Effect of low-protein intake on all-cause mortality in subjects with an estimated glomerular filtration rate higher than 60 mL/min/1.73 m2 with or without albuminuria.

BACKGROUND: We aimed to investigate the effect of a low-protein intake on all-cause mortality in subjects with an estimated glomerular filtration rate (eGFR) ≧60 mL/min/1.73 m2 with or without albuminuria using data from the National Health and Nutrition Examination Survey (NHANES). METHODS: We analysed participants in the NHANES from 2003 to 2010. We excluded participants with an eGFR less than 60 mL/min/1.73 m2 from the analyses. Low-protein intake was defined as a protein intake of less than 0.8 g/kg/day. The Healthy Eating Index 2010 was used to assess diet quality. The vital status of all participants in the NHANES was determined by linking to the National Death Index through the end of 2011. The hazard ratios (HRs) for the association of low-protein intake and mortality were determined using weighted Cox proportional hazards regression models. RESULTS: A total of 7730 participants were included in the analyses. After a median follow up of 4.7 years, 462 participants died. A low-protein intake was associated with a higher risk of mortality (HRs 1.394, 95% CI 1.121-1.734, P = .004) with adjustment for diet quality and relevant risk factors. The higher risk of mortality associated with a low-protein intake was consistent in subjects with or without albuminuria (P interaction .280). CONCLUSION: A protein intake of less than 0.8 g/kg/day was associated with a higher risk of mortality in subjects with an eGFR ≧60 mL/min/1.73 m2 , irrespective of whether they had albuminuria.

Feeding modality is a barrier to adequate protein provision in children receiving continuous renal replacement therapy (CRRT).

BACKGROUND: Critically ill children have a high prevalence of malnutrition. Children with acute kidney injury experience high rates of protein debt. Previous research has indicated that protein provision is positively associated with survival. METHODS: This was a prospective observational study of all patients receiving CRRT for greater than 48 h at our tertiary care institution. Patients with inborn errors of metabolism were excluded. Data collection included energy, protein, and fluid volume intakes, anthropometrics, feeding modality, and route of nutrition intake. RESULTS: Forty-one patients 9 ± 6.8 years of age, 66% male, received CRRT over a 10-month time period. CRRT treatment was 17.3 ± 25 days. Forty-one percent were malnourished via anthropometric criteria at CRRT start. Median protein delivery was 2 g/kg/day (IQR 1.4-2.5). Fifty-one percent received a combination of parenteral nutrition (PN) and enteral/oral feedings (EN), 34% received only PN, and 12% received only EN. Percentage of time meeting protein goals by modality was 27.6%, 34.6%, and 65.3% for those patients receiving solely EN, PN, and EN + PN combination, respectively. When weaned to only EN support from combination PN + EN, the average percentage of time protein goals were met decreased to 20.5% (p < 0.01). CONCLUSIONS: Without PN, patients on enteral/oral nutrition support fail to meet appropriate protein prescription. Transition of parenteral to enteral feeds was identified as a period of nutritional risk in children receiving CRRT.

Parenteral nutrition in intensive care patients: medicoeconomic aspects.

PURPOSE OF REVIEW: Parenteral nutrition (PN) alone or as supplemental parenteral nutrition (SPN) has been shown to prevent negative cumulative energy balance, to improve protein delivery and, in some studies, to reduce infectious morbidity in ICU patients who fail to cover their needs with enteral nutrition (EN) alone. RECENT FINDINGS: The optimization of energy provision to an individualized energy target using either early PN or SPN within 3-4 days after admission has recently been reported to be a cost-saving strategy mediated by a reduction of infectious complications in selected intensive care patients. SUMMARY: EN alone is often insufficient, or occasionally contraindicated, in critically ill patients and results in growing energy and protein deficit. The cost benefit of using early PN in patients with short-term relative contraindications to EN has been reported. In selected patients SPN has been associated with a decreased risk of infection, a reduced duration of mechanical ventilation, a shorter stay in the ICU. Altogether four studies have investigated the costs associated with these interventions since 2012: two of them from Australia and Switzerland have shown that optimization of energy provision using SPN results in cost reduction, conflicting with other studies. The latter encouraging findings require further validation.

The relevance of dietary protein after bariatric surgery: what do we know?

PURPOSE OF REVIEW: The growing obesity epidemic is associated with an increased demand for bariatric surgery with Roux-en-Y Gastric Bypass and Sleeve Gastrectomy as the most widely performed procedures. Despite beneficial consequences, nutritional complications may arise because of anatomical and physiological changes of the gastrointestinal tract. The purpose of this review is to provide an update of the recent additions to our understanding of the impact of bariatric surgery on the intake, digestion and absorption of dietary protein. RECENT FINDINGS: After bariatric surgery, protein intake is compromised because of reduced gastric capacity and aversion for certain foods. A minority of patients reaches the recommended protein intake of minimal 60 g per day, which results in the loss of fat-free mass rather than the desired loss of fat mass. Despite inadequate protein intake, protein digestion and absorption do not seem to be impaired suggesting that other mechanisms could counteract the reduced secretion of digestive enzymes and their delayed inlet. SUMMARY: After bariatric surgery, protein supplementation or diet enrichment could attribute to achieve the minimal recommended protein intake and benefit the amount and composition of postoperative weight loss.

Paricalcitol and Peritoneal Protein Loss in Peritoneal Dialysis: A Double-Center Study.

BACKGROUND/AIMS: Peritoneal protein loss (PPL) is associated with cardiovascular disease and mortality in peritoneal dialysis (PD). Controversial results have been published about the effect of paricalcitol in PPL among PD patients. This study intends to analyze the relationship between paricalcitol and PPL in PD. METHODS: In a retrospective study, prevalent PD patients were divided into 2 groups: "with paricalcitol" and "without paricalcitol". X2-test, Student's t test, Pearson correlation coefficient and Logistic Regression analysis were applied. RESULTS: Eighty-two patients were included. PPL was lower among patients medicated with paricalcitol (5.17 ± 1.71 vs. 6.79 ± 2.10 g/24 h, p = 0.0001). In multivariate analysis, paricalcitol and dialysate/plasma ratio of creatinine (D/P creatinine) were independently related to PPL (OR 4.270 [1.437-12.684], p = 0.009 and OR 0.205 [0.064-0.659], p = 0.008, respectively), adjusted for diabetes. CONCLUSION: Paricalcitol and D/P creatinine were independently related to PPL. Paricalcitol may have an effect on PPL in PD patients.

Associations between neighborhood food environments and deficient protein intake among elderly people in a metropolitan suburb: A case study in Kisarazu city, Japan.

OBJECTIVES: Living in a poor food environment and its association with an increased risk of inadequate nutrient intake are increasingly important issues in Japan due to an increase in the elderly population. METHODS: The present study examined the relationships between neighborhood food environment and the protein and fat intakes of elderly Japanese individuals (n = 181) living in the metropolitan Tokyo suburb of Kisarazu. RESULTS: A logistic regression analysis adjusted for sociodemographic and shopping behavior variables revealed associations between subjectively evaluated poor neighborhood food environment and deficient protein intake. However, there was no significant association between excessive fat intake and neighborhood food environments. CONCLUSION: The findings demonstrate that living in a poor neighborhood food environment, which is becoming increasingly prevalent in Japan and other developed countries, has the potential to result in malnutrition, or at least in a low-quality diet, in elderly populations.

Leucine restores murine hepatic triglyceride accumulation induced by a low-protein diet by suppressing autophagy and excessive endoplasmic reticulum stress.

Although it is known that a low-protein diet induces hepatic triglyceride (TG) accumulation in both rodents and humans, little is known about the underlying mechanism. In the present study, we modeled hepatic TG accumulation by inducing dietary protein deficiency in mice and aimed to determine whether certain amino acids could prevent low-protein diet-induced TG accumulation in the mouse liver. Mice fed a diet consisting of 3 % casein (3C diet) for 7 days showed hepatic TG accumulation with up-regulation of TG synthesis for the Acc gene and down-regulation of TG-rich lipoprotein secretion from hepatocytes for Mttp genes. Supplementing the 3 % casein diet with essential amino acids, branched-chain amino acids, or the single amino acid leucine rescued hepatic TG accumulation. In the livers of mice fed the 3 % casein diet, we observed a decrease in the levels of the autophagy substrate p62, an increase in the expression levels of the autophagy marker LC3-II, and an increase in the splicing of the endoplasmic reticulum (ER) stress-dependent Xbp1 gene. Leucine supplementation to the 3 % casein diet did not affect genes related to lipid metabolism, but inhibited the decrease in p62, the increase in LC3-II, and the increase in Xbp1 splicing levels in the liver. Our results suggest that ER stress responses and activated autophagy play critical roles in low-protein diet-induced hepatic TG accumulation in mice, and that leucine suppresses these two major protein degradation systems. This study contributes to understanding the mechanisms of hepatic disorders of lipid metabolism.

Perinatal low-protein diet alters brainstem antioxidant metabolism in adult offspring.

BACKGROUND AND OBJECTIVES: Studies in humans and animal models have established a close relationship between early environment insult and subsequent risk of development of non-communicable diseases, including the cardiovascular. Whereas experimental evidences highlight the early undernutrition and the late cardiovascular disease relation, the central mechanisms linking the two remain unknown. Owing to the oxidative balance influence in several pathologies, the aim of the present study was to evaluate the effects of maternal undernutrition (i.e. a low-protein (LP) diet) on oxidative balance in the brainstem. METHODS AND RESULTS: Male rats from mothers fed with an LP diet (8% casein) throughout the perinatal period (i.e. gestation and lactation) showed 10× higher lipid peroxidation levels than animals treated with normoprotein (17% casein) at 100 days of age. In addition, we observed the following reductions in enzymatic activities: superoxide dismutase, 16%; catalase, 30%; glutathione peroxidase, 34%; glutathione-S-transferase, 51%; glutathione reductase, 23%; glucose-6-phosphate dehydrogenase, 31%; and in non-enzymatic glutathione system, 46%. DISCUSSION: This study is the first to focus on the role of maternal LP nutrition in oxidative balance in a central nervous system structure responsible for cardiovascular control in adult rats. Our data observed changes in oxidative balance in the offspring, therefore, bring a new concept related to early undernutrition and can help in the development of a new clinical strategy to combat the effects of nutritional insult. Wherein the central oxidative imbalance is a feasible mechanism underlying the hypertension risk in adulthood triggered by maternal LP diet.

Exposure to increased levels of estradiol during development can have long-term effects on the response to undernutrition in female rats.

OBJECTIVES: Undernutrition during development alters the expression of peptides that control energy expenditure and feeding behavior. Estrogens can also modulate these peptides. Here, we analyze whether the early postnatal administration of estradiol modulates the effects of undernutrition on neuroendocrine parameters in adult female Wistar rats. METHODS: Control rats were fed a control diet. Undernourished pups were submitted to a restricted diet with half of the undernourished rats receiving 0.4 mg/kg s.c. of estradiol benzoate (EB) from postnatal day (P) 6 until P13. Quantitative real-time polymerase chain reaction was performed to determine expression in the hypothalamus of agouti-related peptide (AgRP), proopiomelanocortin (POMC), neuropeptide Y (NPY), and cocaine- and amphetamine-regulated transcript. Plasma estradiol, testosterone, and adiponectin levels were measured by enzyme-linked immunosorbent assay. Total and acylated ghrelin levels were measured in plasma by radioimmunoassay. Insulin and leptin were measured by mulitplex immunoassays. RESULTS: Undernourishment decreased body weight, fat mass, plasma leptin and insulin levels, and hypothalamic POMC mRNA levels. An increase in orexigenic signals AgRP and NPY mRNA levels, and in plasma adiponectin levels were found in undernourished animals. Early postnatal treatment with EB to undernourished female rats reversed the effects of undernutrition on adult hypothalamic POMC mRNA levels. In addition, neonatal EB treatment to undernourished females significantly decreased adult plasma testosterone, estradiol, and acylated ghrelin levels. DISCUSSION: Our results suggest that increased estradiol during a critical period of development has the capacity to modulate the alterations that undernutrition produces on energy metabolism.

[SURGICAL COMPLICATIONS IN ACUTE POISONING AND PROTEIN--ENERGY DYSFUNCTION].

The article presents a review of acute surgical pathology and the frequency of its occurrence, complicating alcohol poisoning, cauterizing liquids, narcotic and psychotropic drugs and acute emerging metabolic (protein-energy). The development of surgical complications in poisoning was observed in patients in severe and very severe condition and is accompanied by a sharp increase in mortality (75%) and severe energy dysfunction. The most diverse and difficult flowing surgical complications were encountered in alcohol poisoning and cauterizing liquids.

Maternal taurine supplementation in rats partially prevents the adverse effects of early-life protein deprivation on ß-cell function and insulin sensitivity.

Dietary protein restriction during pregnancy and lactation in rats impairs ß-cell function and mass in neonates and leads to glucose intolerance in adult offspring. Maternal taurine (Tau) supplementation during pregnancy in rats restores ß-cell function and mass in neonates, but its long-term effects are unclear. The prevention of postnatal catch-up growth has been suggested to improve glucose tolerance in adult offspring of low-protein (LP)-fed mothers. The objective of this study was to examine the relative contribution of ß-cell dysfunction and insulin resistance to impaired glucose tolerance in 130-day-old rat offspring of LP-fed mothers and the effects of maternal Tau supplementation on ß-cell function and insulin resistance in these offspring. Pregnant rats were fed i) control, ii) LP, and iii) LP+Tau diets during gestation and lactation. Offspring were given a control diet following weaning. A fourth group consisting of offspring of LP-fed mothers, maintained on a LP diet following weaning, was also studied (LP-all life). Insulin sensitivity in the offspring of LP-fed mothers was reduced in females but not in males. In both genders, LP exposure decreased ß-cell function. Tau supplementation improved insulin sensitivity in females and ß-cell function in males. The LP-all life diet improved ß-cell function in males. We conclude that i) maternal Tau supplementation has persistent effects on improving glucose metabolism (ß-cell function and insulin sensitivity) in adult rat offspring of LP-fed mothers and ii) increasing the amount of protein in the diet of offspring adapted to a LP diet after weaning may impair glucose metabolism (ß-cell function) in a gender-specific manner.

Protein deficiency alters CX3CL1 and endothelin-1 in experimental Trypanosoma cruzi-induced cardiomyopathy.

OBJECTIVE: Chagas heart disease is developed as a result of the infection with Trypanosoma cruzi. Protein malnutrition contributes to secondary immunodeficiency. The aim of this study was to investigate the role of a low protein diet on the production of endothelin-1 and CX3CL1 in blood and cardiac tissue samples in an experimental model with T. cruzi infection. METHODS: Fisher rats were submitted to low protein (6%) and normal protein (15%) diets and then infected with the Y strain of T. cruzi. At days 15 and 120, parasites and immune cells were evaluated. RESULTS: The low protein diet reduced body weight and circulating serum proteins, but promoted elevation of CX3CL1 and endothelin-1 levels in infected animals, which were unable to control blood parasitemia replication. In heart tissue, the low protein diet reduced cardiac CX3CL1, endothelin-1 and leucocyte infiltration in the acute phase, in particular CD68 and CD163 macrophage phenotypes. CONCLUSION: Together, these results highlight the participation of endothelin-1 and CX3CL1 in the inflammatory process of Chagas diesease, both being mediators partially controlled by the host nutritional status.

Treatment of metabolic syndrome by combination of physical activity and diet needs an optimal protein intake: a randomized controlled trial.

BACKGROUND: The recommended dietary allowance (RDA) for protein intake has been set at 1.0-1.3 g/kg/day for senior. To date, no consensus exists on the lower threshold intake (LTI = RDA/1.3) for the protein intake (PI) needed in senior patients ongoing both combined caloric restriction and physical activity treatment for metabolic syndrome. Considering that age, caloric restriction and exercise are three increasing factors of protein need, this study was dedicated to determine the minimal PI in this situation, through the determination of albuminemia that is the blood marker of protein homeostasis. METHODS: Twenty eight subjects (19 M, 9 F, 61.8 ± 6.5 years, BMI 33.4 ± 4.1 kg/m²) with metabolic syndrome completed a three-week residential programme (Day 0 to Day 21) controlled for nutrition (energy balance of -500 kcal/day) and physical activity (3.5 hours/day). Patients were randomly assigned in two groups: Normal-PI (NPI: 1.0 g/kg/day) and High-PI (HPI: 1.2 g/kg/day). Then, patients returned home and were followed for six months. Albuminemia was measured at D0, D21, D90 and D180. RESULTS: At baseline, PI was spontaneously 1.0 g/kg/day for both groups. Albuminemia was 40.6 g/l for NPI and 40.8 g/l for HPI. A marginal protein under-nutrition appeared in NPI with a decreased albuminemia at D90 below 35 g/l (34.3 versus 41.5 g/l for HPI, p < 0.05), whereas albuminemia remained stable in HPI. CONCLUSION: During the treatment based on restricted diet and exercise in senior people with metabolic syndrome, the lower threshold intake for protein must be set at 1.2 g/kg/day to maintain blood protein homeostasis.

Protein intake in renal and hepatic disease.

The kidney and the liver play a central role in protein metabolism. Synthesis of albumin and other proteins occurs mainly in the liver, whereas protein breakdown and excretion are handled through an intricate interaction between these two organ systems. Thus, disease states of either the liver and/or the kidney invariably result in clinically relevant disturbances of protein metabolism. Conversely, metabolic processes regulated by these two organs are directly affected by dietary protein intake. Of particular importance in this respect is the maintenance of acid/base homeostasis. Finally, both the amount and composition of ingested proteins have a direct impact on renal function, especially in a state of diseased kidneys. Consequently, dietary protein intake is of paramount importance in patients with chronic nephropathy and renal insufficiency. Limitation of ingested protein, particularly from animal sources, is crucial in order to slow the progression of chronic kidney disease and impaired renal function. In contrast, patients with chronic renal failure undergoing renal replacement therapy by hemodialysis or peritoneal dialysis, have an increased protein demand. The syndrome of "protein-energy malnutrition" is a relevant factor for morbidity and mortality in this population and requires early detection and vigorous treatment. Protein intake in patients with cirrhosis of the liver should not be diminished as has been earlier suggested but rather increased to 1.0 - 1.2 g/kg body weight/day, in order to prevent protein malnutrition. Moderate restriction depending on protein tolerance (0.5 - 1.2 g/kg body weight/day), with the possible addition of branched chain amino acids (BCAA), has been recommended only in patients with advanced hepatic encephalopathy. Proteins of plant origin are theoretically superior to animal proteins.

Impairment of G-CSF receptor on granulocytic progenitor cells causes neutropenia in protein malnutrition.

OBJECTIVE: It is well known that protein malnutrition (PM) states can affect hematopoiesis, leading to severe leukopenia and reduced number of granulocytes, which act as the first line of defense, and are important to the innate immune response. The aim of this study was to elucidate some of the mechanisms involved in the impairment of granulopoiesis in PM. METHODS: Male C57BL/6 mice were submitted to PM with a low-protein diet containing 2% protein. Control mice were fed a 12% protein-containing diet. Bone marrow histology and the percentage of granulocytic progenitors were evaluated after in vivo granulocyte-colony stimulating factor (G-CSF) stimulus. Cell proliferation, STAT3 signaling, and the expression of G-CSF receptor were evaluated in hematopoietic progenitor cells. RESULTS: Malnourished animals presented with leukopenia associated with reduced number of granulocytes and reduced percentage of granulocytic progenitors; however, no differences were observed in the regulatory granulopoietic cytokine G-CSF. Additionally, the malnourished group presented with impaired response to in vivo G-CSF stimulus compared with control animals. PM was implicated in decreased ability of c-Kit+ cells to differentiate into myeloid progenitor cells and downregulated STAT3 signaling. Furthermore, the malnourished group exhibited reduced expression of G-CSF receptor on granule-monocytic progenitors. This reduced expression was not completely reversible with G-CSF treatment. CONCLUSIONS: This study implies that PM promotes intrinsic alterations to hematopoietic precursors, which result in hematologic changes, mainly neutropenia, observed in peripheral blood in PM states.

The influences of low protein diet on the intestinal microbiota of mice.

Recent research suggests that protein deficiency symptoms are influenced by the intestinal microbiota. We investigated the influence of low protein diet on composition of the intestinal microbiota through animal experiments. Specific pathogen-free (SPF) mice were fed one of four diets (3, 6, 9, or 12% protein) for 4 weeks (n = 5 per diet). Mice fed the 3% protein diet showed protein deficiency symptoms such as weight loss and low level of blood urea nitrogen concentration in their serum. The intestinal microbiota of mice in the 3% and 12% protein diet groups at day 0, 7, 14, 21 and 28 were investigated by 16S rRNA gene sequencing, which revealed differences in the microbiota. In the 3% protein diet group, a greater abundance of urease producing bacterial species was detected across the duration of the study. In the 12% diet protein group, increases of abundance of Streptococcaceae and Clostridiales families was detected. These results suggest that protein deficiency may be associated with shifts in intestinal microbiota.