Levels Of Dietary Protein Intake Research Articles

Effects of Dietary Protein Intake Levels on Peripheral Circadian Rhythm in Mice.

The regulation of the circadian clock plays an important role in influencing physiological conditions. While it is reported that the timing and quantity of energy intake impact circadian regulation, the underlying mechanisms remain unclear. This study investigated the impact of dietary protein intake on peripheral clocks. Firstly, transcriptomic analysis was conducted to investigate molecular targets of low-protein intake. Secondly, mPer2::Luc knock-in mice, fed with either a low-protein, normal, or high-protein diet for 6 weeks, were analyzed for the oscillation of PER2 expression in peripheral tissues and for the expression profiles of circadian and metabolic genes. Lastly, the candidate pathway identified by the in vivo analysis was validated using AML12 cells. As a result, using transcriptomic analysis, we found that the low-protein diet hardly altered the circadian rhythm in the central clock. In animal experiments, expression levels and period lengths of PER2 were different in peripheral tissues depending on dietary protein intake; moreover, mRNA levels of clock-controlled genes and endoplasmic reticulum (ER) stress genes were affected by dietary protein intake. Induction of ER stress in AML12 cells caused an increased amplitude of Clock and Bmal1 and an advanced peak phase of Per2. This result shows that the intake of different dietary protein ratios causes an alteration of the circadian rhythm, especially in the peripheral clock of mice. Dietary protein intake modifies the oscillation of ER stress genes, which may play key roles in the regulation of the circadian clock.

Use of low-protein staple foods in the dietary management of patients with stage 3\u20134 chronic kidney disease: a prospective case-crossover study

ObjectiveMaintaining a low-protein diet (LPD) is important for patients with chronic kidney disease (CKD) to delay renal degradation and alleviate clinical symptoms. For most patients with CKD, it is difficult to maintain the necessary low level of dietary protein intake (DPI). To improve the current dietary management of CKD, we conducted an intervention study by administering low-protein staple foods (LPSF).Design and methodsWe conducted a prospective case-crossover study among 25 patients with stage 3–4 CKD. During the initial 12 weeks of the study, we instructed the patients regarding a standard LPD according to the recommendations of a renal dietitian. In the second stage of the study, we requested the patients taking low-protein rice or low-protein flour (250 g/d) as an LPSF diet instead of regular staple food daily, and followed these patients up for 12 weeks. We compared the DPI, dietary energy intake (DEI), normalized protein equivalent of total nitrogen appearance (nPNA), serum creatinine levels, and nutritional index between baseline and the end of the study.ResultsWe found no change in dietary variables among the patients during the first 12 weeks of the LPD. After subjecting them to an LPSF diet, the corresponding variables showed a pronounced change. The patients’ DPI decreased from 0.88 ± 0.20 to 0.68 ± 0.14 g/kg/d (P < 0.01) and the nPNA value decreased from 0.99 ± 0.18 to 0.87 ± 0.19 g/kg/d (P < 0.01). The high biological value protein intake proportion increased from 42% (baseline) to 57% (P < 0.01) during the 24 weeks. No variation was found in the measured DEI (28.0 ± 5.8 vs 28.6 ± 5.4 kcal/kg/d), nutrition assessment, or renal function and serum creatinine levels.ConclusionOur prospective case-crossover study demonstrated that an LPSF diet can help patients with stage 3–4 CKD reduce DPI and nPNA values, improve the proportion of highly bioavailable proteins, ensure adequate calorie intake, and avoid malnutrition. An LPSF diet is an effective and simple therapy for patients with stage 3–4 CKD.

A-posteriori protein-rich dietary patterns and their association with ten-year transition to metabolically unhealthy status: highlights from a population-based cohort study

Abstract Background/Introduction The role of dietary protein on cardiometabolic health remains complex influenced by concomitant changes in overall diet composition. The quality of protein sources is currently suggested as more detrimental than the level of consumption itself. Purpose The association between different protein-rich dietary patterns and 10-year transition to metabolically unhealthy status in a sample from Greece was evaluated. Methods A prospective study was conducted during 2001–2012 studying n=1,514 men and n=1,528 women (&amp;gt;18 years old) free of CVD. Healthy metabolic status was defined as absence of all NCEP ATP III (2005) metabolic syndrome components. Baseline dietary assessment was based on a validated semi-quantitative food frequency questionnaire. Dietary protein was calculated through standardized food database. Follow-up cardiometabolic assessment (2011–2012) was achieved in n=2,020 participants. Protein-rich dietary patterns were derived through factor analysis in the subsample of participants with high daily protein intake (&amp;gt;15% of total energy intake corresponding to the median consumption level). Patterns were named according to food scores that correlated most with the factor (scores&amp;gt;0.5). Results Overall, six of ten participants lost their metabolically healthy status within a decade. Multiadjusted analysis revealed an inverse yet non-significant association between total energy-standardized protein intake and transition to metabolically unhealthy status [Odds ratio (OR) (high vs. low protein intake)=0.59, 95% Confidence Interval (95% CI) (0.32, 1.10), p=0.09]. Factor analysis extracted three protein-rich dietary patterns, explained 55% of the total variation in intake. Factor A was characterized by increased consumption of processed meet, unprocessed red meat and eggs, factor B was characterized by increased consumption of nuts and seeds, legumes, whole grain products and fish while factor C was characterized by increased consumption of dairy products, poultry and vegetables. Multiadjusted logistic regression analysis revealed that factor B had the strongest protective effect against 10-year transition to metabolically unhealthy status [ORper 1 point increase in factor B score=0.74, 95% CI (0.60, 0.85), p=0.01] followed by a marginally protective effect of factor C [ORper 1 point increase in factor C score=0.89, 95% CI (0.73, 1.05), p=0.07]. Participants with higher adherence to factor A had an increased likelihood to lose their metabolically healthy status [ORper 1 point increase in factor A score=1.15, 95% CI (1.02, 1.30), p=0.04]. Conclusions The present work confirms that within an increased level of dietary protein intake, different cardiometabolic outcomes were observed according to the quality of protein food sources consumed. Funding Acknowledgement Type of funding sources: None.

Effect of Overeating Dietary Protein at Different Levels on Circulating Lipids and Liver Lipid: The PROOF Study.

Background: During overeating, a low protein diet slowed the rate of weight gain and increased the energy cost of the added weight, suggesting that low protein diets reduced energy efficiency. The Protein Overfeeding (PROOF) study explored the metabolic changes to low and high protein diets, and this sub-study examined the changes in body composition and blood lipids when eating high and low protein diets during overeating. Methods: Twenty-three healthy volunteers (M = 14; F = 9) participated in an 8-week, parallel arm study where they were overfed by ~40% with diets containing 5% (LPD = low protein diet), 15% (NPD = normal protein diet), or 25% (HPD = high protein diet) protein. Dual energy X-ray absorptiometry (DXA) and computer tomography (CT) were used to quantify whole body and abdominal fat and intrahepatic lipid, respectively. Metabolites were measured by standard methods. Results: Protein intake and fat intake were inversely related since carbohydrate intake was fixed. Although overeating the LPD diet was associated with a significant increase in high density lipoprotein (HDL)-cholesterol (p < 0.001) and free fatty acids (p = 0.034), and a significant decrease in fat free mass (p < 0.0001) and liver density (p = 0.038), statistical models showed that dietary protein was the main contributor to changes in fat free mass (p = 0.0040), whereas dietary fat was the major predictor of changes in HDL-cholesterol (p = 0.014), free fatty acids (p = 0.0016), and liver fat (p = 0.0007). Conclusions: During 8 weeks of overeating, the level of dietary protein intake was positively related to the change in fat free mass, but not to the change in HDL-cholesterol, free fatty acids, and liver fat which were, in contrast, related to the intake of dietary fat.

Dietary protein interventions to improve nutritional status in end-stage renal disease patients undergoing hemodialysis.

Poor nutritional status is prevalent among end-stage renal disease patients undergoing hemodialysis. Chronic hemodialysis patients show an accelerated decline in skeletal muscle mass and strength, which is associated with higher mortality rates and a reduced quality of life. The current review aims to summarize recent advances regarding underlying causes of muscle loss and interventions that support muscle mass maintenance in patients with chronic hemodialysis. Muscle maintenance in chronic hemodialysis patients is compromised by low dietary protein intake levels, anabolic resistance of skeletal muscle tissue, sedentary behavior, and amino acid removal during hemodialysis. Studies assessing the effect of increased protein intake on nutritional status generally show beneficial results, especially in hypoalbuminemic chronic hemodialysis patients. The muscle protein synthetic response following protein ingestion in chronic hemodialysis patients may be enhanced through incorporation of structured physical activity and/or concurrent ketoacid ingestion. A coordinated program that combines nutritional and physical activity interventions is likely required to attenuate the decline in muscle mass and strength of chronic hemodialysis patients. Nephrologists, dieticians, and exercise specialists should collaborate closely to establish guidelines regarding the appropriate quantity and timing of protein ingestion. In addition, they should provide tailored nutritional and physical activity interventions for chronic hemodialysis patients (see video, Supplemental Digital Content 1, Video abstract, http://links.lww.com/COCN/A14).

Complete replacement of fishmeal by soybean and poultry meals in Pacific whiteleg shrimp feeds: Growth and tolerance to EMS/AHPND and WSSV challenge

Corresponding to projected global population growth, the world's food production systems must likewise enlarge substantially if current levels of dietary protein intake are to be maintained. The anticipated growth curve for global aquaculture, and especially for shrimp farming, which is forecast to double production by 2030, will inevitably result in shortfalls in currently favored dietary ingredients: fishmeal (FM) and fish oil (FO). Servicing the projected FM-FO shortfall with marine products would be a formidable task as economic, social, moral, safety and environmental issues have forced the feed sector to examine the use of alternative, non-marine, ingredients. Herein, various alternative protein and lipid sources were evaluated as substitutes for FM-FO in Pacific whiteleg shrimp diets. Growth trials were coupled to challenges with viral and bacterial pathogens to assess potential benefit or disadvantage of ingredient switching. No differences (P > .05) were observed between control and test diets regarding growth or survival, Average Daily Gain (g d−1) or Specific Growth Rate (% d−1) over a 56-day period. Moreover, response to post-feeding trial challenge with EMS/AHPND or WSSV also did not differ between diets (P > .05). However, there was a difference in size/age responsiveness to bacterial challenge, with younger animals succumbing to infection more rapidly (P ≤ .035). Similar responses were observed for shrimp exposed to WSSV over the first 5-days post-challenge (P ≤ .02) after which survival rates equalized. Overall, the results support the sustained belief that FM-FO constituents of Pacific whiteleg shrimp diets can be totally replaced by non-marine ingredients that are nutritionally equivalent. Improvement in responsiveness to substitute proteins and oils might be further gained with more judicious blending of ingredients and use of other additives. Such manipulations could also result in less expensive sustainable feeds.

Effects of a high protein diet and liver disease in an in silico model of human ammonia metabolism

BackgroundAfter proteolysis, the majority of released amino acids from dietary protein are transported to the liver for gluconeogenesis or to peripheral tissues where they are used for protein synthesis and eventually catabolized, producing ammonia as a byproduct. High ammonia levels in the brain are a major contributor to the decreased neural function that occurs in several pathological conditions such as hepatic encephalopathy when liver urea cycle function is compromised. Therefore, it is important to gain a deeper understanding of human ammonia metabolism. The objective of this study was to predict changes in blood ammonia levels resulting from alterations in dietary protein intake, from liver disease, or from partial loss of urea cycle function.MethodsA simple mathematical model was created using MATLAB SimBiology and data from published studies. Simulations were performed and results analyzed to determine steady state changes in ammonia levels resulting from varying dietary protein intake and varying liver enzyme activity levels to simulate liver disease. As a toxicity reference, viability was measured in SH-SY5Y neuroblastoma cells following differentiation and ammonium chloride treatment.ResultsResults from control simulations yielded steady state blood ammonia levels within normal physiological limits. Increasing dietary protein intake by 72% resulted in a 59% increase in blood ammonia levels. Simulations of liver cirrhosis increased blood ammonia levels by 41 to 130% depending upon the level of dietary protein intake. Simulations of heterozygous individuals carrying a loss of function allele of the urea cycle carbamoyl phosphate synthetase I (CPS1) gene resulted in more than a tripling of blood ammonia levels (from roughly 18 to 60 μM depending on dietary protein intake). The viability of differentiated SH-SY5Y cells was decreased by 14% by the addition of a slightly higher amount of ammonium chloride (90 μM).ConclusionsData from the model suggest decreasing protein consumption may be one simple strategy to decrease blood ammonia levels and minimize the risk of developing hepatic encephalopathy for many liver disease patients. In addition, the model suggests subjects who are known carriers of disease-causing CPS1 alleles may benefit from monitoring blood ammonia levels and limiting the level of protein intake if ammonia levels are high.

Dietary Protein Intake Level Modulates Mucosal Healing and Mucosa-Adherent Microbiota in Mouse Model of Colitis.

Mucosal healing after an inflammatory flare is associated with lasting clinical remission. The aim of the present work was to evaluate the impact of the amount of dietary protein on epithelial repair after an acute inflammatory episode. C57BL/6 DSS-treated mice received isocaloric diets with different levels of dietary protein: 14% (P14), 30% (P30) and 53% (P53) for 3 (day 10), 6 (day 13) and 21 (day 28) days after the time of colitis maximal intensity. While the P53 diet worsened the DSS- induced inflammation both in intensity and duration, the P30 diet, when compared to the P14 diet, showed a beneficial effect during the epithelial repair process by accelerating inflammation resolution, reducing colonic permeability and increasing epithelial repair together with epithelial hyperproliferation. Dietary protein intake also impacted mucosa-adherent microbiota composition after inflammation since P30 fed mice showed increased colonization of butyrate-producing genera throughout the resolution phase. This study revealed that in our colitis model, the amount of protein in the diet modulated mucosal healing, with beneficial effects of a moderately high-protein diet, while very high-protein diet displayed deleterious effects on this process.

Effects of education on low-phosphate diet and phosphate binder intake to control serum phosphate among maintenance hemodialysis patients: A randomized controlled trial.

BackgroundFor phosphate control, patient education is essential due to the limited clearance of phosphate by dialysis. However, well-designed randomized controlled trials about dietary and phosphate binder education have been scarce.MethodsWe enrolled maintenance hemodialysis patients and randomized them into an education group (n = 48) or a control group (n = 22). We assessed the patients’ drug compliance and their knowledge about the phosphate binder using a questionnaire.ResultsThe primary goal was to increase the number of patients who reached a calcium-phosphorus product of lower than 55. In the education group, 36 (75.0%) patients achieved the primary goal, as compared with 16 (72.7%) in the control group (P = 0.430). The education increased the proportion of patients who properly took the phosphate binder (22.9% vs. 3.5%, P = 0.087), but not to statistical significance. Education did not affect the amount of dietary phosphate intake per body weight (education vs. control: −1.18 ± 3.54 vs. −0.88 ± 2.04 mg/kg, P = 0.851). However, the dietary phosphate-to-protein ratio tended to be lower in the education group (−0.64 ± 2.04 vs. 0.65 ± 3.55, P = 0.193). The education on phosphate restriction affected neither the Patient-Generated Subjective Global Assessment score (0.17 ± 4.58 vs. −0.86 ± 3.86, P = 0.363) nor the level of dietary protein intake (−0.03 ± 0.33 vs. −0.09 ± 0.18, P = 0.569).ConclusionEducation did not affect the calcium-phosphate product. Education on the proper timing of phosphate binder intake and the dietary phosphate-to-protein ratio showed marginal efficacy.

Low-protein diet for conservative management of chronic kidney disease: a systematic review and meta-analysis of controlled trials.

BackgroundRecent data pose the question whether conservative management of chronic kidney disease (CKD) by means of a low‐protein diet can be a safe and effective means to avoid or defer transition to dialysis therapy without causing protein‐energy wasting or cachexia. We aimed to systematically review and meta‐analyse the controlled clinical trials with adequate participants in each trial, providing rigorous contemporary evidence of the impact of a low‐protein diet in the management of uraemia and its complications in patients with CKD.MethodsWe searched MEDLINE (PubMed) and other sources for controlled trials on CKD to compare clinical management of CKD patients under various levels of dietary protein intake or to compare restricted protein intake with other interventions. Studies with similar patients, interventions, and outcomes were included in the meta‐analyses.ResultsWe identified 16 controlled trials of low‐protein diet in CKD that met the stringent qualification criteria including having 30 or more participants. Compared with diets with protein intake of >0.8 g/kg/day, diets with restricted protein intake (<0.8 g/kg/day) were associated with higher serum bicarbonate levels, lower phosphorus levels, lower azotemia, lower rates of progression to end‐stage renal disease, and a trend towards lower rates of all‐cause death. In addition, very‐low‐protein diets (protein intake <0.4 g/kg/day) were associated with greater preservation of kidney function and reduction in the rate of progression to end‐stage renal disease. Safety and adherence to a low‐protein diet was not inferior to a normal protein diet, and there was no difference in the rate of malnutrition or protein‐energy wasting.ConclusionsIn this pooled analysis of moderate‐size controlled trials, a low‐protein diet appears to enhance the conservative management of non‐dialysis‐dependent CKD and may be considered as a potential option for CKD patients who wish to avoid or defer dialysis initiation and to slow down the progression of CKD, while the risk of protein‐energy wasting and cachexia remains minimal.

Red Meat Intake and Risk of ESRD.

Randomized controlled trials suggest that protein restriction may retard the progression of CKD toward ESRD. However, the effects of dietary protein intake level and the food sources of dietary protein on the risk of ESRD in the general population remain unclear. We investigated these effects in the Singapore Chinese Health Study, a prospective population-based cohort that recruited 63,257 Chinese adults aged 45-74 years from 1993 to 1998. We collected habitual diet information via a validated semiquantitative food frequency questionnaire and identified ESRD via record linkage with a nationwide registry. In all, 951 cases of ESRD occurred over a mean follow-up of 15.5 years. Regarding total protein intake, compared with the lowest quartile, the three higher quartiles combined had a hazard ratio for ESRD of 1.24 (95% confidence interval [95% CI], 1.05 to 1.46), but the dose-dependent association across the quartiles was not statistically significant (Ptrend=0.16). Red meat intake strongly associated with ESRD risk in a dose-dependent manner (hazard ratio for highest quartile versus lowest quartile,1.40 [95% CI, 1.15 to 1.71; Ptrend<0.001]). Intake of poultry, fish, eggs, or dairy products did not associate with risk of ESRD. In substitution analysis, replacing one serving of red meat with other food sources of protein associated with a maximum relative risk reduction of 62.4% (95% CI, 33.1 to 78.9; P<0.01). Our study shows that red meat intake may increase the risk of ESRD in the general population and substituting alternative sources of protein may reduce the incidence of ESRD.

Dietary Protein Intake in a Multi-ethnic Asian Population of Healthy Participants and Chronic Kidney Disease Patients

Clinical practice guidelines recommend different levels of dietary protein intake in predialysis chronic kidney disease (CKD) patients. It is unknown how effectively these recommendations perform in a multi-ethnic Asian population, with varied cultural beliefs and diets. We assess the profi le of protein intake in a multi-ethnic Asian population, comparing healthy participants and CKD patients. We analysed the 24-hour urine collections of the Asian Kidney Disease Study (AKDS) and the Singapore Kidney Function Study (SKFS) to estimate total protein intake (TPI; g/day). We calculated ideal body weight (IDW; kg): 22.99 × height2 (m). Standard statistical tests were applied where appropriate, and linear regression was used to assess associations of continuous variables with protein intake. There were 232 CKD patients and 103 healthy participants with 35.5% diabetics. The mean TPI in healthy participants was 58.89 ± 18.42 and the mean TPI in CKD patients was 53.64 ± 19.39. By US National Kidney Foundation (NKF) guidelines, 29/232 (12.5%) of CKD patients with measured glomerular filtration rate (GFR) <25 (in mL/min/1.73 m2) had a TPI-IDW of <0.6 g/kg/day. By Caring for Australasians with Renal Impairment (CARI) guidelines, 76.3% (177/232) of CKD patients had TPI-IDW >0.75g/kg/ day. By American Dietetic Association (ADA) guidelines, 34.7% (44/127) of CKD patients with GFR <50 had TPI-IDW between 0.6 to 0.8 g/kg/day. Only 1/6 non-diabetic CKD patients with GFR <20 had a protein intake of between 0.3 to 0.5 g/kg/day. A total of 21.9% (25/114) of diabetic CKD patients had protein intake between 0.8 to 0.9 g/kg/day. On average, the protein intake of most CKD patients exceeds the recommendations of guidelines. Diabetic CKD patients should aim to have higher protein intakes.

The mean dietary protein intake at different stages of chronic kidney disease is higher than current guidelines

The actual dietary protein intake of adults without and with different stages of chronic kidney disease is not known. To evaluate this we performed cross-sectional analyses of 16,872 adults (20 years of age and older) participating in the National Health and Nutrition Examination Survey 2001-2008 who completed a dietary interview by stage of kidney disease. Dietary protein intake was assessed from 24-h recall systematically collected using the Automated Multiple Pass Method. Complex survey analyses were used to derive population estimates of dietary protein intake at each stage of chronic kidney disease. Using dietary protein intake of adults without chronic kidney disease as the comparator, and after adjusting for age, the mean dietary protein intake was 1.30 g/kg ideal body weight/day (g/kgIBW/d) and was not different from stage 1 or stage 2 (1.28 and 1.25 g/kgIBW/d, respectively), but was significantly different in stage 3 and stage 4 (1.22 and 1.13 g/kgIBW/d, respectively). These mean values appear to be above the Institute of Medicine requirements for healthy adults and the NKF-KDOQI guidelines for stages 3 and 4 chronic kidney disease. Thus, the mean dietary protein intake is higher than current guidelines, even after adjusting for age.

Calcium absorption and bone density in immature horses fed two levels of crude protein

Research in other animal models indicate that high protein diets increase urinary calcium (Ca) excretion and may lead to a negative Ca balance and reduced bone density. This study was undertaken to determine the effects of two common levels of dietary protein intake on physiological parameters, Ca absorption, and bone density in immature horses. Sixteen 10-month old horses were blocked by age and sex into two dietary treatments. The control diet (C) was formulated using common ingredients to provide 100% of the National Research Council (NRC) for crude protein (CP), while the high protein diet (H) was formulated at 150% of NRC recommendations. Lower than expected dietary intake resulted in mean protein intake of 769±16 g/d in C and 978±18 g/d in H, equivalent to 91% and 116% of NRC, respectively. Blood, urine, and faeces were collected during the 112-day study to determine pH and mineral balance. Radiographs of the left third metacarpal were used to estimate bone density via radiographic bone aluminum equivalence (RBAE). Although urine pH decreased over time (P&lt;0.001), no change in blood or urine pH was observed due to diet. Faecal pH, normalised to day 0, was significantly lower in H (P&lt;0.02). Faecal Ca loss was greater in H (P&lt;0.005); while Ca absorption and absorption as a percent of intake were lower for H (P&lt;0.02). RBAE of dorsal and palmar cortices increased over time (P&lt;0.001), but no differences were observed between diets. While excess dietary protein decreased faecal pH, increased faecal Ca excretion, and decreased Ca absorption, there appeared to be no effect on bone density over the course of this study.

A high protein diet upregulates whole‐body protein turnover during energy deficit

The effects of dietary protein level on whole‐body protein turnover (WBPTO) during energy deficit (ED) are not well described. Using a randomized‐block design, 24 males and five females (21 ± 3 yr) participated in a controlled trial. Volunteers consumed either standard (SP; 0.8 g·kg−1·d−1), moderate (MP; 1.6 g·kg−1·d−1), or high (HP; 2.4 g·kg−1·d−1) protein diets for 31 days. A weight maintenance (WM, days 1–10) period was followed by 21 days of ED (days 11–31), during which energy intake was restricted to 60% of total daily energy expenditure. Whole‐body protein breakdown, synthesis, and oxidation were determined at rest during WM (day 10) and ED (day 31) using primed, continuous [13C]‐leucine infusions. Volunteers lost (P &lt; 0.05) 3.3 ± 0.9 kg body mass in response to ED regardless of dietary protein level. Protein breakdown decreased (P &lt; 0.05) in response to ED for SP and MP diets, but did not change for HP. Synthesis decreased (P &lt; 0.05) following ED regardless of dietary protein level. Protein oxidation (μmol·kg−1·h−1) increased linearly between SP (9.7 ± 0.5), MP (11.8 ± 0.5), and HP (13.9 ± 0.5) diets during WM, with increased oxidation observed only for HP (16 ± 0.7) during ED (diet‐by‐energy interaction, P &lt; 0.05). These data demonstrate that the level of dietary protein intake modulates WBPTO during sustained ED, as consumption of a high protein diet upregulates WBPTO during ED.

Level of dietary protein intake affects glucose turnover in endurance-trained men

BackgroundTo examine the effects of higher-protein diets on endogenous glucose metabolism in healthy, physically active adults, glucose turnover was assessed in five endurance-trained men (age 21.3 ± 0.3 y, VO2peak 70.6 ± 0.1 mL kg-1 min-1) who consumed dietary protein intakes spanning the current dietary reference intakes.FindingsUsing a randomized, crossover design, volunteers consumed 4 week eucaloric diets providing either a low (0.8 g kg-1 d-1; LP), moderate (1.8 g kg-1 d-1; MP), or high (3.6 g kg-1 d-1; HP) level of dietary protein. Glucose turnover (Ra, glucose rate of appearance; and Rd glucose rate of disappearance) was assessed under fasted, resting conditions using primed, constant infusions of [6,6-2H2] glucose. Glucose Ra and Rd (mg kg-1 min-1) were higher for MP (2.8 ± 0.1 and 2.7 ± 0.1) compared to HP (2.4 ± 0.1 and 2.3 ± 0.2, P < 0.05) and LP (2.3 ± 0.1 and 2.2 ± 0.1, P < 0.01) diets. Glucose levels (mmol/L) were not different (P > 0.05) between LP (4.6 ± 0.1), MP (4.8 ± 0.1), and HP (4.7 ± 0.1) diets.ConclusionsLevel of protein consumption influenced resting glucose turnover in endurance athletes in a state of energy balance with a higher rate of turnover noted for a protein intake of 1.8 g kg-1 d-1. Findings suggest that consumption of protein in excess of the recommended dietary allowance but within the current acceptable macronutrient distribution range may contribute to the regulation of blood glucose when carbohydrate intake is reduced by serving as a gluconeogenic substrate in endurance-trained men.

Metabolic Adjustments to Varying Protein Intake in Harbor Seals (Phoca vitulina): Evidence from Serum Free Amino Acids

Effects of varying dietary protein intake on serum free amino acid (FAA) concentrations were studied in harbor seals (Phoca vitulina) fed two different prey fish diets: either exclusively low-fat, high-protein walleye pollock (Theragra chalcogramma) or high-fat, relatively high-energy-density Pacific herring (Clupea pallasi). Significant differences in FAA concentrations and patterns were observed between the two diets. All essential amino acids (EAA), except methionine and phenylalanine, and two nonessential amino acids (NEAA), glycine and tyrosine, decreased when the diet was switched from herring to pollock and increased on switching back to herring. Both total EAA concentrations and EAA : NEAA ratios decreased with the elevated protein intake typical of a low-fat pollock diet, indicating an inverse correlation between EAA concentrations and dietary protein intake levels. We propose that differing dietary protein intake, caused by differences in macronutrient composition of the two prey fish species, induced a change in protein metabolism that was reflected in blood-circulating amino acids. These findings suggest that surveys of amino acid profiles may be useful to partially determine the protein metabolic status of harbor seals.

Menu Suggestion: An Effective Way to Improve Dietary Compliance in Peritoneal Dialysis Patients

Poor compliance with the dietary prescriptions is quite common in dialysis patients. We believe that most of the noncompliance is caused by the patient's poor understanding of the dietary prescription. Therefore, in the present study, we tried to investigate the role of menu suggestion in improving the patient's compliance with the dietary prescription. A longitudinal cohort study conducted at an outpatient dialysis clinic. Seventy clinically stable patients on peritoneal dialysis were included in this prospective study during April 1, 2004, to November 31, 2004, in a single center. Patients who had significant cognitive impairment and thus did not understand the food contents during the training course were not eligible for enrollment. All the patients were randomly assigned to 1 of 2 groups. Group 1 patients received the traditional patient education method. Group 2 patients additionally received individualized menu suggestions based on their food preferences and education on how to exchange the foods at equivalent amounts according to the exchange list. At present, there are no clear optimal dietary protein intake levels for peritoneal dialysis patients. Our experience is that a dietary protein intake level of 0.8 to 1.2 g/kg/d can maintain our patients in a good nutritional status. Thereafter, in this study we prescribed the dietary protein intake level at 0.8 to 1.2 g/kg/d and defined compliance as meeting this target protein intake level. There were 35 patients in each group. The compliance was 22.9% in group 1 and 57.1% in group 2 (P < .05). Our study suggests that menu suggestion may be an effective way of improving the compliance with the diet in peritoneal dialysis patients. It improves the patient's understanding of the dietary prescription.

Long–term dietary high protein intake up–regulates tissue specific gene expression of uncoupling proteins 1 and 2 in rats

The consequences of chronic high protein (HP) diets are discussed controversially and are not well understood. Rats adapted to HP exposure show an increased amino acid and fat oxidation and lower feed energy efficiency. We hypothesized that the dietary protein level can affect gene expression of uncoupling protein (UCP) homologues which is suggested to be involved in thermogenesis, substrate oxidation, and energy expenditure. To assess the mRNA expression of UCP homologues in various tissues of rats fed HP diets and to relate UCP gene expression to various parameters of substrate and energy metabolism. To obtain further indications for the possible involvement of UCP in reducing feed energy efficiency under conditions of HP exposure. Adult rats were adapted to casein based diets containing either 13.8% (adequate, AP), 25.7% (medium, MP), or 51.3 % (high, HP) crude protein. Rats were fed for 8 wk and killed in the postabsorptive state. Energy expenditure and mRNA expression were measured using indirect calorimetry and Northern blot analysis, respectively. Pearson correlation coefficients were calculated to determine relationships between UCP mRNA expression and metabolic parameters. Hepatic UCP2 mRNA expression was increased by MP and HP diets compared to AP diet. In skeletal muscle UCP2 mRNA expression was lowest under MP conditions. UCP1 mRNA expression in brown adipose tissue (BAT) was significantly increased by HP exposure. The values were inversely associated with feed energy efficiency and positively with energy expenditure and oxygen consumption in the dark period. Skeletal muscle UCP2 and -3 mRNA expression strongly correlated with the plasma free fatty acid concentration, whereas BAT UCP1 and hepatic UCP2 gene expression did not. Our results indicate that hepatic UCP2 and BAT UCP1 mRNA expression is related to the level of dietary protein intake. This suggests a role of UCPs in substrate oxidation and in thermogenesis under conditions of HP exposure.

Growth hormone and amino acid supply interact synergistically to control insulin-like growth factor-I production and gene expression in cultured ovine hepatocytes.

Many of the anabolic effects of growth hormone (GH) are indirect, occurring through GH-stimulated production of insulin-like growth factor-I (IGF-I) by the liver. As well as being regulated by GH, plasma IGF-I concentrations have been demonstrated to depend upon the level of dietary protein intake, with low protein diets being associated with reduced circulatory IGF-I levels. This inhibitory effect cannot be reversed by GH injection, suggesting that liver sensitivity to GH becomes impaired.To investigate the mechanisms through which protein supply affects GH sensitivity, primary cultures of ovine hepatocytes were grown in defined media, containing various proportions (0.2, 1.0 and 5.0) of jugular amino acid concentrations in fed sheep. Production of IGF-I by these cells was measured after 24 and 48 h in culture by radioimmunoassay. In the first 24-h period basal IGF-I production was the same in all defined media, and GH caused an approximately 2-fold increase in IGF-I release in cells grown in 1.0xor 5.0xamino acid media (P<0.01). Although GH appeared to increase IGF-I release in this period for cells grown in 0.2xamino acid media, this effect was not statistically significant. In the period from 24-48 h in defined media, both basal and GH-stimulated IGF-I production was dependent on amino acid availability (P<0.05 and P<0.001 respectively). Factorial analysis of variance demonstrated a strong positive interaction (P<0.001) between the effects of amino acid availability and GH, such that GH increased IGF-I production by more than 2-fold in cells grown in 5.0xamino acid media (P<0.01) but had no effect on production by cells grown in 1.0xor 0.2xamino acid media. Measurement of steady state concentrations of exon 1-derived IGF-I mRNAs using an RNase protection assay demonstrated that the observed effects on IGF-I peptide secretion were strongly associated with parallel effects at the RNA level. Incorporation of (35)S-methionine into cellular proteins over a 4-h period starting 20 h after transfer to defined culture media was not significantly reduced in 1.0xcompared with 5.0x amino acid media, although rates under both of these conditions were significantly higher than those seen in 0.2xamino acid media (P<0.01). The lack of correspondence between the dose-dependent effects of amino acid supply on cellular protein synthesis and those on basal and GH-stimulated IGF-I production, suggests that amino acid supply modulates IGF-I production through selective mechanisms. Steady state levels of the CCAAT/enhancer-binding protein beta (C/EBPbeta) isoforms, liver-enriched activating protein (LAP) and liver-enriched inhibitory protein (LIP) were determined by Western blotting. When levels of LAP were expressed relative to LIP levels in the same extracts, a significant decrease in the LAP:LIP ratio was observed in response to amino acid limitation (P<0.05). These data strengthen earlier arguments that synergistic interaction between the effects of amino acids and GH on hepatic IGF-I gene expression underlie nutrition-dependent changes in circulating IGF-I titres. The association between these effects and altered levels of C/EBPbeta isoforms suggests that CCAAT/enhancer mediated control of IGF-I gene expression may be involved in this phenomenon.