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British Journal of Experimental... Apr 1978Four groups of 10 young adult Wistar male rats were fed on a protein-free diet for periods of 7, 28, 56 and 84 days. Control groups were fed on a 20% casein diet. Food...
Four groups of 10 young adult Wistar male rats were fed on a protein-free diet for periods of 7, 28, 56 and 84 days. Control groups were fed on a 20% casein diet. Food intake and body weights of rats were registered. Plasma protein levels and liver weight and fat content were determined. Sections of the caudate lobe were studied histologically. Fatty changes were classified in three grades. Protein-deficient rats exhibited loss of body weight and had low levels of plasma protein concentration. Liver lost weight after 7 days of protein deficiency; there was a gradual reduction in liver weight as periods of protein deprivation were longer. After 7 days, liver fat concentration was not significantly higher than in the respective control group; it was significantly higher in all the other malnourished animals. As periods of protein deprivation were longer, fatty changes became more severe. Other hepatic lesions were found in 5 of the 10 rats submitted to the longest period of protein deficiency. One of the rats showed a diffuse cellular atrophy, 2 animals showed an extensive haemorrhagic necrosis, another showed a focal area of reticulum collapse and the last exhibited a distortion of the normal architecture of the liver due to diffuse reticulum collapse and early nodular regeneration; these 2 last rats showed early fibrosis in portal areas. The findings suggest that other deficiencies may complicate the protein deficiency when rats are given a protein-free diet over prolonged periods. Even if the proteindeficient diet has protective nutrients, it may be that, when rats eat less food, as occurs in prolonged experiments, deficiency of one or all of these elements can occur, depending on their relative amount in diet.
Topics: Animals; Blood Proteins; Fatty Liver; Lipid Metabolism; Liver; Male; Necrosis; Organ Size; Protein Deficiency; Rats
PubMed: 656316
DOI: No ID Found -
British Journal of Industrial Medicine Jul 1970250-259. In order to determine whether the dietary deficiency, which may occur in miners in India, is likely to influence their response to silica dust, two...
250-259. In order to determine whether the dietary deficiency, which may occur in miners in India, is likely to influence their response to silica dust, two experiments were carried out on rats. In both experiments rats were exposed to silica dust by intratracheal inoculation of saline suspension, the dose being sufficient to cause marked fibrosis in normal rats. In the first experiment rats were fed on a multiple deficient diet and in the second on a diet grossly deficient in protein but otherwise adequate. Although these diets caused other evidence of dietary deficiency, in neither group was there any difference in the extent of silicotic fibrosis as assessed by histological or biochemical methods.
Topics: Animals; Collagen; Deficiency Diseases; Diet; India; Lung; Male; Mining; Occupational Diseases; Organ Size; Protein Deficiency; Rats; Silicon Dioxide; Silicosis; Trachea
PubMed: 4317610
DOI: 10.1136/oem.27.3.250 -
Nutrition Reviews Jan 2008Patients with end-stage liver disease often reveal significant protein-energy malnutrition, which may deteriorate after listing for transplantation. Since malnutrition... (Review)
Review
Patients with end-stage liver disease often reveal significant protein-energy malnutrition, which may deteriorate after listing for transplantation. Since malnutrition affects post-transplant survival, precise assessment must be an integral part of pre- and post-surgical management. While there is wide agreement that aggressive treatment of nutritional deficiencies is required, strong scientific evidence supporting nutritional therapy is sparse. In practice, oral nutritional supplements are preferred over parenteral nutrition, but enteral tube feeding may be necessary to maintain adequate calorie intake. Protein restriction should be avoided and administration of branched-chain amino acids may help yield a sufficient protein supply. Specific problems such as micronutrient deficiency, fluid balance, cholestasis, encephalopathy, and comorbid conditions need attention in order to optimize patient outcome.
Topics: Humans; Liver Diseases; Liver Transplantation; Nutrition Assessment; Nutrition Therapy; Nutritional Physiological Phenomena; Postoperative Care; Preoperative Care; Protein-Energy Malnutrition
PubMed: 18254884
DOI: 10.1111/j.1753-4887.2007.00005.x -
Physiological Reports Dec 2018Malnutrition remains a major health problem in low- and middle-income countries. During low protein intake, <0.67 g/kg/day, there is a loss of nitrogen (N ) balance,...
Malnutrition remains a major health problem in low- and middle-income countries. During low protein intake, <0.67 g/kg/day, there is a loss of nitrogen (N ) balance, due to the unavailability of amino acid for metabolism and unbalanced protein catabolism results. However, there are individuals, who consume the same low protein intake, and preserve N balance for unknown reasons. A novel factor, the gut microbiota, may account for these N balance differences. To investigate this, we correlated gut microbial profiles with the growth of four murine strains (C57Bl6/J, CD-1, FVB, and NIH-Swiss) on protein deficient (PD) diet. Results show that a PD diet exerts a strain-dependent impact on growth and N balance as determined through analysis of urinary urea, ammonia and creatinine excretion. Bacterial alpha diversity was significantly (P < 0.05, FDR) lower across all strains on a PD diet compared to normal chow (NC). Multi-group analyses of the composition of microbiomes (ANCOM) revealed significantly differential microbial signatures between the four strains independent of diet. However, mice on a PD diet demonstrated differential enrichment of bacterial genera including, Allobaculum (C57Bl6/J), Parabacteroides (CD-1), Turicibacter (FVB), and Mucispirillum (NIH-Swiss) relative to NC. For instance, selective comparison of the CD-1 (gained weight) and C57Bl6/J (did not gain weight) strains on PD diet also demonstrated significant pathway enrichment of dihydroorodate dehydrogenase, rRNA methyltransferases, and RNA splicing ligase in the CD-1 strains compared to C57Bl6/J strains; which might account in their ability to retain growth despite a protein deficient diet. Taken together, these results suggest a potential relationship between the specific gut microbiota, N balance and animal response to malnutrition.
Topics: Animals; Gastrointestinal Microbiome; Male; Mice; Mice, Inbred C57BL; Nitrogen; Phenotype; Protein Deficiency
PubMed: 30516001
DOI: 10.14814/phy2.13932 -
Canadian Medical Association Journal Feb 1969
Topics: Gynecomastia; Humans; Kidney Failure, Chronic; Male; Methyldopa; Prolactin; Protein Deficiency; Renal Dialysis
PubMed: 5765409
DOI: No ID Found -
Hormone Research 2007Fetal growth retardation is a fetal adaptation in response to inadequate supply of oxygen and/or nutrients. Animal models of intrauterine growth retardation are an... (Review)
Review
Fetal growth retardation is a fetal adaptation in response to inadequate supply of oxygen and/or nutrients. Animal models of intrauterine growth retardation are an invaluable tool to question the genetic, molecular and cellular events that determine fetal growth and development. Rodent and non-litter bearing animals are mammalian system with similar embryology,anatomy and physiology to humans. Utilization of these systems has led to a greater understanding of the pathophysiology and consequences of intrauterine growth retardation. These observations are comparable to that observed in humans born small for gestational age, and are of interest because of the known association between poor fetal growth and development of adult disease. All the experimental manipulations described here have altered a number of metabolic and physiological variables, but the pattern of alterations seems to vary with the procedure and species employed. This review describes animal models for intrauterine growth retardation and assesses their potentials and limitations at aiming to improve strategies for the prevention of adult disease.
Topics: Animals; Caloric Restriction; Cardiovascular Diseases; Disease Models, Animal; Female; Fetal Growth Retardation; Glucocorticoids; Guinea Pigs; Humans; Hypoxia; Infant, Newborn; Infant, Small for Gestational Age; Kidney Diseases; Ligation; Mice; Pregnancy; Pregnancy in Diabetics; Protein Deficiency; Rats; Sheep; Stress, Physiological; Swine; Uterus
PubMed: 17351325
DOI: 10.1159/000100545 -
Journal of Neurochemistry Jan 2017Early malnutrition is a risk factor for depression and schizophrenia. Since the offspring of malnourished dams exhibit increased brain levels of serotonin (5-HT), a...
Early malnutrition is a risk factor for depression and schizophrenia. Since the offspring of malnourished dams exhibit increased brain levels of serotonin (5-HT), a tryptophan-derived neurotransmitter involved in the pathophysiology of these mental disorders, it is believed that the deleterious effects of early malnutrition on brain function are due in large part to altered serotoninergic neurotransmission resulting from impaired tryptophan (Trp) metabolism. However, tryptophan is also metabolized through the kynurenine (KYN) pathway yielding several neuroactive compounds including kynurenic (KA), quinolinic (QA) and xanthurenic (XA) acids. Nevertheless, the impact of perinatal malnutrition on brain kynurenine pathway metabolism has not been examined to date. Here, we used ultra-performance liquid chromatography-tandem mass spectrometry for the simultaneous quantification of tryptophan and a set of seven compounds spanning its metabolism through the serotonin and kynurenine pathways, in the brain of embryos and adult offspring of rat dams fed a protein-restricted (PR) diet. Protein-restricted embryos showed reduced brain levels of Trp, serotonin and KA, but not of KYN, XA, or QA. In contrast, PR adult rats exhibited enhanced levels of Trp in the brainstem and cortex along with increased concentrations of 5-HT, kynurenine and XA. The levels of XA and KA were also increased in the hippocampus of adult PR rats. These results show that early protein deficiency induces selective and long-lasting changes in brain kynurenine metabolism. Given the regulatory role of KYN pathway metabolites on brain development and function, these changes might contribute to the risk of developing psychiatric disorders induced by early malnutrition.
Topics: Age Factors; Animals; Brain; Dietary Proteins; Female; Kynurenic Acid; Kynurenine; Lactation; Male; Pregnancy; Prenatal Exposure Delayed Effects; Protein Deficiency; Rats; Rats, Wistar
PubMed: 27778340
DOI: 10.1111/jnc.13874 -
Vaccine Oct 2018Low efficacy of rotavirus (RV) vaccines in developing African and Asian countries, where malnutrition is prevalent, remains a major concern and a challenge for global...
BACKGROUND
Low efficacy of rotavirus (RV) vaccines in developing African and Asian countries, where malnutrition is prevalent, remains a major concern and a challenge for global health.
METHODS
To understand the effects of protein malnutrition on RV vaccine efficacy, we elucidated the innate, T cell and cytokine immune responses to attenuated human RV (AttHRV) vaccine and virulent human RV (VirHRV) challenge in germ-free (GF) pigs or human infant fecal microbiota (HIFM) transplanted gnotobiotic (Gn) pigs fed protein-deficient or -sufficient bovine milk diets. We also analyzed serum levels of tryptophan (TRP), a predictor of malnutrition, and kynurenine (KYN).
RESULTS
Protein-deficient pigs vaccinated with oral AttHRV vaccine had lower protection rates against diarrhea post-VirHRV challenge and significantly increased fecal virus shedding titers (HIFM transplanted but not GF pigs) compared with their protein-sufficient counterparts. Reduced vaccine efficacy in protein-deficient pigs coincided with altered serum IFN-α, TNF-α, IL-12 and IFN-γ responses to oral AttHRV vaccine and the suppression of multiple innate immune parameters and HRV-specific IFN-γ producing T cells post-challenge. In protein-deficient HIFM transplanted pigs, decreased serum KYN, but not TRP levels were observed throughout the experiment, suggesting an association between the altered TRP metabolism and immune responses.
CONCLUSION
Collectively, our findings confirm the negative effects of protein deficiency, which were exacerbated in the HIFM transplanted pigs, on innate, T cell and cytokine immune responses to HRV and on vaccine efficacy, as well as on TRP-KYN metabolism.
Topics: Animals; Feces; Germ-Free Life; Humans; Infant; Microbiota; Protein Deficiency; Rotavirus; Rotavirus Vaccines; Swine; Tryptophan; Vaccines, Attenuated
PubMed: 30219368
DOI: 10.1016/j.vaccine.2018.09.008 -
Infection and Immunity Oct 1982Groups of female adult rats were fed either isocaloric protein-free or 18% protein diets for various intervals. Four days before sacrifice, the animals were immunized...
Groups of female adult rats were fed either isocaloric protein-free or 18% protein diets for various intervals. Four days before sacrifice, the animals were immunized either with sheep erythrocytes or with a trinitrophenyl-lipopolysaccharide (TNP-LPS) conjugate. Spleen lymphoid cell populations, spleen plaque-forming cells, and serum hemolysins were measured. A persistent diminution, proportional to the duration of protein deprivation, was observed in all parameters studied after immunization with the T-dependent antigen, sheep erythrocytes. The immune dysfunction was more pronounced for hemolysin titers, which became undetectable after 15 days of protein-free diet. The response of the protein-free group to the T-independent antigen (TNP-LPS) after 15 days of diet was only 34% of the control. When a T-cell lymphokine, macrophage migration inhibitory factor, was measured, a normal response was observed in the protein-free group. Feeding a normal diet rapidly restored the spleen plaque-forming cell populations to 60% of normal after 4 days and to 100% after 6 days. Protein starvation influenced the production of antibodies more than it did the number of antibody-forming cells. The nutritional impairment of immunoglobulin synthesis appears to be reversible.
Topics: Animals; Antibody Formation; Antigens, T-Independent; B-Lymphocytes; Female; Macrophage Migration-Inhibitory Factors; Protein Deficiency; Rats; Rats, Inbred Strains; T-Lymphocytes; T-Lymphocytes, Helper-Inducer
PubMed: 6216214
DOI: 10.1128/iai.38.1.195-200.1982 -
American Journal of Respiratory and... Feb 2019CC16 (club cell secretory protein-16), a member of the secretoglobin family, is one of the most abundant proteins in normal airway secretions and has been described as a...
RATIONALE
CC16 (club cell secretory protein-16), a member of the secretoglobin family, is one of the most abundant proteins in normal airway secretions and has been described as a serum biomarker for obstructive lung diseases.
OBJECTIVES
To determine whether low CC16 is a marker for airway pathology or is implicated in the pathophysiology of progressive airway damage in these conditions.
METHODS
Using human data from the birth cohort of the Tucson Children's Respiratory Study, we examined the relation of circulating CC16 levels with pulmonary function and responses to bronchial methacholine challenge from childhood up to age 32 years. In wild-type and CC16 mice, we set out to comprehensively examine pulmonary physiology, inflammation, and remodeling in the naive airway.
MEASUREMENTS AND MAIN RESULTS
We observed that Tucson Children's Respiratory Study participants in the lowest tertile of serum CC16 had significant deficits in their lung function and enhanced airway hyperresponsiveness to methacholine challenge from 11 years throughout young adult life. Similarly, CC16 mice had significant deficits in lung function and enhanced airway hyperresponsiveness to methacholine as compared with wild-type mice, which were independent of inflammation and mucin production. As compared with wild-type mice, CC16 mice had significantly elevated gene expression of procollagen type I, procollagen type III, and α-smooth muscle actin, areas of pronounced collagen deposition and significantly enhanced smooth muscle thickness.
CONCLUSIONS
Our findings support clinical observations by providing evidence that lack of CC16 in the lung results in dramatically altered pulmonary function and structural alterations consistent with enhanced remodeling.
Topics: Adolescent; Adult; Animals; Biomarkers; Child; Disease Models, Animal; Female; Humans; Lung; Lung Diseases, Obstructive; Male; Mice; Protein Deficiency; Uteroglobin; Young Adult
PubMed: 30543455
DOI: 10.1164/rccm.201807-1345OC