Low-protein Diet Group Research Articles

Effect of low protein diets added with protease on growth performance, nutrient digestibility of weaned piglets and growing-finishing pigs.

The objective of this study was to evaluate the effects of low protein diets added with protease on growth performance, nutrient digestibility, and blood profiles of weaned piglets and growing-finishing pigs. A total of 96 weaned pigs ([Yorkshire × Landrace] × Duroc) with average body weight (BW) of 6.99 ± 0.21 kg were used in a 20-week experiment. The dietary treatments were arranged in a 2 × 3 factorial design. Treatments were as follows: In phase 1 (1–2 weeks), two protein levels as high protein (HP; 19.0%), low protein (LP; 17.0%), and three protease (PT) levels (PT0, 0%; PT1, 0.3%; and PT2, 0.5%); in phase 2 (3–4 weeks), protein levels (HP, 18.05%; LP, 16.15%) and protease levels (0%, 0.3%, and 0.5%); in phase 3 (5–12 weeks), protein levels (HP, 17.1%; LP, 15.3%) and protease level (0%, 0.15%, and 0.3%); in phase 4 (13–20 weeks), protein levels (HP, 16.15%; LP, 14.45%) and protease level (0%, 0.15%, and 0.3%). At 4 weeks and 20 weeks after treatment, BW was higher (p < 0.050) in the PT2 group than PT0 group. From weeks 0 to 4, average daily gain (ADG) and feed efficiency (G/F) were higher (p = 0.006 and p = 0.014; p = 0.014 and p = 0.044, respectively) in the PT2 group than PT0 and PT1 groups. From weeks 16 to 20, ADG and G/F were higher (p < 0.001 and p = 0.009; p = 0.004 and p = 0.033, respectively) in the PT2 group than PT0 and PT1 groups. Crude protein (CP) digestibility was higher (p = 0.013, p = 0.014, and p = 0.035, respectively) in the low protein (LP) group than high protein (HP) group at weeks 4, 12, and 20. At weeks 4 and 20, the LP diet group had lower (p < 0.001 and p = 0.001, respectively) blood urea nitrogen (BUN) levels than the HP diet group. Therefore, a low CP diet added with protease could increase growth performance and CP digestibility of weaned piglets and growing-finishing pigs.

Fermented Feed Supplement Relieves Caecal Microbiota Dysbiosis and Kidney Injury Caused by High-Protein Diet in the Development of Gosling Gout.

Simple SummaryRecently, high-protein complete feed has been increasingly used in the Chinese goose industry, increasing the outbreaks of gout in goslings. We found that high-protein diets are implicated in the kidney injury and gut microbiota dysbiosis associated with the occurrence of gout in goslings. Fermented feed, containing many helpful intestinal probiotics and metabolites for birds, shows potential for the protection of gut microbiota. We found that fermented feed supplement alleviates the gout occurrence caused by the high-protein diets and improves renal function, because of its regulations of caecal microbiota. Fermented feed increased Lactobacillus and decreased Enterococcus in the cecum of goslings. We suggest that goose farmers should strictly control the proportion of protein in gosling feed and consider using fermented feed as an effective measure to control the outbreak of gosling gout.Firstly, forty-eight 1-day-old goslings were randomly allocated to four groups and were fed diets containing crude protein (CP) at different concentrations: 160, 180, 200, and 220 g/kg in Experiment One. We found a dose-dependent relationship between the dietary protein levels and morbidity of gosling gout. The concentration of serum uric acid (UA), creatinine (Cr), and urea nitrogen (UN), and the activity of xanthine oxidase in the 220CP groups were significantly higher than those in the low-protein diet groups. Beneficial microbes, including Akkermansia, Lactococcus, and Butyricicoccus were enriched in the ceca of healthy goslings, while the microbes Enterococcus, Enterobacteriaceae, and Bacteroides were enriched in those with gout. Then, we explored the effects of fermented feed on gosling gout caused by high-protein diets in Experiment Two. A total of 720 1-day-old goslings were randomly allotted to four experimental groups: CN (162.9 g/kg CP), CNF (167.5 g/kg CP, replacing 50 g/kg of the basal diet with fermented feed), HP (229.7 g/kg CP, a high-protein diet), and HPF (230.7 g/kg CP, replacing 50 g/kg of the high-protein diet with fermented feed). We found that the cumulative incidence of gout increased in the HP group compared with that in the control, but decreased in the HPF group compared to that in the HP group. Similarly, the concentration of serum UA in the HP group was higher than that in the CN group, but decreased in the HPF group. Meanwhile, compared with the HP group, using fermented feed in diets decreased the abundance of Enterococcus in the ceca of goslings, while increasing the abundance of Lactobacillus. These results suggest that appropriate dietary protein levels and the fermented feed supplement might relieve the kidney injury and gut microbiota dysbiosis caused by high-protein diets in the development of gosling gout.

Gestational protein restriction alters the RANKL/OPG system in the dental germ of offsprings

ObjectiveEvaluate the dentinogenesis in the offspring of rats submitted to gestational protein restriction (GPR). Design: The offspring were evaluated at the 21st day of gestation (21 dG). Assessments were made of morphological parameters and the RANKL/OPG system - bone tissue maturation markers - in the upper incisor tooth germ. Pregnant 10-week-old female Wistar rats were divided into normal protein (NP, 17% casein, n = 5) and low protein (LP, 6% casein, n = 5) diet groups. At 21 dG, the offspring maxillae were collected for histomorphometric and immunohistochemical analyses. Results: The LP group showed decreased thickness of the dentin and odontoblast cell layers on the tooth germ. GPR led to decreased OPG expression and increased RANKL expression in the incisor germ. Conclusion: The results suggested that gestational protein restriction altered odontoblast RANKL/OPG expression and decreased dentin matrix deposition and thickness in tooth development.

A More Oxidized Plasma Albumin Redox State and Lower Plasma HDL Particle Number Reflect Low-Protein Diet Ingestion in Adult Rats

Plasma albumin (ALB) redox state reflects protein nutritional status, but how it differs from other protein nutrition biomarkers remains to be fully elucidated. This study aimed to delineate the characteristics of plasma ALB redox state as a protein nutrition biomarker. Adult male Wistar rats were maintained on an AIN-93 M [14% casein, control (CT)] diet or an AIN-93 M-based 5% casein [low protein (LP)] diet ad libitum for 4 wk. Plasma samples were repeatedly obtained from the same rats at weeks 0-4, ALB redox state was determined by HPLC, and the concentrations of conventional protein nutrition biomarkers, ALB and transthyretin (TTR), were compared between the groups by Student t test. Body mass, relative muscle masses, plasma proteome, and plasma lipids at week 4 were also compared. Plasma ALB redox state shifted to a more oxidized state in the LP diet group compared with the CT diet group at weeks 1-4. The LP diet group also showed significantly lower plasma ALB concentrations at weeks 1 and 2 (13% and 11% lower, respectively) and significantly lower TTR concentration at week 1 (21% lower) compared with the CT diet group, but these concentrations did not differ significantly at weeks 3 and 4. After 4 wk, body mass and relative soleus and gastrocnemius muscle masses did not differ, but the relative plantaris muscle mass tended to be 4% lower (1.75 compared with 1.68 g/kg body mass) in the LP diet group compared with the CT group (P=0.06). The LP diet group also had a significantly lower HDL particle number than the CT group (30% lower). A more oxidized plasma ALB redox state and lower plasma HDL particle number reflect LP diet ingestion in adult rats, which did not exhibit changes of plasma ALB and TTR concentrations.

Plasma albumin redox state is superior to conventional biomarkers to indicate the presence of potential protein undernutrition

AbstractThe redox state of plasma albumin would reflect albumin synthesis rate, and could be useful to demonstrate the presence of potential protein undernutrition. Aiming to delineate the characteristics of plasma albumin redox state as a nutritional biomarker, adult male Wistar rats were maintained on AIN-93M (14% casein, control diet) or an AIN-93M-based low protein diet (5% casein) ad libitum for 4 weeks, and the two groups were compared by examining plasma albumin redox state, plasma/serum levels of conventional biomarkers for protein nutritional status, and plasma proteome. While no significant difference was seen in body weight at the end of the experimental period, plantaris muscle mass trended lower in the low protein diet group, implicating the manifestation of moderate protein undernutrition. The redox of plasma albumin was shifted to more oxidized state in the low protein diet group, and the shift persisted during the entire experimental period. In contrast, the levels of conventional biomarkers, plasma albumin and prealbumin, were initially decreased in the low protein diet group, and the differences were then dissolved later in the experimental period. Similarly, the levels of other biomarkers, plasma transferrin and serum retinol-binding protein-4, did not differ significantly at the end of the experimental period. Plasma proteomic analysis revealed that the abundances of proteins that constitute high-density lipoprotein (HDL), apolipoprotein A-II and paraoxonase-1, were decreased in the low protein diet group, which were then validated by confirming decreases in plasma HDL level, plasma HDL-cholesterol level, and serum paraoxonase-1 activity in the low protein diet group. According to epidemiological reports, dietary protein intake is positively associated with plasma HDL-cholesterol level, and the risk factors of cardiovascular diseases, including lower HDL-cholesterol level, are closely related to frailty. Thus, it can be conceived that moderate dietary protein insufficiency would increase cardiovascular risks, such as reduction in HDL level and function (paraoxonase-1 activity), which could prime the onset of amyotropic diseases later in life, such as sarcopenia and frailty. Collectively, moderate dietary protein insufficiency would lead to decreased skeletal muscle mass, and also attenuate circulating HDL level and function, which could even aggravate the attenuation of skeletal muscle accretion; the redox state of plasma albumin would be instrumental over conventional biomarkers as an indicator of potentially protein undernourished status.

Evaluation of phosphorus, calcium, and magnesium content in commercially available foods formulated for healthy cats.

BackgroundHigh dietary phosphorus (P) and low calcium‐to‐phosphorus ratio (Ca:P) are associated with kidney damage in cats. There are no established guidelines for dietary P maximum for cats.ObjectivesTo quantify crude protein, P, Ca, and magnesium (Mg) concentrations in cat foods and compare among food formats (dry, canned, raw), primary protein ingredients, protein concentrations (low, moderate, high), grain‐free versus grain‐containing foods, foods intended for adult maintenance versus all life stages, and cost.SamplesEighty‐two commercial nonprescription cat foods.MethodsDescriptive study. Mineral concentrations were measured using inductively coupled argon plasma‐optical emission spectroscopy. Crude protein was measured using the Dumas nitrogen combustion method. Mineral and crude protein concentrations were compared among food categories.ResultsTwenty‐seven foods contained ≥3.6 g P/1000 kcal metabolizable energy (ME), of which 7 exceeded 4.8 g/1000 kcal ME. Thirteen foods had low Ca:P ratio (≤1.0). The low‐protein diet group had no products ≥3.6 g P/1000 kcal ME, which was significantly different compared to the high‐protein diet group (52% of products had ≥3.6 g P/1000 kcal ME; P = .01). No significant differences in P content and Ca:P ratio were found among other diet categories. Canned foods had significantly lower Mg compared to dry (P < .001) and raw (P = .007) foods. Declared minimum P and Ca were significantly lower than analyzed concentrations (P = .0005 and P = .003, respectively).Conclusions and Clinical ImportanceThe high number of foods with high P and low Ca suggest that pet food regulatory reform should be considered.

A high-protein diet, not isolated BCAA, is associated with skeletal muscle mass index in patients with gastrointestinal cancer.

Patients with cancer are susceptible to experiencing the loss of skeletal muscle mass. Thus, the purpose of this study was to evaluate whether a high-protein diet (HPD) or isolated branched-chain amino acid (BCAA) intake is associated with an increased skeletal muscle mass index (SMI) in patients with cancer of the gastrointestinal tract. This cross-sectional, observational study included 106 patients with gastrointestinal tract tumors. Food consumption was estimated using 24-h food recall. Patients were divided into two groups: a low-protein diet (LPD) group (≤1.2 g · kg · d-1) and a high-protein diet (HPD) group (>1.2 g · kg · d-1). Appendicular muscle mass (ASM) was calculated using Lee's formula, and its values were divided by the square of the height of the patient to obtain SMI values. Differences were considered significant when the probability they occurred by chance was <5% (P < 0.05). Of 106 patients assessed, 69 (65%) consumed a diet consistent with specifications of the LPD group and 37 (35%) consumed a diet consistent with HPD intake. Logistic regression after adjusting for sex and caloric and carbohydrate consumption showed an association between SMI and HPD (odds ratio, 4.19; 95% confidence interval, 1.06-16.56; P < 0.001) but not with BCAA. Daily total protein intake, but not isolated BCAA or leucine, was able to predict an increase in SMI in 43% of patients considered (P=0.006). Thus, HPD was associated with SMI, and total protein intake was a better predictor of SMI than BCAAs. HPD is a cost-effective way to enhance SMI, rather than focusing on the ingestion of isolated BCAAs.

Establishment of an ovalbumin-induced bronchial asthma model in mice with intrauterine growth retardation

To establish and evaluate an ovalbumin (OVA)-induced bronchial asthma model in mice with intrauterine growth retardation (IUGR), and to explore the molecular mechanism of relationship between IUGR and asthma. A total of 16 pregnant BALB/c female mice were divided into a low-protein diet group (n=8) and a normal-protein diet group (n=8), which were fed with low-protein (8%) diet and normal-protein (20%) diet respectively. The neonatal mice were weighed 6 hours after birth. Sixteen male neonatal mice with IUGR were randomly chosen from the low-protein diet group and enrolled in the IUGR group, and 16 male neonatal mice from the normal-protein diet group were enrolled in the control group. Blood samples were collected from the mice in both groups for testing of blood glucose. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum insulin level. The mice in the control group were randomized into a control + PBS group and a control + OVA group (n=8 each). The mice in the IUGR group were randomized into an IUGR + PBS group and an IUGR + OVA group (n=8 each). Six-week-old mice in the control + OVA and IUGR + OVA groups were subjected to intraperitoneal injection of 2 mg/mL OVA for sensitization and aerosol inhalation of 1% OVA for challenge. Mice in the control + PBS group and the IUGR + PBS group were treated with an equivalent amount of PBS. ELISA was used to determine serum IgE level in the mice in each group. Bronchoalveolar lavage fluid (BLF) was collected from the mice in each group for cell counting. The lung tissue of the mice in each group was stained with hematoxylin and eosin to observe pathological changes. The body weight at 6 hours after birth was significantly lower for neonatal mice in the low-protein diet group compared with those in the normal-protein diet group (P<0.01). The IUGR group had a significantly lower serum insulin level than the control group (P<0.01). The IUGR + PBS group had a significantly lower IgE level than the control + PBS group (P<0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had a significantly increased IgE level, and the IgE level was significantly higher in the IUGR + OVA group than in the control + OVA group (P<0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had significantly increased counts of leukocytes, eosinophils, lymphocytes, and macrophages in the BLF (P<0.01). The pulmonary alveoli of OVA-induced IUGR mice showed massive inflammatory cell infiltration and damage of intercellular continuity. Meanwhile, airway epithelial cell proliferation, bronchial wall thickening, bronchial lumen narrowing, and massive inflammatory cell infiltration around the bronchi and the vascular wall were observed. An OVA-induced bronchial asthma model has been successfully established in the mice with IUGR induced by low-protein diet, which provides a basis for further study of the molecular mechanism of relationship between IUGR and airway inflammation.

Effect Royal Jelly against Low Protein Diet Induced Hepatic Damage in Male Rats

Background: Proteins play the most important role in the structure and function of liver. Royal Jelly (RJ) as a honey bee secretion has antioxidant activities. This study was designed to evaluate the effects of RJ against hepatic damage in rats induced by Low Protein Diet (LPD). Materials and Methods: Forty‑eight male rats were randomly assigned into 6 groups: sham and LPD (%8 protein) groups; RJ groups (200 mg/kg RJ for 5 months and 200 mg/kg RJ for 10 months, orally) and LPD + RJ groups (200 mg/kg RJ orally + LPD for 5 months and 200 mg/kg RJ orally and LPD for 10 months). Griess technique was hired for determination of serum Nitric Oxide (NO) level. Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT) and Alkaline Phosphatase (ALP) concentrations were determined for liver functional disturbances value. In addition, Thiobarbituric acid reactive species, antioxidant capacity, the diameter of hepatocytes and the Central Hepatic Vein (CHV) were investigated. Results: LPD significantly increased the liver Malondialdehyde (MDA) and NO levels, the mean diameter of CHV and hepatocyte, hepatic enzymes and decreased tissue Ferric Reducing Ability of Plasma (FRAP) level compared to the sham group (P< 0.01). The RJ and RJ + LPD in all treatments significantly reduced the mean diameter of hepatocyte and CHV, hepatic enzymes, liver MDA and NO levels and increased tissue FRAP level compared to the LPD group (P< 0.01). Conclusion: RJ administration recovers the hepatic injury due to oxidative stress by LPD in rats.

The low-protein diet for chronic kidney disease: 8 years of clinical experience in a nephrology ward.

BackgroundGuidelines indicate that a low-protein diet (LPD) delays dialysis in severe chronic kidney disease (CKD). We assessed the value of these guidelines by performing a retrospective analysis in our renal clinical practice.MethodsThe analysis was performed from 1 January 2010 to 31 March 2018 in 299 CKD Stage 4 patients followed for 70 months in collaboration with a skilled nutritionist. The patients included 43 patients on a controlled protein diet (CPD) of 0.8 g/kg/day [estimated glomerular filtration rate (eGFR) 20–30 mL/min/1.73 m2 body surface (b.s.)], 171 patients on an LPD of 0.6 g/kg/day and 85 patients on an unrestricted protein diet (UPD) who were not followed by our nutritionist (LPD and UPD, eGFR <20 mL/min/1.73 m2 b.s.).ResultseGFR was higher in CPD patients than in UPD and LPD patients (21.9 ± 7.4 mL/min/1.73 m2 versus 17.6 ± 8.00 mL/min/1.73 m2 and 17.1 ± 7.5 mL/min/1.73 m2; P = 0.008). The real daily protein intake was higher in UPD patients than in LPD and CDP patients (0.80 ± 0.1 g/kg/day versus 0.6 ± 0.2 and 0.63 ± 0.2 g/kg/day; P = 0.01). Body mass index (BMI) was stable in the LPD and CPD groups but decreased from 28.5 ± 4.52 to 25.4 ± 3.94 kg/m2 in the UPD group (P < 0.001). The renal survival of UPD, LPD and CPD patients was 47.1, 84.3 and 90.7%, respectively, at 30 months (P < 0.001), 42.4, 72.0 and 79.1%, respectively, at 50 months (P < 0.001) and 42.4, 64.1 and 74.4%, respectively, at 70 months (P < 0.001). The LPD patients started dialysis nearly 24 months later than the UPD patients. Diet was an independent predictor of dialysis [−67% of RR reduction (hazard ratio = 0.33; confidence interval 0.22–0.48)] together with a reduction in BMI.ConclusionsAn LPD recommended by nephrologists in conjunction with skilled dietitians delays dialysis and preserves nutritional status in severe CKD.

Impact of gestational low protein diet and postnatal bisphenol A exposure on chemically induced mammary carcinogenesis in female offspring rats.

This study evaluated the effect of gestational low protein diet (LPD) and/or postnatal bisphenol A (BPA) exposure on mammary gland development and carcinogenesis in female offspring. Pregnant Sprague-Dawley rats were fed a normal protein diet (NPD, 17% protein) or LPD (6% protein). At weaning, female offspring were distributed in four groups (NPD, LPD, NPD + BPA, and LPD + BPA) and received vehicle or BPA in drinking water (0.1%), during postnatal day (PND) 21 to 51. On PND 51, some female offspring were euthanized or received a single dose of 7,12-dimethylbenzoanthracene (DMBA, 30 mg/kg, i.g.) and were euthanized on PND 250. On PND 51, neither gestational LPD nor postnatal BPA exposure, individually or in combination, significantly altered the development of mammary gland tree, mean number of terminal structures or estrogen receptor beta (ER-β), proliferating cell nuclear antigen (PCNA) or caspase-3 protein expression in the mammary tissue. A significant reduction in mammary epithelial area (%) was observed in both LPD groups and a significant increase in ER-α protein expression was detected only in LPD group. In LPD + BPA group was observed a significant increase in both fat pad area (%) and in mean number of mammary epithelial cells positive for progesterone receptor (PR). On PND 250, the groups that received BPA presented lower latency and higher tumor incidence and tumor multiplicity and LPD + BPA group more aggressive tumors. These findings suggest that postnatal BPA exposure associated with gestational LPD is able to induce morphological changes in the mammary gland and increase susceptibility to mammary carcinogenesis.

Efficacy of low-protein diet in diabetic nephropathy: a meta-analysis of randomized controlled trials

PurposeWe aimed to systematically assess the efficacy of low-protein diet preventing progression of diabetic nephropathy based on randomized controlled trials (RCTs).MethodsA systematic and electronic search was conducted. Initial searches of literature updated to September 2018 were made using the following databases including CNKI, VIP, Wanfang, Cochrane, PubMed, and Embase using the index words for qualified RCTs. Additional searches were performed to identify linked literature sources. Data of RCTs on low-protein diet versus control diet, efficacy analysis of kidney function, nutritional status or proteinuria were extracted. Random effects model and fixed effects model were applied to combine the data which were further analyzed by Chi-squared test and I2tests. The main outcomes were then analyzed through the use of relative risks (RR), mean difference (MD) and its 95% confidence interval (95% CI).ResultsTwenty articles were included in the present meta-analysis with a total of 690 patients in the low-protein diet group (LPD) and a total of 682 patients in the control group. Moderate to strong evidence indicated that LPD was significantly effective for decreasing the urinary albumin excretion rate (SMD:0.62, 95%CI:0.06–1.19) and proteinuria (SMD:0.69, 95%CI:0.22–1.16) versus the control group. No statistical difference, however, was found in glycosylated hemoglobin (SMD:0.17, 95%CI:-0.18–0.51), serum creatinine (SMD:0.20, 95%CI:-0.26–0.66), as well as glomerular filtration rate (SMD:0.21, 95%CI:-0.29–0.71) between the two groups.ConclusionThe current meta-analysis reveals an effective role of low-protein diet in improving diabetic nephropathy. However, the small number of involved patients may limit the accuracy of results. High-quality RCTs with a larger sample size in the future are required to confirm the current findings.

Impacts of low-protein diet on the hippocampal CA1 neurons and learning deficits in rats

Introduction: Proteins are the essential part of all organism cells. Nutrition plays the most important role in the structure and function of the brain. CA1 region belongs to hippocampus and plays a vital role in converting short-term to long-term memory. This study was designed to assess the effects of low-protein diet on hippocampal region CA1 and learning deficit in rats. Materials and Methods: In this study, 30 male rats were randomly assigned to two groups: control group and low-protein diet group (8% protein). Animals in a low-protein diet group have eaten food with low protein daily for 10 months. Body weight was measured. Transcardiac perfusion method was applied to tissue fixation. Passive avoidance learning of animals was examined by the shuttle-box apparatus technique. The number of dendritic spines was investigated by the Golgi staining technique. Furthermore, Cresyl violet staining method was used to determine the number of neurons in the hippocampal region CA1. Results: The passive avoidance learning of the low-protein diet rats was reduced significantly compared to the control ones (P

Very low protein diet plus ketoacid analogs of essential amino acids supplement to retard chronic kidney disease progression.

BackgroundA very low protein diet (VLPD) with ketoacid analogs of essential amino acids (KA/EAA) administration can remarkably influence protein synthesis and metabolic disturbances of patients with advanced chronic kidney disease (CKD), and may also slow the decline in renal function.MethodsA retrospective cohort study was carried out to monitor renal progression and metabolic and nutritional status among 140 patients with CKD stage III or IV. One group (n = 70) was on a low protein diet (LPD) with 0.6 g of protein intake, and another group (n = 70) was on a VLPD with 0.3 g of protein and KA/EAA supplementation of 100 mg/kg/day for 12 months.ResultsAt 12-month follow-up, estimated glomerular filtration rate (GFR) significantly decreased from 41.6 ± 10.2 to 36.4 ± 8.8 mL/min/1.73 m2 (P < 0.001) and urine protein increased from 0.6 ± 0.5 to 0.9 ± 1.1 g/day (P = 0.017) in the LPD group, but no significant changes in estimated GFR and urine protein were found in the VLPD plus KA/EAA group. A significant mean difference in rate of change in estimated GFR (−5.2 ± 3.6 mL/min/1.73 m2 per year; P < 0.001) was observed between the two groups. After Cox regression analysis, treatment with VLPD plus KA/EAA significantly protected against the incidence of declining GFR > 10% annually (adjusted hazard ratio, 0.42; 95% confidence interval, 0.23–0.79; P = 0.006) and significant correlations were found between using VLPD plus KA/EEA and increased GFR.ConclusionVLPD supplementation with KA/EAA is associated with delayed renal progression while preserving the nutritional status in the patients with CKD. Co-administration of VLPD and KA/EAA may prove an effective alternative to conservative management of CKD.

Hydroalcoholic extract of Brazilian green propolis modulates inflammatory process in mice submitted to a low protein diet

The occurrence of inflammation and protein malnutrition is an aggravating risk factor for morbidity and mortality in the clinical setting. The green propolis, a natural product made by Apis mellifera bees from Baccharis dracunculifolia resin, has therapeutic potential to modulate chronic inflammation. However, its effect on inflammation in an impaired nutritional status is not known. The aim of this study was to characterize the effects of the administration of the hydroalcoholic extract of the green propolis in the chronic inflammatory process of mice submitted to a low-protein diet. For this, we used the subcutaneous implantation of sponge disks as an inflammatory model and the animals were distributed in the following groups: standard protein diet (12% protein content), control treatment; standard protein diet, propolis treatment; low-protein diet (3% protein content), control treatment; low-protein diet, propolis treatment. Propolis was given daily at a dose of 500 mg/kg (p.o.) during a period of 7 or 15 days. Our main findings show that animals fed with standard protein diet and treated with propolis had low levels of red blood cells, hemoglobin, and hematocrit, with the subsequent reestablishment of these levels, in addition to monocyte count elevation and higher TNF levels after one week of treatment. In the low-protein diet group, the propolis treatment provided a significant recovery in weight and maintenance of total serum protein levels at the end of two weeks of treatment. Histological analysis showed propolis reduced the inflammatory infiltrate in the sponges of both standard and low-protein diet groups. In addition, the propolis extract presented antiangiogenic effect in both groups. Therefore, our data suggests that the hydroalcoholic extract of the green propolis promotes weight recovery and avoid the reduction of protein levels, in addition to inhibit inflammation and angiogenesis in animals fed with a low-protein diet.

Effect of a normal protein diet on oxidative stress and organ damage in malnourished rats

We investigated the effects of three weeks of renutrition with a normal protein diet on oxidant/antioxidant status in malnourished rats using biochemistry and histology. Eighteen young Wistar rats were divided into three groups: control group was fed on a normal protein diet; malnourished group was fed on low protein diet and renourished group was fed on low protein diet followed by a normal protein diet. Serum albumin was evaluated. Malondialdehyde, protein carbonyl, superoxide dismutase and catalase levels were determined in the intestine, muscle and liver. Intestinal and hepatic damage were assessed by histological examination. Protein malnutrition resulted in a significant decrease of body weight, albumin level, villus length, intraepithelial lymphocytes counts (IELC) and superoxide dismutase level (liver and muscle). However, catalase activity increased significantly in muscle and gut but there was no difference in liver. In all organs, malondialdehyde and protein carbonyl content of malnourished group showed a significant increase. Interestingly, a normal protein diet for three weeks resulted in a return to normal levels of superoxide dismutase, albumin, malondialdehyde and protein carbonyl in all organs. Catalase activity decreased in the muscle and gut and exhibited no significant difference in the liver. The renutrition diet enhanced also the recovery of intestinal epithelium by increasing villus length. Hepatic damage of rats fed normal protein diet was markedly reduced (macrovesicular steatosis decreased by 45%). The normal protein diet could improve the oxidant/antioxidant imbalance and organ damage induced by protein malnutrition.

Low-Protein Diets Decrease Porcine Nitrogen Excretion but with Restrictive Effects on Amino Acid Utilization.

Reducing dietary crude protein (CP) intake effectively decreases nitrogen excretion in growing-finishing pigs but at the expense of poor growth when dietary CP content is reduced by ≥3%. In this study, we investigated the main disadvantages of low-protein diets supplemented with lysine, methionine, threonine, and tryptophan in pigs. First, changes in the nitrogen balance in response to differences in dietary CP content (18%, 15%, and 13.5%) were investigated in barrows (40 kg). Then, barrows (40 kg) surgically fitted with catheters in the mesenteric vein, portal vein, hepatic vein, and carotid artery were used to investigate changes in amino acid (AA) metabolism in the portal-drained viscera and liver in response to differences in dietary CP content. The results showed that low-protein diets reduced fecal and urinary nitrogen excretion ( P < 0.05) meanwhile resulted in significant decreases in nitrogen retention ( P < 0.05). Moreover, a reduction in the dietary CP content from 18% to 13.5% resulted in decreases in the net portal fluxes of NH3, glycine, and alanine as well as in the urea production in the liver ( P < 0.05), whereas their values as a percentage of nitrogen intake did not decline ( P > 0.05). The net portal fluxes of nonessential AA (NEAA) were reduced in the low-protein diet groups ( P < 0.05), while essential AA consumption in the liver increased ( P < 0.05). Thus, low-protein diets result in reductions in both nitrogen excretion and retention, and NEAA deficiency may be a major disadvantage of low-protein diets.

Effect of oregano essential oil and benzoic acid supplementation to a low-protein diet on meat quality, fatty acid composition, and lipid stability of longissimus thoracis muscle in pigs

BackgroundConsumers are becoming increasingly interested in food containing appropriately high concentration of intramuscular fat (IMF) and polyunsaturated fatty acids (PUFA). The supplementation of feed with antioxidants decreases degradation of lipids in muscles thereby enhances nutritional and sensory properties of meat. Two experiments were conducted to determine the effects of adding oregano essential oil (OEO) and benzoic acid (BA) to low-protein, amino acid-supplemented diets on meat quality, sensory profile, fatty acid composition, and lipid oxidation of longissimus thoracis (LT) muscle in pigs.MethodsIn Exp. 1, 21 barrows were housed in metabolism cages and randomly allotted to 1 of 3 diets. The three diets were normal protein diet (NPD), medium protein diet (MPD) and low protein diet (LPD) with 1% and 2% less than NPD, respectively. In Exp. 2, 36 barrows were randomly divided into three experimental groups, namely, NPD, LPD, and identical LPD supplemented with blends of OEO (250 mg/kg feed) and BA (1000 mg/kg feed) (LPOB) groups.ResultsNo significant effects of diets on meat quality were observed in Exp. 1. The b*45min, tenderness, and IMF content in LPD muscle were higher than those in NPD and LPOB muscle. The LT muscle in LPD group contained a higher percentage of oleic acid (C18:1n-9) and a lower percentage of linoleic acid (C18:2n-6) than those in NPD group. Dietary LPOB improved oxidative stability, total superoxide dismutase, and glutathione peroxidase but decreased drip loss in LT muscle.ConclusionsThese findings suggest that growing-finishing pigs fed with a low-protein, amino acid-supplemented diet show a high content of intramuscular fat in the longissimus thoracis muscle. Dietary LPOB enhances the anti-oxidative status by improving antioxidative capacity but deteriorates the sensory attributes by decreasing IMF content of meat.

Maternal Low-Protein Diet Modulates Glucose Metabolism and Hepatic MicroRNAs Expression in the Early Life of Offspring †.

Emerging studies revealed that maternal protein restriction was associated with increased risk of type 2 diabetes mellitus in adulthood. However, the mechanisms of its effects on offspring, especially during early life of offspring, are poorly understood. Here, it is hypothesized that impaired metabolic health in offspring from maternal low-protein diet (LPD) is associated with perturbed miRNAs expression in offspring as early as the weaning age. We examined the metabolic effects on the C57BL/6J mice male offspring at weaning from dams fed with LPD or normal chow diet (NCD) throughout pregnancy and lactation. Maternal LPD feeding impaired metabolic health in offspring. Microarray profiling indicated that mmu-miR-615, mmu-miR-124, mmu-miR-376b, and mmu-let-7e were significantly downregulated, while, mmu-miR-708 and mmu-miR-879 were upregulated in LPD offspring. Bioinformatic analysis showed target genes were mapped to inflammatory-related pathways. Serum tumor necrosis factor-α (TNF-α) levels were higher and interleukin 6 (IL-6) had a tendency to be elevated in the LPD group. Finally, both mRNA and protein levels of IL-6 and TNF-α were significantly increased in the LPD group. Our findings provide novel evidence that maternal LPD can regulate miRNAs expression, which may be associated with chronic inflammation status and metabolic health in offspring as early as the weaning age.

The reduced/oxidized state of plasma albumin is modulated by dietary protein intake partly via albumin synthesis rate in rats

The reduced/oxidized state of plasma albumin is influenced by many factors, including chronic diseases and strenuous training. Recently, the reduced/oxidized state has also been shown to be associated with dietary protein and energy intakes in rats. We hypothesized that dietary protein intake may modulate the reduced/oxidized state of plasma albumin by altering the rate of albumin synthesis and that the reduced/oxidized state could therefore serve as a novel marker of protein undernutrition. We tested this hypothesis by examining male growing rats placed on a low-protein or energy-restriction diet. In the 4-week experiment, animals fed a low-protein diet (3% casein), whose dietary intakes were lower than those fed control diet (20% casein), showed significant decreases in plasma albumin level and the ratio of the reduced form of albumin to total albumin. Animals given the same amount of control diet as the low-protein diet group (approximately 30% energy restriction) also showed the above decreases, albeit to much more limited extents. The ratio of reduced to total plasma albumin correlated significantly with plasma albumin fractional synthesis rate. When animals were maintained on the low-protein diet for as long as 12 weeks and then fed the control diet for 1 week, the decreased ratio of reduced to total plasma albumin, but not plasma albumin level, resolved rapidly. The reduced/oxidized state of plasma albumin would thus reflect dietary protein status via plasma albumin turnover including the fractional synthesis rate and could prove useful as a sensitive marker of protein undernutrition.