Effect Of Dietary Protein Restriction Research Articles

Correlated changes in stress resistance and biochemical parameters in response to long-term protein restriction in Drosophila melanogaster.

Studies in fruit flies, Drosophila melanogaster, have observed considerable variation in the effect of dietary protein restriction (PR) on various fitness traits. In addition, not only are there inconsistent results relating lifespan to stress resistance, but also the long-term effects of PR are unexplored. We study PR implementation across generations (long term) hypothesizing that it will be beneficial for fitness traits, stress resistance and storage reserves due to nutritional plasticity transferred by parents to offspring in earlier Drosophila studies. By imposing two concentrations of PR diets (50% and 70% of control protein) from the pre-adult and adult (age 1 day) stages of the flies, we assessed the stage-specific and long-term effect of the imposed PR. All long-term PR flies showed increased resistance against the tested stressors (starvation, desiccation, H2O2-induced oxidative stress). In addition, we also found long-term PR-induced increased stress resistance across generations. The PR flies also possessed higher protein and triglyceride (TG) content, reduced glucose and unaffected glycogen levels. We also assayed the effect of returning the PR flies to control (AL) food for a single generation and assessed their biochemical parameters to witness the transient PR effect. It was seen that TG content upon reversal was similar to AL flies except for PRI70 males; however, the glucose levels of PR males increased, while they were consistently lower in females. Taken altogether, our study suggests that long-term PR implementation contributes to increased stress resistance and was found to influence storage reserves in D. melanogaster.

Effects of Dietary Protein Restriction on Nutritional Status of Hemodialysis Patients

Haemodialysis is one of the three renal replacement therapies in which waste products and excess fluid are removed from blood when kidneys stop functioning properly. Protein catabolism is increased as patients lose some protein during haemodialysis treatment. Sufficient protein intake is of great significance, yet prevalence of inadequate protein consumption persists due to various reasons, resulting protein-energy malnutrition (PEM). The studies regarding low protein intake among haemodialysis patients is lower compared to studies conducted on non-dialysis chronic kidney disease (CKD) patients. The purpose of this study was to investigate the prevalence of protein restriction practices and its effect in nutritional status of haemodialysis patients. The study was descriptive exploratory analysis among 150 haemodialysis patients at one of the largest dialysis center of Kathmandu district using anthropometric, biochemical, clinical and dietary (ABCD) assessments. Among 150 haemodialysis patients, majority (63.3%) were male. 71.3% were undergoing haemodialysis for more than 1 to 5 years and 82.7% doing twice a week in- center haemodialysis. According to serum albumin report, 66.7% were identified as PEM. Body mass index (BMI) result also classified 3.3% as underweight. It was concluded that the effect of protein restriction resulted as malnourished among certain patients. The underlying causes for consuming low protein diets were associated with dislike to protein-rich foods, financial constraints, lack of awareness, and other factors. Establishing regular consultations with dieticians and closely monitoring dietary patterns appeared as crucial approaches for enhancing the nutritional status of these patients. It is essential to acknowledge that protein requirements vary based on different stages of CKD and the presence of concurrent health conditions. Consistent follow-up by a multidisciplinary team, utilizing a range of nutrition assessment methods specified for haemodialysis patients is vital step.

Effects of Dietary Protein Restriction on Colonic Microbiota of Finishing Pigs.

This study is aimed at the effects of low-protein diets with four amino acids balanced on serum biochemical parameters and colonic microflora of finishing pigs. Fifty-four healthy (Duroc × Landrace × Yorkshire) hybrid barrows with an average body weight of 70.12 ± 4.03 kg were randomly assigned to one of three dietary treatments with three barrows per pen and six pens per treatment. The barrows were fed a normal protein diet (NP), a low-protein diet (LP), and a very low-protein diet (VLP). Compared with the NP diet, reduced dietary protein did not influence serum biochemical parameters (p > 0.05). The valeric acid was significantly increased with the VLP diet (p < 0.05). Compared with the NP diets, the abundance of Terrisporobacter (13.37%) Clostridium_sensu_stricto_1 (23.37%) and Turicibacter (2.57%) increased to 21.04, 33.42 and 13.68% in LP diets and 16.72, 43.71 and 14.61% in VLP diets, while the abundance of Lactobacillus (9.30%) and Streptococcus (25.26%) decreased to 3.57 and 14.50% in LP diets and 1.86 and 4.07% in VLP diets. Turicibacter and Clostridium_sensu_stricto_6 had a powerful negative correlation with the content of valeric acid (p < 0.01), while Peptococcus and Clostridia_UCG-014 had a very solid positive correlation (p < 0.01). In conclusion, reducing dietary protein level can improve colon microbiota composition, especially reducing the abundance of bacteria related to nitrogen metabolism, but has no significant effect on SCFA except valeric acid. In addition, reduction in the dietary protein level by 5.48% had more different flora than that of 2.74% reduction in dietary CP level.

Low-protein diet is inversely related to the incidence of chronic kidney disease in middle-aged and older adults: results from a community-based prospective cohort study.

Dietary protein intake can modulate renal health. However, the effect of dietary protein restriction on kidney function in the general population remains unclear. This study aimed to examine the association between total protein intake and new-onset chronic kidney disease (CKD) in Korean adults. We included 7339 participants from the Korean Genome and Epidemiology Study. Participants were divided into low-protein diet (LPD, < 0.8g/kg/day), normal-protein diet (NPD, 0.8-1.3g/kg/day), and high-protein diet (HPD, > 1.3g/kg/day) groups. New-onset CKD was defined as two consecutive events of estimated glomerular filtration rate < 60mL/min/1.73 m2. Multivariable Cox hazard regression analysis was conducted to examine the association of total protein intake with new-onset CKD. Subgroup analyses according to diabetes mellitus (DM) status were performed. We performed the same analyses by dividing participants into total protein, plant protein, and animal protein intake tertiles. During a median follow-up of 13.7years, 633 (8.7%) participants newly developed CKD. The fully adjusted hazard ratios (HR) with 95% confidence interval (CI) for incident CKD of the LPD and HPD groups compared with the NPD group were 1.49 (1.18-1.87) and 0.63 (0.45-0.87), respectively. The HR (95% CI) of the highest tertile group of plant protein intake for incident CKD was 0.72 (0.54-0.93), compared with that of the lowest tertile group. Similar trends were observed only in the non-DM subgroup, not in the DM subgroup. Protein intake, especially plant proteins, was negatively associated with the incidence of new-onset CKD in middle-aged and older Korean adults.

Using complex behavior to understand brain mechanisms in health and disease.

Using complex behavior to understand brain mechanisms in health and disease.

Dynamic effects of dietary protein restriction on body weights, food consumption, and protein preference in C57BL/6J and Fgf21-KO mice.

Single-case experimental designs (SCEDs) are rarely used in behavioral neuroscience despite their potential benefits. The current study used a SCED to evaluate the effects of dietary protein restriction in C57BL/6J and Fgf21-knockout (KO) mice on body weight, food consumption, and protein preference and changes in those outcome measures were quantified using multilevel linear models. In C57BL/6J mice, rate of weight gain was lower and food consumption and protein preference higher during periods of low (4% kcal) protein diet feeding compared to periods of normal (18% kcal) protein diet feeding. In Fgf21-KO mice, who do not produce the liver-derived hormone FGF21, rate of weight gain and protein preference were not substantially affected by diet although food consumption was slightly higher during periods of low protein diet than periods of normal protein diet. These results demonstrate that protein restriction dynamically regulates physiological and behavioral responses at the individual mouse level and that FGF21 is necessary for those responses. Further, the current results demonstrate how a SCED can be used in behavioral neuroscience research, which entails both scientific and practical benefits.

Very low-density lipoprotein receptor increases in a liver-specific manner due to protein deficiency but does not affect fatty liver in mice

Very low-density lipoprotein receptor (VLDLR) is a member of the LDL receptor family that is involved in the uptake of VLDL into cells. Increased hepatic VLDLR under endoplasmic reticulum (ER) stress has been shown to cause fatty liver. In this study, the effect of dietary protein restriction on hepatic VLDLR and the role of VLDLR in fatty liver were investigated using Vldlr knockout (KO) mice. Growing wild-type (WT) and KO mice were fed a control diet containing 20% ​​protein or a low protein diet containing 3% protein for 11 days. In WT mice, the amount of hepatic Vldlr mRNA and VLDLR protein increased by approximately 8- and 7-fold, respectively, due to protein restriction. Vldlr mRNA and protein levels increased in both type 1 and type 2 VLDLR. However, neither Vldlr mRNA nor protein levels were significantly increased in heart, muscle, and adipose tissue, demonstrating that VLDLR increase due to protein restriction occurred in a liver-specific manner. Increased liver triglyceride levels during protein restriction occurred in KO mice to the same extent as in WT mice, indicating that increased VLDLR during protein restriction was not the main cause of fatty liver, which was different from the case of ER stress.

The effect of dietary protein restriction in a case of molybdenum cofactor deficiency with MOCS1 mutation

Molybdenum cofactor deficiency (MoCD) is an autosomal recessive inborn error of metabolism that results from mutations in genes involved in molybdenum cofactor (Moco) biosynthesis. MoCD is characterized clinically by intractable seizures and severe, rapidly progressing neurodegeneration leading to death in early childhood in the majority of known cases. We report on a patient with an unusual late disease onset and mild phenotype, characterized by delayed development and a decline triggered by a febrile illness and a subsequent dystonic movement disorder. Magnetic resonance imaging showed abnormal signal intensities of the bilateral basal ganglia. Blood and urine chemistry tests demonstrated remarkably low serum and urinary uric acid levels. A urine sulfite test was positive. Specific diagnostic workup showed elevated levels of xanthine and hypoxanthine in serum with increased urinary sulfocysteine (SSC) levels. Genetic analysis revealed a homozygous missense mutation at c.1510C > T (p.504R > W) in exon 10 of the MOCS1 in isoform 7 (rs1387934803). At age 1 year 4 months, the patient was placed on a low protein diet to reduce cysteine load and accumulation of sulfite and SCC in tissues. At 3 months after introduction of protein restriction, the urine sulfite test became negative and the urine SCC level was decreased. After starting the protein restriction diet, dystonic movement improved, and the patient's course progressed without regression and seizures. Electroencephalogram findings were remarkably improved. This finding demonstrates that the dietary protein restriction suppresses disease progression in mild cases of MoCD and suggests the effectiveness of dietary therapy in MoCD.

FGF21 signaling in glutamatergic neurons is required for weight loss associated with dietary protein dilution

Alterations in macronutrient intake can have profound effects on energy intake and whole-body metabolism. For example, reducing protein intake increases energy expenditure, increases insulin sensitivity and decreases body weight in rodents. Fibroblast growth factor 21 (FGF21) signaling in the brain is necessary for the metabolic effects of dietary protein restriction and has more recently been proposed to promote protein preference. However, the neuron populations through which FGF21 elicits these effects are unknown. Here, we demonstrate that deletion of β-klotho in glutamatergic, but not GABAergic, neurons abrogated the effects of dietary protein restriction on reducing body weight, but not on improving insulin sensitivity in both diet-induced obese and lean mice. Specifically, FGF21 signaling in glutamatergic neurons is necessary for protection against body weight gain and induction of UCP1 in adipose tissues associated with dietary protein restriction. However, β-klotho expression in glutamatergic neurons was dispensable for the effects of dietary protein restriction to increase insulin sensitivity. In addition, we report that FGF21 administration does not alter protein preference, but instead promotes the foraging of other macronutrients primarily by suppressing simple sugar consumption. This work provides important new insights into the neural substrates and mechanisms behind the endocrine control of metabolism during dietary protein dilution.

Short-term protein restriction at advanced age stimulates FGF21 signalling, energy expenditure and browning of white adipose tissue.

Dietary protein restriction has been demonstrated to improve metabolic health under various conditions. However, the relevance of ageing and age-related decline in metabolic flexibility on the effects of dietary protein restriction has not been addressed. Therefore, we investigated the effect of short-term dietary protein restriction on metabolic health in young and aged mice. Young adult (3months old) and aged (18months old) C57Bl/6J mice were subjected to a 3-month dietary protein restriction. Outcome parameters included fibroblast growth factor 21 (FGF21) levels, muscle strength, glucose tolerance, energy expenditure (EE) and transcriptomics of brown and white adipose tissue (WAT). Here, we report that a low-protein diet had beneficial effects in aged mice by reducing some aspects of age-related metabolic decline. These effects were characterized by increased plasma levels of FGF21, browning of subcutaneous WAT, increased body temperature and EE, while no changes were observed in glucose homeostasis and insulin sensitivity. Moreover, the low-protein diet used in this study was well-tolerated in aged mice indicated by the absence of adverse effects on body weight, locomotor activity and muscle performance. In conclusion, our study demonstrates that a short-term reduction in dietary protein intake can impact age-related metabolic health alongside increased FGF21 signalling, without negatively affecting muscle function. These findings highlight the potential of protein restriction as a strategy to induce EE and browning of WAT in aged individuals.

Effects of Short-Term Dietary Protein Restriction on Blood Amino Acid Levels in Young Men.

Pre-clinical studies show that dietary protein restriction (DPR) improves healthspan and retards many age-related diseases such as type 2 diabetes. While mouse studies have shown that restriction of certain essential amino acids is required for this response, less is known about which amino acids are affected by DPR in humans. Here, using a within-subjects diet design, we examined the effects of dietary protein restriction in the fasted state, as well as acutely after meal feeding, on blood plasma amino acid levels. While very few amino acids were affected by DPR in the fasted state, several proteinogenic AAs such as isoleucine, leucine, lysine, phenylalanine, threonine, tyrosine, and valine were lower in the meal-fed state with DPR. In addition, the non-proteinogenic AAs such as 1- and 3-methyl-histidine were also lower with meal feeding during DPR. Lastly, using in silico predictions of the most limiting essential AAs compared with human exome AA usage, we demonstrate that leucine, methionine, and threonine are potentially the most limiting essential AAs with DPR. In summary, acute meal feeding allows more accurate determination of which AAs are affected by dietary interventions, with most essential AAs lowered by DPR.

Short communication: Dietary protein restriction and conjugated linoleic acid supplementation in dairy cows affect milk composition, the cheese-making process, and cheese quality

We used 20 mid-lactating Holstein cows, housed in 4 pens according to a Latin square design, to evaluate the effects of dietary protein restriction (crude protein: 12.3 vs. 15.0% dry matter) and conjugated linoleic acid supplementation (CLA: 6.34 g/d of C18:2cis-9,trans-11 and 6.14 g/d of C18:2trans-10,cis-12) on milk composition, coagulation, curd firming and syneresis modeling, and cheese yield and quality (96 small cheeses). Dietary crude protein restriction, suggested as a way to reduce N excretion in farming, caused a reduction in milk protein content (-4%,), milk casein (-3.8%), lactose (-1%), cheese soluble protein (-16.8%), and the cheese maturation index (-15%), and a correlated increase in cheese fat content (+7.5%) and the fat to protein ratio (+18%). A modest reduction (-0.9%) in milk fat recovery in the curd did not affect cheese yield. The addition of CLA to the cows' diet, suggested as a way to improve N use efficiency and the nutritional value of dairy products, caused substantial alterations to the milk composition, cheese-making process, and cheese quality. The CLA reduced the fat (-12.3%), protein (-2%), casein (-2.2%), lactose (-1.0), and total solids (-4%) contents of milk, tended to delay coagulation, and weakened curd firming. The CLA reduced the fresh cheese yield (-7.5%) and cheese solids (-8.2%) because of the lower nutrient content of the milk, but also because of a lower recovery of milk protein in the curd (-0.9%) and lower total solids (-4.5%). It also reduced the fat content in the ripened cheese (-11.8%), as well as the fat to protein ratio (-19.4%) as a result of having increased the protein content (+9.3%). Last, it increased the lightness of the paste of the ripened cheeses (+3.3%), and especially the shear force (+16.3%). Dietary crude protein restriction, and CLA addition in particular, substantially altered the milk composition, cheese-making process, and cheese quality, and therefore needs to be carefully evaluated. Further studies are required to shed light on the causes of these modifications.

227-LB: Dietary Protein Restriction Induced–FGF21 Improves Metabolic Health during Aging

Aging and obesity are risk factors linked to the impairment of both energy and glucose homeostasis. Conversely, reducing caloric intake or the intake of select macronutrients or amino acids, including dietary protein restriction (DPR) and methionine restriction, defends against the detrimental effects of aging and obesity. Our data demonstrate that DPR increases energy expenditure and improves glucose homeostasis, and that the metabolic hormone FGF-21 coordinates these adaptive responses to protein restriction in young mice. However, the role of FGF-21 in mediating the effects of DPR during aging remains unclear. C57BL6 mice were fed either a normal protein (NP) or a low protein diet (LP), beginning at either young (3-months) or middle (12-months) age. A separate group of middle-aged mice were fed either a high-fat (HFD) diet or a high-fat, low-protein (HFLP) diet. Bodyweight and food intake were assessed weekly in all groups. Energy expenditure and glucose tolerance were assessed at 12 and 20 months of age in young mice and 16 months of age in middle aged-mice. Serum collected at sacrifice was used to measure FGF-21 levels. LP diet increased energy expenditure and food intake, and reduced body weight gain, in both young and middle-aged mice (P&amp;lt;0.05), and HFLP-diet similarly reduced body weight gain relative to HFD-fed controls (P&amp;lt;0.05). Glucose tolerance was improved in LP-fed young mice, and in LP and HFLP fed middle-aged mice (P&amp;lt;0.05). Lastly, FGF-21 levels were increased in both young and middle-aged mice in response to LP-diet (P&amp;lt;0.05), and in response to HFLP in middle-aged mice (P&amp;lt;0.05). These data indicate that the interaction of age or diet-induced obesity does not blunt the effects of DPR to induce-FGF-21, reduce body weight gain, increase energy expenditure, or improve glucose homeostasis. Disclosure C.M. Hill: None. D. McDougal: None. C. Morrison: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (R01DK105032, F32DK115137); Pennington Biomedical/Louisiana Nutrition Obesity Center (P30DK072476)

FGF21, not GCN2, influences bone morphology due to dietary protein restrictions

BackgroundDietary protein restriction is emerging as an alternative approach to treat obesity and glucose intolerance because it markedly increases plasma fibroblast growth factor 21 (FGF21) concentrations. Similarly, dietary restriction of methionine is known to mimic metabolic effects of energy and protein restriction with FGF21 as a required mechanism. However, dietary protein has been shown to be required for normal bone growth, though there is conflicting evidence as to the influence of dietary protein restriction on bone remodeling. The purpose of the current study was to evaluate the effect of dietary protein and methionine restriction on bone in lean and obese mice, and clarify whether FGF21 and general control nonderepressible 2 (GCN2) kinase, that are part of a novel endocrine pathway implicated in the detection of protein restriction, influence the effect of dietary protein restriction on bone. MethodsAdult wild-type (WT) or Fgf21 KO mice were fed a normal protein (18 kcal%; CON) or low protein (4 kcal%; LP) diet for 2 or 27 weeks. In addition, adult WT or Gcn2 KO mice were fed a CON or LP diet for 27 weeks. Young New Zealand obese (NZO) mice were placed on high-fat diets that provided protein at control (16 kcal%; CON), low levels (4 kcal%) in a high-carbohydrate (LP/HC) or high-fat (LP/HF) regimen, or on high-fat diets (protein, 16 kcal%) that provided methionine at control (0.86%; CON-MR) or low levels (0.17%; MR) for up to 9 weeks. Long bones from the hind limbs of these mice were collected and evaluated with micro-computed tomography (μCT) for changes in trabecular and cortical architecture and mass. ResultsIn WT mice the 27-week LP diet significantly reduced cortical bone, and this effect was enhanced by deletion of Fgf21 but not Gcn2. This decrease in bone did not appear after 2 weeks on the LP diet. In addition, Fgf21 KO mice had significantly less bone than their WT counterparts. In obese NZO mice dietary protein and methionine restriction altered bone architecture. The changes were mediated by FGF21 due to methionine restriction in the presence of cystine, which did not increase plasma FGF21 levels and did not affect bone architecture. ConclusionsThis study provides direct evidence of a reduction in bone following long-term dietary protein restriction in a mouse model, effects that appear to be mediated by FGF21.

Dietary protein restriction increases hepatic leptin receptor mRNA and plasma soluble leptin receptor in male rodents.

Leptin is an adipokine that regulates adipose tissue mass through membrane-anchored leptin receptor (Ob-R). Extracellular domain of Ob-R in plasma is called soluble leptin receptor (sOb-R), and is the main leptin-binding protein. Based on a previous DNA microarray analysis that showed induction of hepatic Ob-R mRNA in low-protein diet-fed mice, this study aimed to clarify the effect of dietary protein restriction on hepatic Ob-R mRNA and plasma sOb-R levels. First, the effect of protein restriction on hepatic Ob-R mRNA level was examined together with fasting and food restriction using male rats as common experimental model for nutritional research. Hepatic Ob-R mRNA level was increased by feeding low-protein diet for 7 d, although not significantly influenced by 12-h fasting and sixty percent restriction in food consumption. Then, effect of protein restriction on liver Ob-R and plasma sOb-R was investigated using male mice because specific sOb-R ELISA was more available for mice. Hepatic Ob-R mRNA level was also increased in protein restricted-mice although it did not increase in hypothalamus. Hepatic Ob-R protein was decreased, whereas plasma sOb-R was increased by protein restriction. Because the concentration of sOb-R increased without changing plasma leptin concentration, free leptin in plasma was significantly reduced. The direct effect of amino acid deprivation on Ob-R mRNA level was not observed in rat hepatoma cells H4IIE cultured in amino acid deprived medium. In conclusion, dietary protein restriction increased hepatic Ob-R mRNA, resulting in increased plasma sOb-R concentration, which in turn, reduces plasma free leptin level and may modulate leptin activity.

Effects of dietary protein restriction followed by realimentation on growth performance and liver transcriptome alterations of lamb

The present study aimed to investigate the compensatory effect of early protein restriction followed by a realimentation on growth performance of lamb and to explore the transcriptomic changes in liver. Thirty-two lambs with an initial birth weight of 2.3 ± 0.20 kg that were weaned on day 15 were randomly divided into two groups. The lambs were fed a basal diet with normal protein level (NPL, protein level in the milk replacer and starter, 25 and 21%, respectively) or low protein level (LPL, protein level in the milk replacer and starter, 19 and 15%, respectively) from 15 to 60 d, after which all lambs consumed the same diet with a normal protein level from 61 to 90 d. Protein restriction led to a significant decrease in average daily gain (ADG), body weight and liver weight (P < 0.05). Transcriptome analysis showed that 302 or 12 differentially expressed genes (DEGs) were identified during the restriction or recovery periods, respectively (P < 0.05). The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that DEGs enriched in nutrient metabolism and antioxidant capacity were down-regulated, while vessel development and immunity response-related genes up-regulated. The genes involved in metabolism of tyrosine were still down-regulated in the realimentation phase. Studies in this area indicated the accelerated growth effect of early protein restriction followed by a realimentation on growth performance of lambs and explored the transcriptomics change of liver which can help to develop feeding strategies to optimize the use of feedstuffs and in providing a new perspective for the study of early nutrition and epigenetics in later life.

Medical Nutrition Therapy for Patients with Non–Dialysis-Dependent Chronic Kidney Disease: Barriers and Solutions

Medical Nutrition Therapy for Patients with Non–Dialysis-Dependent Chronic Kidney Disease: Barriers and Solutions

Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints

Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of energy expenditure during protein restriction requires UCP1, promotes a resistance to cold stress, and is dependent on the concomitant hyperphagia. Wildtype, Ucp1-KO and Fgf21-KO mice were placed on control and low protein (LP) diets to assess changes in energy expenditure, food intake and other metabolic endpoints. Deletion of Ucp1 blocked LP-induced increases in energy expenditure and food intake, and exacerbated LP-induced weight loss. While LP diet increased energy expenditure and Ucp1 expression in an FGF21-dependent manner, neither LP diet nor the deletion of Fgf21 influenced sensitivity to acute cold stress. Finally, LP-induced energy expenditure occurred even in the absence of hyperphagia. Increased energy expenditure is a primary metabolic effect of dietary protein restriction, and requires both UCP1 and FGF21 but is independent of changes in food intake. However, the FGF21-dependent increase in UCP1 and energy expenditure by LP has no effect on the ability to acutely respond to cold stress, suggesting that LP-induced increases in FGF21 impact metabolic but not thermogenic endpoints.

Adult dietary protein has age- and context-dependent effects on male post-copulatory performance.

The highly conserved effect of dietary protein restriction on lifespan and ageing is observed in both sexes and across a vast range of taxa. This extension of lifespan is frequently accompanied by a reduction in female fecundity, and it has been hypothesized that individuals may reallocate resources away from reproduction and into somatic maintenance. However, effects of dietary protein restriction on male reproduction are less consistent, suggesting that these effects may depend on other environmental parameters. Using the neriid fly, Telostylinus angusticollis, we examined age-specific effects of adult dietary protein restriction on male post-copulatory reproductive performance (fecundity and offspring viability). To explore the context dependence of these effects, we simultaneously manipulated male larval diet and adult mating history. We found that protein-restricted males sired less viable offspring at young ages, but offspring viability increased with paternal age and eventually exceeded that of fully fed males. The number of eggs laid by females was not affected by male dietary protein, whereas egg hatching success was subject to a complex interaction of male adult diet, age, larval diet and mating history. These findings suggest that effects of protein restriction on male reproduction are highly context dependent and cannot be explained by a simple reallocation of resources from reproduction to somatic maintenance. Rather, these effects appear to involve changes in the scheduling of male reproductive investment with age.

Effects of dietary protein restriction on muscle fiber characteristics and mTORC1 pathway in the skeletal muscle of growing-finishing pigs.

BackgroundTo investigate the effects of dietary crude protein (CP) restriction on muscle fiber characteristics and key regulators related to protein deposition in skeletal muscle, a total of 18 growing-finishing pigs (62.30 ± 0.88 kg) were allotted to 3 groups and fed with the recommended adequate protein (AP, 16 % CP) diet, moderately restricted protein (MP, 13 % CP) diet and low protein (LP, 10 % CP) diet, respectively. The skeletal muscle of different locations in pigs, including longissimus dorsi muscle (LDM), psoas major muscle (PMM) and biceps femoris muscle (BFM) were collected and analyzed.ResultsResults showed that growing-finishing pigs fed the MP or AP diet improved (P < 0.01) the average daily gain and feed: gain ratio compared with those fed the LP diet, and the MP diet tended to increase (P = 0.09) the weight of LDM. Moreover, the ATP content and energy charge value were varied among muscle samples from different locations of pigs fed the reduced protein diets. We also observed that pigs fed the MP diet up-regulated (P < 0.05) muscular mRNA expression of all the selected key genes, except that myosin heavy chain (MyHC) IIb, MyHC IIx, while mRNA expression of ubiquitin ligases genes was not affected by dietary CP level. Additionally, the activation of mammalian target of rapamycin complex 1 (mTORC1) pathway was stimulated (P < 0.05) in skeletal muscle of the pigs fed the MP or AP diet compared with those fed the LP diet.ConclusionThe results suggest that the pigs fed the MP diet could catch up to the growth performance and the LDM weight of the pigs fed the AP diet, and the underlying mechanism may be partly due to the alteration in energy status, modulation of muscle fiber characteristics and mTORC1 activation as well as its downstream effectors in skeletal muscle of different locations in growing-finishing pigs.Electronic supplementary materialThe online version of this article (doi:10.1186/s40104-016-0106-8) contains supplementary material, which is available to authorized users.