made on our understanding of energy balance regulation and thermogenesis.

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, O 3 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 O 3 exposure. Heart SOD and GPx, however, were not affected by ozone or diet. The pulmonary and hepatic effects due to diet and O 3 further illustrate the importance of nutritional status when assessing the health effects of O 3 exposure.

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.