Excess Dietary Protein Research Articles

Dietary protein decreases exercise endurance through rapamycin-sensitive suppression of muscle mitochondria

Loss of physical performance is linked not only to decreased activity in daily life but also to increased onset of cardiovascular diseases and mortality. A high-protein diet is recommended for aged individuals in order to preserve muscle mass; however, the regulation of muscle mitochondria by dietary protein has not been clarified. We investigated the long-term effects of a high-protein diet on muscle properties, focusing especially on muscle mitochondria. Mice were fed a high-protein diet from the age of 8 wk and examined for mitochondrial properties and exercise endurance at the ages of 20 and 50 wk. Compared with normal chow, a high-protein diet significantly decreased the amount of muscle mitochondria, mitochondrial activity, and running distance at 50 wk, although it increased muscle mass and grip power. Inhibition of TORC1-dependent signal pathways by rapamycin from 8 wk suppressed the decline in mitochondria and exercise endurance observed when mice were fed the high-protein diet in association with preserved AMPK activity. Collectively, these findings suggest a role for dietary protein as a suppressor of muscle mitochondria and indicate that the age-associated decline in exercise endurance might be accelerated by excessive dietary protein through rapamycin-sensitive suppression of muscle mitochondria.

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<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<0.02). Faecal Ca loss was greater in H (P<0.005); while Ca absorption and absorption as a percent of intake were lower for H (P<0.02). RBAE of dorsal and palmar cortices increased over time (P<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.

Maternal dietary protein restriction and excess affects offspring gene expression and methylation of non-SMC subunits of condensin I in liver and skeletal muscle

Recent evidence indicates that maternal nutrition during pregnancy influences gene expression in offspring through epigenetic alterations. In the present study we evaluated the effect of protein excess and deficiency during porcine pregnancy on offspring hepatic and skeletal muscular expression patterns of key genes of methionine metabolism (DNMT1, DNMT3a, DNMT3b, BHMT, MAT2B and AHCYL1), condensin I subunit genes (NCAPD2, NCAPG and NCAPH), important for chromosome condensation and segregation, global DNA methylation and gene-specific DNA methylation. German Landrace sows were randomly assigned to control (CO), high protein (HP) and low protein (LP) diet groups. Tissue samples of offspring were collected from fetal (dpc95), newborn (dpn1), weanling (dpn28) and finisher pigs (dpn188). Gene expression of DNMT1, DNMT3a and DNMT3b was influenced by both HP and LP diets, indicating an involvement of DNA methylation in fetal programming by maternal protein supply. Moreover, hepatic global methylation was significantly affected by protein restriction at dpc95 (p = 0.004) and by protein excess at dpn188 (p = 0.034). Gene expression in fetal liver was significantly different between CO and LP for NCAPD2 (p = 0.0005), NCAPG (p = 0.0009) and NCAPH (p < 0.0001). In skeletal muscle, LP fetuses had significantly altered gene expression of NCAPD2 (p = 0.020) and NCAPH (p = 0.001), compared with CO. Furthermore, NCAPG was differentially methylated among LP, HP and CO; indeed, a significant positive correlation was detected with transcript amount in fetal pigs (r = 0.47, p = 0.002). These data demonstrate that both restriction and excess dietary protein during pregnancy alters the offspring’s epigenetic marks and influences gene expression.

Effects of limited and excess protein intakes of pregnant gilts on carcass quality and cellular properties of skeletal muscle and subcutaneous adipose tissue in fattening pigs1,2

The aim of this study was to investigate whether dietary protein intake of gilts during gestation below (50%) or above (250%) recommendations affects body composition, carcass and meat quality, and properties of skeletal muscle and subcutaneous adipose tissue (SCAT) in offspring at d 83 and 188 of age. German Landrace gilts were fed isoenergetic gestation diets (~13.7 MJ of ME/kg) containing a low (LP, 6.5%; n = 18), an adequate (AP, 12.1%; n = 20), or a high (HP, 30%; n = 16) protein content from mating until farrowing. Within 48 h of birth, offspring were cross-fostered to sows fed a standard diet. On d 83 of age, no effects of the LP diet on BW and body composition were detected, whereas HP pigs showed a slight growth delay (P = 0.06) associated with increased relative weights of small intestine (P < 0.01) and brain (P = 0.08), and reduced relative thymus weight (P < 0.01). On d 188 of age, BW was not different among the dietary groups. However, the carcass of LP pigs contained less (P = 0.01) lean and more (P = 0.07) fat compared with AP and HP pigs, which was only pronounced in pigs originating from large litters (P < 0.05). Like skeletal muscles (P = 0.06), the heart muscle weighed less (P = 0.02) in LP than AP pigs. Compared with AP pigs, LP pigs exhibited a fewer (P = 0.09) total number of myofibers in semitendinosus muscle plus LM both at d 83 and 188 of age, whereas total muscular DNA was less (P = 0.02) at d 188 only. The mRNA abundance of IGF2 measured on d 188 was reduced in SCAT (P = 0.03) and LM (P = 0.07) of LP compared with AP pigs. No changes in muscular fiber type frequency, capillary density, or creatine kinase activity, as well as SCAT adipocyte size and number, were observed at either stages of age. Meat quality characteristics remained unchanged at d 83, whereas Warner-Bratzler shear force value in LM was decreased (P = 0.03) in LP compared with AP pigs on d 188 of age. The results suggest that the maternal LP diet impairs prenatal myofiber formation, reduces the potential of postnatal lean growth related to reduced IGF2 mRNA expression and myonuclear accumulation, and consequently changes carcass quality toward reduced lean proportion and improved tenderness at market weight. In contrast, except for a slight transient growth delay, excess dietary protein during gestation seems to have little effect on the fetal programming of postnatal muscle and adipose tissue phenotype of the progeny.

Metabolic responses to high protein diet in Korean elite bodybuilders with high-intensity resistance exercise

BackgroundHigh protein diet has been known to cause metabolic acidosis, which is manifested by increased urinary excretion of nitrogen and calcium. Bodybuilders habitually consumed excessive dietary protein over the amounts recommended for them to promote muscle mass accretion. This study investigated the metabolic response to high protein consumption in the elite bodybuilders.MethodsEight elite Korean bodybuilders within the age from 18 to 25, mean age 21.5 ± 2.6. For data collection, anthropometry, blood and urinary analysis, and dietary assessment were conducted.ResultsThey consumed large amounts of protein (4.3 ± 1.2 g/kg BW/day) and calories (5,621.7 ± 1,354.7 kcal/day), as well as more than the recommended amounts of vitamins and minerals, including potassium and calcium. Serum creatinine (1.3 ± 0.1 mg/dl) and potassium (5.9 ± 0.8 mmol/L), and urinary urea nitrogen (24.7 ± 9.5 mg/dl) and creatinine (2.3 ± 0.7 mg/dl) were observed to be higher than the normal reference ranges. Urinary calcium (0.3 ± 0.1 mg/dl), and phosphorus (1.3 ± 0.4 mg/dl) were on the border of upper limit of the reference range and the urine pH was in normal range.ConclusionsIncreased urinary excretion of urea nitrogen and creatinine might be due to the high rates of protein metabolism that follow high protein intake and muscle turnover. The obvious evidence of metabolic acidosis in response to high protein diet in the subjects with high potassium intake and intensive resistance exercise were not shown in this study results. However, this study implied that resistance exercise with adequate mineral supplementation, such as potassium and calcium, could reduce or offset the negative effects of protein-generated metabolic changes. This study provides preliminary information of metabolic response to high protein intake in bodybuilders who engaged in high-intensity resistance exercise. Further studies will be needed to determine the effects of the intensity of exercise and the level of mineral intakes, especially potassium and calcium, which have a role to maintain acid-base homeostasis, on protein metabolism in large population of bodybuilders.

Dietary protein regulates hepatic constitutive protein anabolism in rats in a dose-dependent manner and independently of energy nutrient composition

We had previously observed that drastic increases in protein consumption greatly modified hepatic protein anabolism in rats, but the confounding effects of other macronutrient changes or a moderate protein increase to generate the same modifications have not yet been established. This study examined the metabolic and hormonal responses of rats subjected to 14-day isoenergetic diets containing normal, intermediate, or high-protein levels (NP: 14% of energy, IP: 33%, HP: 50%) and different carbohydrate (CHO) to fat ratios within each protein level. Fasted or fed rats (n = 104) were killed after the injection of a flooding dose of (13)C-valine. The hepatic protein content increased in line with the dietary protein level (P < 0.05). The hepatic fractional synthesis rates (FSR) of protein were significantly influenced by both the protein level and the nutritional state (fasted vs. fed) (P < 0.0001) but not by the CHO level, reaching on average 110%/day, 92%/day, and 83%/day in rats fed the NP, IP, and HP diets, respectively. The FSR of plasma albumin and muscle did not differ between diets, while feeding tended to increase muscle FSR. Proteolysis, especially the proteasome-dependent system, was down-regulated in the fed state in the liver when protein content increased. Insulin decreased with the CHO level in the diet. Our results reveal that excess dietary protein lowers hepatic constitutive, but not exported, protein synthesis rates, independently of the other macronutrients, and related changes in insulin levels. This response was observed at the moderate levels of protein intake (33%) that are plausible in a context of human consumption.

Limited and excess dietary protein during gestation affects growth and compositional traits in gilts and impairs offspring fetal growth1,2

The aim of this study was to investigate whether dietary protein intake during gestation less than or greater than recommendations affects gilts growth and body composition, gestation outcome, and colostrum composition. German Landrace gilts were fed gestation diets (13.7 MJ of ME/kg) containing a low (n = 18; LP, 6.5% CP), an adequate (n = 20; AP, 12.1%), or a high (n = 16; HP, 30%) protein content corresponding to a protein:carbohydrate ratio of 1:10.4, 1:5, and 1:1.3, respectively, from mating until farrowing. Gilts were inseminated by semen of pure German Landrace boars and induced to farrow at 114 d postcoitum (dpc; Exp. 1). Energy and protein intake during gestation were 33.3, 34.4, and 35.8 MJ of ME/d (P < 0.001) and 160, 328, and 768 g/d, respectively, in LP, AP, and HP gilts (P < 0.001). From insemination to 109 dpc, BW gain was least in LP (42.1 kg), intermediate in HP (63.1 kg), and greatest in AP gilts (68.3 kg), whereas increase of backfat thickness was least in gilts fed the HP diet compared with LP and AP diets (3.8, 5.1, 5.0 mm; P = 0.01). Litter size, % stillborn piglets, and mummies were unaffected (P > 0.28) by the gestation diet. Total litter weight tended to be less in the offspring of LP and HP gilts (14.67, 13.77 vs. 15.96 kg; P = 0.07), and the percentage of male piglets was greater in litters of HP gilts (59.4%; P < 0.01). In piglets originating from LP and HP gilts, individual birth weight was less (1.20, 1.21 vs. 1.40 kg; P = 0.001) and birth weight/crown-rump length ratio was reduced (45.3, 46.4 vs. 50.7 g/cm; P = 0.003). Colostrum fat (7.8, 7.4 vs. 8.1%) and lactose concentrations (2.2, 2.1 vs. 2.6%) tended to be reduced in LP and HP gilts (P = 0.10). In Exp. 2, 28 gilts (LP, 10; AP, 9; HP, 9) were treated as in Exp. 1 but slaughtered at 64 dpc. At 64 dpc, LP gilts were 7% lighter than AP gilts (P = 0.03), whereas HP gilts were similar to AP gilts. Body composition was markedly altered in response to LP and HP feeding with less lean (P < 0.01) and greater fat content (P = 0.02 to 0.04) in LP and less fat content (P = 0.02 to 0.04) in HP gilts. Fetal litter weight and number, and embryonic survival at 64 dpc were not affected by the diets. These results indicated that gestation diets containing protein at 50 and 250% of recommendations and differing in protein:carbohydrate ratio led to marked changes in protein and fat metabolism in gilts resulting in fetal growth retardation of 15%, which mainly occurred during the second half of gestation.

A scientific review of the reported effects of vegan nutrition on the occurrence and prevalence of cancer and cardiovascular disease

That there exists an increased prevalence of non-communicable diseases is not readily disputed, though best practice for remedying these afflictions remains highly contentious. This paper investigates the influence of a wholly herbivorous (or vegan) diet on two leading non-communicable diseases (cancer and cardiovascular disease (CVD)). Relevant aspects considered are the biochemical effects of varying dietary concentrations of protein, calcium, essential fatty acids, cholesterol and cobalamin (B 12 ). Current literature and research investigating interactions between each focal compound and either cancer or CVD was assessed (noting where compounds influence both diseases simultaneously, the impact considered greatest in significance was chosen). Results are typically complex and indirect, with primary effects leading to secondary effects involving other compounds (including counterbalancing other focal compounds), and ancillary effects on comorbidity factors of the focal diseases. Outcomes included: weak risk reduction for colorectal and breast cancer due to a decreased propensity toward excessive dietary protein intake; possible risk reduction of prostate cancer from reduced calcium intake; cancer risk promotion due to disproportionate intakes of omega-3 relative to omega-6; CVD risk reduction from reduced cholesterol intake and insufficient evidence to consider B 12 intake either promotive or predisposing for CVD. Caution is advised attributing dietary recommendations to these findings, as high levels of contention exist between authors due to disparate study results. Greater unanimity may be borne from future trials.

Effects of feeding excess dietary crude protein from soybean meal and dried distillers grains with solubles on nursery pig performance (2010)

Two experiments were conducted to determine the effects of feeding excess dietary CP to nursery pigs. In Exp. 1, a total of 105 nursery pigs (PIC TR4 x 1050, initially 22.9 lb and 35 d of age) were used in a 21-d growth assay to determine the effects of feeding excess CP from soybean meal to nursery pigs. The pigs were fed a pelleted commercial starter diet for the first 14 d after weaning, and the experimental treatments were fed for the next 21 d. Treatments consisted of 3 corn-soybean meal-based diets formulated to different CP levels: (1) 22.5%, (2) 25%, and (3) 27.5% CP. Increasing CP from 22.5 to 27.5% had no effect (P > 0.19) on ADG, ADFI, or F/G. In Exp. 2, a total of 105 nursery pigs (PIC TR4 x 1050, initially 22.1 lb and 35 d of age) were used in a 21-d growth assay to determine the effects of excess CP from dried distillers grains with solubles (DDGS) on nursery pig growth. The pigs were fed a pelleted commercial starter diet for the first 14 d after weaning and the experimental treatments for the next 21 d. Treatments were corn-soybean meal-based diets formulated to 22.9 and 25% CP and a diet with 30% DDGS formulated to 25% CP. Increasing the CP concentration had no effect (P > 0.12) on ADG, ADFI, or F/G. However, pigs fed the DDGS had poorer (P < 0.04) F/G compared to pigs fed the corn-soybean meal-based diet formulated to 25% CP. Our data suggest that nursery pigs can tolerate CP levels up to 27.5% without negative effects on growth performance. Additionally, the inclusion of 30% DDGS in nursery pig diets did not have a significant impact on ADG or ADFI, but did negatively affect F/G.; Swine Day, Manhattan, KS, November 18, 2010

WPŁYW POZIOMU MOCZNIKA I BIAŁKA W MLEKU NA WSKAŹNIKI PŁODNOŚCI KRÓW

An analysis of the effect of milk urea and protein levels in four consecutive lactations on fertility indices of Blackand- White Polish Holstein-Friesian cows, milk recorded in the Kujawsko-Pomorskie province has been made. Poorer fertility indices were found in first-calf heifers and second lactation cows receiving energy-deficient diets and in older (third and fourth lactation) cows receiving excess dietary protein and energy. Best fertility was found in young cows fed excess protein (>3.60%) regardless of milk urea levels, and in older cows having lower and optimum levels regardless of protein levels. Cow fertility is differentiated more by milk protein levels than by urea content. Fertility parameters were poorer in first and second lactation cows than in older cows. The coefficients of correlation between milk urea and protein levels and fertility indices were very low, with the only significant differences between protein content vs. calving interval and reproductive rest period.

Blackspot seabream ( Pagellus bogaraveo) lipogenic and glycolytic pathways appear to be more related to dietary protein level than dietary starch type

The lipogenic potential of carbohydrate type on blackspot seabream was determined using two isolipidic (10%) and isonitrogenous (45%) diets containing either crude (CS) or gelatinized corn starch (GS). A third diet containing a lower protein level (35%) and gelatinized starch (GS) was also tested to determine if any lipogenic effect detected was due to carbohydrate and not from excess dietary protein. The three diets were formulated to have similar energy (21 kJ g − 1 DM) content. Triplicate groups of fish (24 g initial body weight) were fed each dietary treatment by hand to apparent satiety for 90 days. Both starch type and dietary protein level significantly affected growth. Fish fed the CS diet increased voluntary feed intake (VFI) and digestible protein intake resulting in both higher final body weight (FBW) and daily growth index (DGI). Although the lower protein level (35%) increased VFI, this increase was not enough to reach the same digestible protein intake observed in fish fed the high protein level (45%), resulting in lower FBW and DGI. Despite the differences observed in growth, nutrient gain and hence whole body composition were not affected by starch type (CS vs GS) or dietary protein level (35 vs 45%). Similarly, glycaemia was not affected by starch type or dietary protein level in any of the treatments, with the highest values being observed at 4 h post feeding. On the other hand, both starch type and dietary protein level significantly affected insulin levels 2 h after feeding. Plasma lipid levels showed no significant differences at 2 and 24 h post feeding, regardless of dietary treatment. A reduction of 10% dietary protein level (45 to 35%) markedly depressed (> 40%) hepatic activities of lipogenic enzymes (glucose-6-phosphate dehydrogenase, G6PD; malic enzyme, ME; fatty acid synthetase, FAS), and significantly increased PK activities at each postprandial time (2, 4 and 24 h). Starch type did not cause any significant effect on hexokinase (HK), glucokinase (GK), pyruvate kinase (PK) (glycolysis) or glucose-6-phosphatase (G6Pase) (gluconeogenesis) postprandial hepatic activities. Blackspot seabream lipogenic and glycolytic pathway regulation appear to be more related to dietary protein level than to dietary starch type.

The potential of land animal protein ingredients to replace fish meal in diets for cuneate drum,Nibea miichthioides, is affected by dietary protein level

A net pen experiment was carried out to examine the effect of dietary protein level on the potential of land animal protein ingredients as fish meal substitutes in practical diets for cuneate drum Nibea miichthioides. Two isocaloric basal (control) diets were formulated to contain 400 g kg-1 herring meal but two different digestible protein (DP) levels (400 versus 350 g kg-1). At each DP level, dietary fish meal level was reduced from 400 to 280, 200, 80 and 0 g kg-1 by incorporating a blend that comprised of 600 g kg-1 poultry by-products meal (PBM), 200 g kg-1 meat and bone meal (MBM), 100 g kg-1 feather meal (FEM) and 100 g kg-1 blood meal (BLM). Cuneate drum fingerling (initial weight 42 g fish-1) were fed the test diets for 8 weeks. Fish fed the test diets exhibited similar feed intake. Final body weight, feed conversion ratio and nitrogen retention efficiency was not significantly different between fish fed the basal diets containing 350 and 400 g kg-1 DP. Weight gain decreased linearly with the reduction of dietary fish meal level at the 350 g kg-1 DP level, but did not decrease with the reduction of dietary fish meal level at the 400 g kg-1 DP level. Results of the present study suggest that fish meal in cuneate drum diets can be completely replaced with the blend of PBM, MBM, FEM and BLM at the 400 g kg-1 DP level, based on a mechanism that excessive dietary protein compensate lower contents of bio-available essential amino acid in the land animal protein ingredients relative to fish meal.

Protein-induced alterations in murine hepatic α-aminoadipate δ-semialdehyde synthase activity are mediated posttranslationally

The molecular mechanisms responsible for alterations in lysine alpha-ketoglutarate reductase (LKR) activity are unknown. Therefore, the aim of these studies was to discern the mechanism(s) responsible for induction of hepatic LKR activity in rodents fed excess dietary protein. Four studies were conducted that used 84 mice. Mice were fed either a high-protein (50% casein) or adequate-protein (20% casein) diet in powder form in study 1 and a high-protein (46% casein) or adequate-protein (21% casein) diet in pellet form in the remaining studies. No significant differences in weight gain between the mice fed the different diets were detected. As expected, mice fed high-protein diets had a greater (P< .05) LKR activity in all 4 experiments. Mice fed high- and adequate-protein diets for 8 days showed no difference (P> .1) in alpha-aminoadipate delta-semialdehyde synthase (AASS) mRNA in experiment 1. However, after pooling the data from the remaining 3 experiments, mice receiving the high-protein diet had greater (P< .05) AASS mRNA compared to mice fed the adequate protein diet. In this investigation, no differences (P> .1) in AASS protein abundance were detected. The results are consistent with a mechanism in which posttranslational regulation is responsible for hepatic induction of LKR activity in mice fed high-protein diets.

Pet Food Safety: Dietary Protein

The goal of this article was to review the evidence surrounding the risks posed by insufficient or excessive dietary protein. Dietary protein is required to provide essential amino acids and replenish protein reserves. When intake is deficient, protein turnover slows and lean body mass is gradually depleted. These changes lead to increased morbidity and mortality. Dogs can maintain nitrogen balance (typically used to define minimum requirements in adults), yet be in a protein-depleted state due to physiologic adaptations. Preservation of protein turnover and lean body mass requires about threefold more protein than nitrogen balance. The ability of excess dietary protein to induce renal pathology was studied in both dogs with chronic kidney failure and older dogs without kidney failure. Numerous studies have confirmed that protein does not adversely affect the kidneys. However, phosphorus- and protein-restricted diets are clinically beneficial in dogs with existing chronic kidney failure. Protein restriction for healthy older dogs is not only unnecessary, it can be detrimental. Protein requirements actually increase by about 50% in older dogs, while their energy requirements tend to decrease. When insufficient protein is provided, it can aggravate the age-associated loss of lean body mass and may contribute to earlier mortality. Older dogs should receive at least 25% of their calories from protein, typically provided by diets containing at least 7 g protein/100 Kcal ME.

Dietary protein intake is an independent and dose‐dependent regulator of hepatic anabolism in rats fed high protein diets

We previously observed that drastic increases in protein consumption greatly modify hepatic protein anabolism in rats, yet the confounding effects of the other macronutrient changes and the ability of a moderate protein increase to produce the same effects are not established. This study examined the metabolic and hormonal responses of rats submitted to 14‐d isoenergetic diets with normal, intermediary or high protein levels (NP:14% of energy, IP: 33%, HP: 50%) and different carbohydrate (CHO) to fat ratios within each protein level. Fasted or fed rats (n=96) were killed after injection of a flooding dose of 13C‐valine. Hepatic protein content increased with the dietary protein level (P&lt;0.05). The hepatic fractional synthesis rates (FSR) of protein were significantly influenced by both the protein level and the nutritional state (fasted vs. fed) (P&lt;0.0001) but not by the CHO/fat ratio and reached on average 110%/d, 92%/d and 83%/d in rats fed the NP, IP and HP diets, respectively. Muscle FSR did not differ among diets. Insulin levels significantly decreased with both increasing protein level and decreasing CHO/fat ratio. Our results reveal that excess dietary protein inhibits hepatic protein synthesis rates independently of the other macronutrients and the related changes in insulin levels. This response is observed at moderate levels of protein intake (33%) that are plausible in human consumption.

Effects of excess dietary crude protein from soybean meal and dried distillers grains with solubles in diets for finishing pigs (2008)

A total of 180 pigs (90 barrows and 90 gilts, average initial weight of 148 lb) were used in a 67-d experiment to determine the effects of excess dietary CP on growth performance and carcass measurements in finishing pigs. The pigs were sorted by ancestry and blocked by weight with 12 pigs per pen and 5 pens per treatment. Treatments were cornsoybean meal-based diets formulated to 15.3 and 18.3% CP and a corn-soybean-DDGSbased diet formulated to 18.3% CP. Feed and water were consumed on an ad libitum basis until the pigs were slaughtered (average final weight of 282 lb) at a commercial abattoir. Pigs fed diets with high CP had lower (P < 0.001) final weight, ADG, ADFI, and HCW, but these results were caused entirely by the diet with 40% DDGS. Our results indicated that diets with 40% DDGS decreased growth performance and economically important carcass measurements. However, the excess CP in those diets does not seem to be the culprit.

Nutrition and cardiovascular disease: Putting a pathogenic framework into focus

In the last two decades it has become clear that dietary recommendations are a key element in the management of cardiovascular disease (CVD). An expanding body of evidence indicates that certain dietary patterns can influence cardiovascular health and primary prevention of CVD by modifying risk factors such as obesity, dyslipidemia, and hypertension as well as factors involved in systemic inflammation, insulin sensitivity, oxidative stress, endothelial function, thrombosis, and cardiac rhythm [1–3]. In the last century dietary and exercise habits have changed, with greater abundance of refined foods and a more sedentary lifestyle, resulting in the rising prevalence of obesity in Western countries [4,5]. In the present Spotlight Issue, we present a series of review articles and original papers with the aim of investigating the various dietary profiles and pathogenic mechanisms that have emerged in the literature and the major studies that investigated their effectiveness in modifying cardiovascular risk. However, we need to keep in mind that long-term adherence can become a problem with some dietary advice that uses severe restriction of certain food groups. Indeed, in trials that investigated the effectiveness of low-carbohydrate diets in inducing weight loss, the attrition rates ranged between 24% and 39%. In most of these trials, comparable attrition rates were observed in subjects assigned to a low-fat diet [6–8]. More important, when a major change in the proportion of one macronutrient is imposed, compensatory changes in the proportions of other macronutrients will naturally occur. In the case of low-carbohydrate diets, there is a concern that excessive dietary protein intake without appropriate quantity of water and beverages can occur and potentially increase long-term risks for nephrolithiasis [9]. Furthermore, when dietary fat intake is severely restricted, biochemical evidence of essential fatty acid deficiency can result. Some clinical consequences have been reported, including episodic … *Corresponding author. Tel./fax: +39 081 293399. Email address: claunap{at}tin.it

Amino acids injure mesangial cells by advanced glycation end products, oxidative stress, and protein kinase C

In diabetes, high intake of dietary protein exacerbates responses associated with kidney damage. Increased levels of amino acids could injure cells by providing free amino groups for glycation reactions leading to advanced glycation end products (AGEs). Rat mesangial cells were cultured with increased amino acids designed to resemble protein feeding, high glucose (30.5 mmol/L), and, the combination, amino acids/high glucose. AGEs, reactive oxygen species (ROS), protein kinase C (PKC) activity and production, and mitogen-activated protein (MAP) kinase-extracellular signal regulated kinase (ERK) 1,2 activity were measured. Inhibitors were used to determine roles of these processes in fibrosis and/or AGE formation. AGE immunostaining increased when cells were cultured in amino acids and was comparable to that observed with high glucose. In amino acids/high glucose, AGE immunostaining appeared even greater. Amino acids, high glucose, and amino acids/high glucose induced ROS production. Aminoguanidine and vitamin E prevented AGE accumulation and induction of protein and mRNA for fibrosis markers [transforming growth factor-beta1 (TGF-beta1), fibronectin, and collagen IV]. PKC and ERK 1,2 activity increased with amino acids, high glucose, and amino acids/high glucose. PKC-beta inhibition prevented ERK 1,2 activation and fibrosis induction. ERK 1,2 inhibition also blocked the fibrosis response. A profibrotic injury response occurred in mesangial cells exposed to amino acids, with or without high glucose, by formation of AGE, oxidative stress, and activation of the PKC-beta and MAP kinase-ERK 1,2 signal pathway. These observations provide new insight into cellular mechanisms of kidney damage produced by excess dietary protein, particularly in diabetes.

298. Dietary protein does not influence mitochondrial distribution in the 2-cell mouse embryo

Excess dietary protein can negatively influence fertility. The underlying mechanisms remain to be completely elucidated; however, variations in reproductive tract pH, and ammonium and urea concentrations have been implicated. Mouse embryos cultured in the presence of ammonium showed a shift in mitochondrial distribution away from the nucleus towards the cell cortex, suggestive of reduced mitochondrial activity, ATP production and embryo viability. In this study we determined the effect of dietary protein in vivo, on mitochondrial distribution in the 2-cell mouse embryo. Five-week-old Swiss female mice (n = 10) were fed low (9%), medium (14%) or high (25%) dietary protein for 3weeks; feed intake and body weight were recorded weekly. At 8 weeks of age mice were primed with 5 IU of PMSG, then 5 IU hCG 48 h later, and mated overnight with males of proven fertility. Forty hours post-hCG females were sacrificed, their oviducts collected and flushed with media. The total number of 2-cell embryos and oocytes retrieved were recorded. Active mitochondria were stained in the 2-cell embryos using Mitotracker Green (Molecular Probes), and were visualised using confocal microscopy. Density of perinuclear and cortical staining was determined in Photoshop 7.0, using an established method. Females fed the medium diet consumed significantly less and gained less weight than those fed the low or high diet (Table 1), despite similar final body weights (data not shown). Females fed the low diet tended to have a lower ovulation rate and fewer 2-cell embryos than females consuming the other diets (Table 1, P &gt; 0.05). There was no significant effect of dietary protein on the distribution of mitochondria between the perinuclear and cortical region of the embryo, which may be reflective of lower in vivo ammonium levels compared to those described in culture.

Nutrition and feed management strategies to reduce nutrient excretions and odors from swine manure

Manipulation of the pig's diet to reduce nutrient excretions and odors is feasible and practical. Avoiding excessive dietary protein, using high quality protein sources, and feeding low protein, amino acid supplemented diets are practices that will reduce the N in excreta. Avoiding excessive overages of dietary P, balancing diets on an available P basis, and use of phytase as a dietary supplement offers potential for further reducing the P in manure. Use of reduced or organic forms of Cu, Zn, Fe and Mg will reduce excretion of these nutrients in manure. Feeding management technologies that will enhance feed efficiencies and reduce nutrient excretion include feeding for phase, sex and genetic ability of the animal. Reducing the intact protein levels in diets and balancing with synthetic amino acids, use of low levels of specific non-starch polysaccharides (NSP; soybean hulls, sugar beet pulp), and maintaining the proper acid-base balance and buffering in the diet can significantly reduce odorous compounds. Greater nutrient reductions may be possible through the development of specialty feed ingredients that will be used for specific animal diets. Research to fine-tune the diets for production systems is needed.