Muscle Protein Content Research Articles

Improvement of muscle quality in tilapia (Oreochromis niloticus) with dietary faba bean (Vicia faba L.).

Tilapia (Oreochromis niloticus) is a freshwater fish which is farmed worldwide. Improving the muscle quality of fish has become a major goal while maintaining a sustainable aquaculture system. This research attempts to assess the effect of 0% (FB0), 40%(FB40), 50%(FB50), 60%(FB60) and 70% (FB70) faba bean on the texture parameter, histological analysis, proximate, amino acids, and fatty acids composition in tilapia fed 90 days. The results showed that hardness, chewiness, and shear force of tilapia muscle fed FB60, and FB70 were considerably more in comparison to fish fed FB0 at 90 days (p < 0.05). Tilapia fed faba beans had higher muscle fiber density, wider spaces between muscle fibers and smaller fiber diameter, with the greatest difference in tilapia fed FB60. The total protein content in tilapia fed FB40 was considerably more in comparison to in fish fed FB70 (p < 0.05), where the total protein content in muscle first increased and then reduced with increasing dietary faba bean level. The muscle ∑TAA, ∑EAA, valine, tyrosine, cysteine, aspartic acid, methionine, isoleucine, glutamic acid, leucine, arginine, and serine, contents in tilapia fed FB60 were much more in contrast to in fish fed FB0 (p < 0.05), which initially increased and then reduced with increasing dietary faba bean level. The muscle ∑PUFA content in tilapia fed dietary faba beans was greater compared with fish fed FB0, whereas the ∑SFA contents in tilapia fed FB50 and FB60 were lower in contrast to in fish fed FB0. In summary, dietary faba beans can improve muscle texture, muscle fibers, amino acids content and fatty acids content in tilapia. The research's results make a contribution to the improved knowledge of the association among muscle quality in tilapia and dietary faba beans.

Organic production of gilthead sea bream (Sparus aurata) using organic certified green pea protein and seaweed. Effects on growth, feed conversion and final product quality.

The aim of this study was to evaluate the use of novel ingredients such as green pea protein and Ascophyllum nodosum, a brown seaweed for the replacement of fish meal in feeds suitable for organic production. The growth, feed utilization and fillet composition of gilthead seabream were examined under a lab scale trial and based on the results a large-scale field trial was conducted in the facilities of Galaxidi marine farms in order to compare a novel feed with a typical commercial feed suitable for organic production.Final weight, growth rate and somatic indices of the fish fed these alternative ingredients did not show significant differences compared to the control group fed the commercial diet. Muscle protein content was higher in the fish fed the higher inclusion level of green pea protein, whereas lipid content was lower in both experimental diets. Fatty acid composition, in terms of n-3 and n-6 polyusaturated (PUFA), eicosapentanoic (EPA) and docosahexaenoic (DHA) acid content was higher in the muscle of the fish fed the experimental diets. In the case of the liver, the fatty acid profile reflected the feed composition, and the fish fed the diet with an inclusion of 19% green pea protein showed a lower content of protein and a higher content of n-6 PUFA, and monounsaturated fatty acids (MUFA).In view of the results obtained, the ingredients assayed in this study could be used in organic feed formulations as alternatives to fish meal obtained from trimmings since no negative effects were detected neither on fish growth, muscle composition, fish health nor end product quality and nutritional value.

The Emerging Importance of Cirsimaritin in Type 2 Diabetes Treatment.

Cirsimaritin is a dimethoxy flavon that has different biological activities such as antiproliferative, antimicrobial, and antioxidant activities. This study aims to investigate the anti-diabetic effects of cirsimaritin in a high-fat diet and streptozotocin-(HFD/STZ)-induced rat model of type 2 diabetes mellitus (T2D). Rats were fed HFD, followed by a single low dose of STZ (40 mg/kg). HFD/STZ diabetic rats were treated orally with cirsimaritin (50 mg/kg) or metformin (200 mg/kg) for 10 days before terminating the experiment and collecting plasma, soleus muscle, adipose tissue, and liver for further downstream analysis. Cirsimaritin reduced the elevated levels of serum glucose in diabetic rats compared to the vehicle control group (p < 0.001). Cirsimaritin abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control rats (p < 0.01). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the diabetic rats treated with cirsimaritin compared to the vehicle controls. The skeletal muscle and adipose tissue protein contents of GLUT4 (p < 0.01 and p < 0.05, respectively) and pAMPK-α1 (p < 0.05) were upregulated following treatment with cirsimaritin. Cirsimaritin was able to upregulate GLUT2 and AMPK protein expression in the liver (p < 0.01, <0.05, respectively). LDL, triglyceride, and cholesterol were reduced in diabetic rats treated with cirsimaritin compared to the vehicle controls (p < 0.001). Cirsimaritin reduced MDA, and IL-6 levels (p < 0.001), increased GSH levels (p < 0.001), and reduced GSSG levels (p < 0.001) in diabetic rats compared to the vehicle control. Cirsimaritin could represent a promising therapeutic agent to treat T2D.

Medial Gastrocnemius Muscle Properties of Children With Cerebral Palsy After Different Tone Treatments: A Pilot Study.

Spasticity in children with cerebral palsy can be managed by a spectrum of approaches, from conservative therapy, to temporary botulinum toxin A injections, to permanent transection of sensory nerves with a selective dorsal rhizotomy. This pilot study investigated whether these three tone management approaches are associated with histological and biochemical properties of the medial gastrocnemius. A convenience sample of children with cerebral palsy undergoing gastrocnemius lengthening surgery was enrolled. Intraoperative biopsies were obtained from three individuals (one each: minimal tone treatment; frequent gastrocnemius botulinum toxin A injections; previous selective dorsal rhizotomy). All individuals had plantarflexor contractures, weakness, and impaired motor control before the biopsy. Differences between participants were observed for muscle fiber cross-sectional area, fiber type, lipid content, satellite cell density, and centrally located nuclei. The most pronounced difference was the abundance of centrally located nuclei in the botulinum toxin A participants (52%) compared with the others (3-5%). Capillary density, collagen area and content, and muscle protein content were similar across participants. Several muscle properties seemed to deviate from reported norms, although age- and muscle-specific references are sparse. Prospective studies are necessary to distinguish cause and effect and to refine the risks and benefits of these treatment options.

Partial replacement of soybean meal by yellow mealworm (Tenebrio molitor) meal influences the flesh quality of Nile tilapia (Oreochromis niloticus).

This study investigated the effects of yellow mealworm meal (YM) replacing soybean meal (SBM) at different proportions (0%, 15%, 30% and 45%, referred as YM0, YM15, YM30 and YM45, respectively) on the flesh quality of Nile tilapia. A total of 360 fish (70.0±0.12g) were randomly divided into 4 groups (3 tanks per group). Fish were fed the experimental diet twice daily for 10wk. The results showed that muscle protein content significantly decreased in YM30 and YM45, while the lipid content significantly decreased in YM45 (P<0.05). The essential amino acids and flavor amino acids of the muscle were not affected by the YM substitution, while saturated fatty acid content decreased in YM30 and YM45 compared with YM0 (P<0.05). Fillets in YM45 had higher hardness, gumminess, and a higher proportion of thin myofibers (≤100μm, P<0.05) than those in other groups. Further analysis revealed that apoptosis and atrophy related genes were up-regulated, while the muscle antioxidant capacity decreased significantly in YM45 (P<0.05), which may be related to the high acid value in YM45 diet. Our findings indicated that YM could replace up to 30% SBM without substantially altering the flesh quality. When the replacement ratio increased to 45%, the flesh quality would change. Special attention should be paid to avoid feed rancidity which may affect the flesh quality of fish.

High Protein Diet Has Beneficial Effects in Murine Muscular Dystrophy

In normal muscle there is a delicate balance between muscle protein synthesis and protein degradation. It is believed that this balance is disturbed in muscular dystrophy (MD) by decreased muscle protein synthesis and/or increased muscle protein degradation, resulting in net catabolism. In an attempt to reduce or reverse this catabolism, a high protein diet (HPD, 50% protein) was fed to dystrophic mice (129/ReJ dy) for 4 wk. The effects on muscle biochemistry, muscle function and muscle morphology were compared with those in dystrophic mice fed a normal diet (NPD, 20% protein) and in nondystrophic mice (NORM) also fed the 20% protein diet. Compared with NORM mice, NPD mice demonstrated greater rates of muscle protein synthesis (P < 0.05) as measured by the incorporation of labeled phenylalanine into muscle, greater protein degradation (P < 0.01) as measured by urinary 3-methylhistidine excretion, and lower muscle protein concentration (P < 0.01). When dystrophic mice were fed HPD for 4 wk, protein degradation was lower (P < 0.01) and muscle protein concentration greater (P < 0.01) than in NPD mice. These biochemical improvements were accompanied by greater morphological uniformity of muscle fibers, higher volume density of muscle fibers per unit area of muscle (P < 0.01), and lower shape factor (P < 0.01). Functionally, HPD led to improved muscle endurance (P < 0.01) and increased hind-limb utilization (P 0.01). We conclude that in murine dystrophy, HPD decreases net muscle catabolism, principally by decreasing muscle protein degradation, resulting in improvement in muscle morphology, strength and function.

Exposure to waterborne cadmium induce disorder of lipid metabolism, antioxidant system and autophagy in the muscle of crayfish Procambarus clarkii

Cadmium (Cd) is a non-essential toxic metal in the body, which can cause harmful effects on the aquatic environment and aquatic organisms. In this study, the effects of acute Cd exposure on lipid metabolism disorder, oxidative stress and autophagy in abdominal muscles of Procambarus clarkii were investigated, as well the underlying molecular mechanisms were explored. P. clarkii were exposed to 0 (control), 1 and 5 mg Cd/l, respectively, for 5 days. We found that TG content, fas, hsl, and cpt1 gene expression levels, as well as the Srebp1 protein content in abdominal muscle decreased with the Cd concentrations increased, indicating that acute Cd exposure induced disorder of lipid metabolism in the abdominal muscle of P. clarkii. Further studies showed that acute Cd exposure provoked oxidative stress in the abdominal muscle of P. clarkii by increasing the accumulation of malondialdehyde (MDA) in the abdominal muscle. The oxidative stress of abdominal muscle induced by acute Cd exposure may be due to the reduction of catalases (CAT) and glutathione peroxidase (GPX) enzyme activities and Nrf2 protein content in the nucleus. The expression levels of autophagy-related genes (beclin1, atg101, atg13, atg3, atg4b, atg5, atg7, lc3a, lc3c atg9a) were also affected by acute Cd exposure, suggesting that acute Cd exposure also affected autophagy activity in abdominal muscle of P. clarkii. Our research indicates that waterborne acute Cd exposure can induce lipid metabolism disorder, and oxidative stress, and inhibit the expression of genes that trigger autophagy in the abdominal muscle of P. clarkii. These results may be useful for understanding the mechanism of Cd muscular toxicity in crustaceans.

The protective role of vitamin C on intestinal damage induced by high-dose glycinin in juvenile Rhynchocypris lagowskii Dybowski

This study was to evaluate the mitigative effects of vitamin C (VC) on growth inhibition and intestinal damage induced by glycinin in juvenile Rhynchocypris lagowskii Dybowski. 270 healthy juvenile Rhynchocypris lagowskii Dybowski (4.65 ± 0.04 g) were randomly divided into 3 treatments, and fed with control diet, 80 g/kg glycinin diet and 80 g/kg glycinin+200 mg/kg VC diet respectively for 8 weeks. The results showed that glycinin significantly decreased the weight gain rate, specific growth rate, protein efficiency rate, feed efficiency rate and feeding rate of fish compared with the control group (P < 0.05), while VC supplementation improved the growth performance and feed utilization efficiency, and reached a level similar to the control group. Similarly, VC significantly increased the crude protein content of muscle and whole-body, and hepatopancreas and intestinal protease activities of fish fed with glycinin diet (P < 0.05). The distal intestine of fish in glycinin group showed typical damage characteristics, including breakage and atrophy of intestinal mucosal fold, and increased intestinal mucosal permeability. However, fish fed the glycinin + VC diet showed an unimpaired normal intestinal morphology. Usefully, VC supplementation could also restore impaired immune function and antioxidant capacity. VC down-regulated the mRNA levels of pro-inflammatory cytokines TNF‐α and IL-1β, and up-regulated the mRNA levels of anti-inflammatory cytokines IL-10 and TGF-β in the distal intestine of fish fed with glycinin. Furthermore, glycinin exposure could reduce the mRNA levels of HO-1, CAT and GPx by inhibiting the activation of Nrf2-Keap1 signaling pathway, while VC supplementation reversed this phenomenon and maintained the homeostasis of antioxidant defense system. Concluded, glycinin causes growth inhibition, digestive dysfunction and intestinal damage of Rhynchocypris lagowskii Dybowski, while sufficient VC intake is beneficial for fish to resist the adverse effects of glycinin.

Breaking up sedentary time to improve glucose control in a population at risk for developing type 2 diabetes (BURST2D study): a randomized controlled trial

Background: To compare the acute and chronic effects of frequent, short physical activity (PA) bouts spread throughout the day to a time-matched intervention consisting in a single continuous daily bout of PA on glucose control and potential underlying mechanisms in adults at risk of developing type 2 diabetes (T2D). Methods: BURST2D is a single-center, parallel-group, randomized controlled trial, in which sedentary adults with overweight/obesity and pre-diabetes (18-45 y, BMI: 25-40 kg/m2, fasting glucose: 100-125 mg/dL or 2h glucose: 140-199 mg/dL or HbA1c: 5.7-6.4%) will be randomly assigned to one of two 3-month PA interventions: BREAK, nine bouts of 5-min brisk walking performed every hour for nine consecutive hours (45-min/d total), 5 days/wk; ONE, one continuous 45-min bout of brisk walking, 5 days/wk. Primary outcomes will be daily glycemic mean and variability, fasting glucose and HbA1c, postprandial plasma glucose and insulin, glucose kinetics, and content of skeletal muscle proteins related to insulin signaling and glucose uptake. Secondary outcomes will be whole-body insulin sensitivity, 24-h total substrate oxidation, postprandial triglycerides, daily PA and sedentary behavior (SB) patterns, knowledge and attitude towards PA and SB, barriers and facilitators to intervention compliance, self-perceived appetite, mood, and sleep. Outcomes will be assessed at baseline and after one month and/or three months of intervention. Conclusions: This study will establish the acute and chronic effects of breaking up SB, independent of increases in PA, on glucose control and underlying mechanisms in adults with pre-diabetes. Results will advance the science of T2D prevention. Trial registration: This study is registered with the ClinicalTrials.gov, registry number NTC05041491.

New Treatment for Type 2 Diabetes Mellitus Using a Novel Bipyrazole Compound.

2',3,3,5'-Tetramethyl-4'-nitro-2'H-1,3'-bipyrazole (TMNB) is a novel bipyrazole compound with unknown therapeutic potential in diabetes mellitus. This study aims to investigate the anti-diabetic effects of TMNB in a high-fat diet and streptozotocin-(HFD/STZ)-induced rat model of type 2 diabetes mellitus (T2D). Rats were fed HFD, followed by a single low dose of STZ (40 mg/kg). HFD/STZ diabetic rats were treated orally with TMNB (10 mg/kg) or (200 mg/kg) metformin for 10 days before terminating the experiment and collecting plasma, soleus muscle, adipose tissue, and liver for further downstream analysis. TMNB reduced the elevated levels of serum glucose in diabetic rats compared to the vehicle control group (p &lt; 0.001). TMNB abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control rats (p &lt; 0.001). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the diabetic rats treated with TMNB compared to the vehicle controls. The skeletal muscle and adipose tissue protein contents of GLUT4 and AMPK were upregulated following treatment with TMNB (p &lt; 0.001, &lt; 0.01, respectively). TMNB was able to upregulate GLUT2 and AMPK protein expression in liver (p &lt; 0.001, &lt; 0.001, respectively). LDL, triglyceride, and cholesterol were reduced in diabetic rats treated with TMNB compared to the vehicle controls (p &lt; 0.001, 0.01, respectively). TMNB reduced MDA and IL-6 levels (p &lt; 0.001), and increased GSH level (p &lt; 0.05) in diabetic rats compared to the vehicle controls. Conclusion: TMNB ameliorates insulin resistance, oxidative stress, and inflammation in a T2D model. TMNB could represent a promising therapeutic agent to treat T2D.

Acute resistance exercise training does not augment mitochondrial remodelling in master athletes or untrained older adults.

Background: Ageing is associated with alterations to skeletal muscle oxidative metabolism that may be influenced by physical activity status, although the mechanisms underlying these changes have not been unraveled. Similarly, the effect of resistance exercise training (RET) on skeletal muscle mitochondrial regulation is unclear. Methods: Seven endurance-trained masters athletes ([MA], 74 ± 3years) and seven untrained older adults ([OC]. 69 ± 6years) completed a single session of knee extension RET (6 x 12 repetitions, 75% 1-RM, 120-s intra-set recovery). Vastus lateralis muscle biopsies were collected pre-RET, 1h post-RET, and 48h post-RET. Skeletal muscle biopsies were analyzed for citrate synthase (CS) enzyme activity, mitochondrial content, and markers of mitochondrial quality control via immunoblotting. Results: Pre-RET CS activity and protein content were ∼45% (p < .001) and ∼74% greater in MA compared with OC (p = .006). There was a significant reduction (∼18%) in CS activity 48h post-RET (p < .05) in OC, but not MA. Pre-RET abundance of individual and combined mitochondrial electron transport chain (ETC) complexes I-V were significantly greater in MA compared with OC, as were markers of mitochondrial fission and fusion dynamics (p-DRP-1Ser616, p-MFFSer146, OPA-1 & FIS-1, p < .05 for all). Moreover, MA displayed greater expression of p-AMPKThr172, PGC1α, TFAM, and SIRT-3 (p < .05 for all). Notably, RET did not alter the expression of any marker of mitochondrial content, biogenesis, or quality control in both OC and MA. Conclusion: The present data suggest that long-term aerobic exercise training supports superior skeletal muscle mitochondrial density and protein content into later life, which may be regulated by greater mitochondrial quality control mechanisms and supported via superior fission-fusion dynamics. However, a single session of RET is unable to induce mitochondrial remodelling in the acute (1h post-RET) and delayed (48h post-RET) recovery period in OC and MA.

Isorhamnetin Reduces Glucose Level, Inflammation, and Oxidative Stress in High-Fat Diet/Streptozotocin Diabetic Mice Model.

Background: Isorhamnetin is a flavonoid that is found in medical plants. Several studies showed that isorhamnetin has anti-inflammatory and anti-obesity effects. This study aims to investigate the anti-diabetic effects of isorhamnetin in a high-fat diet and Streptozotocin-(HFD/STZ)-induced mice model of type 2 diabetes. Materials and Methods: Mice were fed with HFD followed by two consecutive low doses of STZ (40 mg/kg). HFD/STZ diabetic mice were treated orally with isorhamnetin (10 mg/kg) or (200 mg/kg) metformin for 10 days before sacrificing the mice and collecting plasma and soleus muscle for further analysis. Results: Isorhamnetin reduced the elevated levels of serum glucose compared to the vehicle control group (p < 0.001). Isorhamnetin abrogated the increase in serum insulin in the treated diabetic group compared to the vehicle control mice (p < 0.001). The homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in diabetic mice treated with isorhamnetin compared to the vehicle controls. Fasting glucose level was significantly lower in diabetic mice treated with isorhamnetin during the intraperitoneal glucose tolerance test (IPGTT) (p < 0.001). The skeletal muscle protein contents of GLUT4 and p-AMPK-α were upregulated following treatment with isorhamnetin (p > 0.01). LDL, triglyceride, and cholesterol were reduced in diabetic mice treated with isorhamnetin compared to vehicle control (p < 0.001). Isorhamnetin reduced MDA, and IL-6 levels (p < 0.001), increased GSH levels (p < 0.001), and reduced GSSG levels (p < 0.05) in diabetic mice compared to vehicle control. Conclusions: Isorhamnetin ameliorates insulin resistance, oxidative stress, and inflammation. Isorhamnetin could represent a promising therapeutic agent to treat T2D.

Sublethal Toxicity of Copper Sulphate (CuSO4 ) on Protein, amino acids changes in Liver, Kidney and Muscle of the fish Mystus vittatus

The present study indicates the toxic effects of Copper Sulphate on fish. The sublethal toxicity of Copper Sulphate on protein content in liver, kidney and muscle of fish Mystus vittatus have been studied. The fish exposed to sublethal concentration of 1/20th (low), and 1/10th (high) for the period of 10, 20 and 30 days. The results showed decrease in the protein content and increase in the amino acid content in liver, kidney and muscle of fish Mystus vittatus. The significant reduction in protein content and elevated levels of amino acids is apparently indicative of the toxic effect of Copper Sulphate on biochemical parameter and organism’s response to the toxic stress.

Glutamine and leucine administration attenuates muscle atrophy in sepsis

AimsThis study investigated whether l-glutamine (Gln) and/or l-leucine (Leu) administration could attenuate muscle atrophy in a mouse model of cecal ligation and puncture (CLP)-induced sepsis. Materials and methodsSeptic mice were given a daily intraperitoneal injection of Gln, Leu, or Gln plus Leu, and mice were sacrificed on either day 1 or 4 after CLP. Blood and muscles were collected for analysis of amino acid contents and markers related to protein degradation, muscle regeneration, and protein synthesis. Key findingsLeu treatment alone increased both muscle mass and total muscle protein content on day 4 after CLP. Gln administration reduced muscular Gln contents on day 1 and enhanced plasma Gln levels on day 4. Higher plasma branched-chain amino acid (BCAA) abundances and lower muscular BCAA levels were observed in Leu-treated mice on day 4. Gln and Leu individually suppressed muscle expressions of the E3 ubiquitin ligase genes, Trim63 and Fbxo32, on day 4 after CLP. As to muscle expressions of myogenic genes, both Gln and Leu upregulated Myog expression on day 1, but Leu alone enhanced Myf5 gene expression, whereas Gln plus Leu increased MyoD and Myog expression levels on day 4. Akt/mammalian target of rapamycin (mTOR) signaling was only activated by Gln and Leu when individually administered. SignificanceGln and/or Leu administration reduces sepsis-induced muscle degradation and promotes myogenic gene expressions. Leu treatment alone had more-pronounced effects on maintaining muscle mass during sepsis. A combination of Gln and Leu failed to show synergistic effects on alleviating sepsis-induced muscle atrophy.

Comparison of the Retention Rates of Synthetic and Natural Astaxanthin in Feeds and Their Effects on Pigmentation, Growth, and Health in Rainbow Trout (Oncorhynchus mykiss).

The coloring efficiency and physiological function of astaxanthin in fish vary with its regions. The aim of this study was to compare the retention rates of dietary astaxanthin from different sources and its effects on growth, pigmentation, and physiological function in Oncorhynchus mykiss. Fish were fed astaxanthin-supplemented diets (LP: 0.1% Lucantin® Pink CWD; CP: 0.1% Carophyll® Pink; EP: 0.1% Essention® Pink; PR: 1% Phaffia rhodozyma; HP: 1% Haematococcus pluvialis), or a diet without astaxanthin supplementation, for 56 days. Dietary astaxanthin enhanced pigmentation as well as the growth of the fish. The intestinal morphology of fish was improved, and the crude protein content of dorsal muscle significantly increased in fish fed with astaxanthin. Moreover, astaxanthin led to a decrease in total cholesterol levels and alanine aminotransferase and aspartate aminotransferase activity in plasma. Fish fed on the CP diet also produced the highest level of umami amino acids (aspartic acid and glutamic acid). Regarding antioxidant capacity, astaxanthin increased Nrf2/HO-1 signaling and antioxidant enzyme activity. Innate immune responses, including lysozyme and complement systems, were also stimulated by astaxanthin. Lucantin® Pink CWD had the highest stability in feed and achieved the best pigmentation, Essention® Pink performed best in growth promotion and Carophyll® Pink resulted in the best flesh quality. H. pluvialis was the astaxanthin source for achieving the best antioxidant properties and immunity of O. mykiss.

Substitution of soybean meal with Clostridium autoethanogenum protein in grass carp (Ctenopharygodon idella) diets: Effects on growth performance, feed utilization, muscle nutritional value and sensory characteristics

Iso-nitrogenous and iso-lipidic diets replace 0 %, 30 %, and 100 % of soybean meal (SBM) with Clostridium autoethanogenum protein (CAP) (namely, CAP0, CAP30 and CAP100) were prepared to evaluate their effects on the growth performance, feed utilization, muscle nutritional value and sensory characteristics of grass carp. The results indicated that the growth performance and feed utilization of grass carp fed a diet containing CAP groups were comparable to those of the control group (P > 0.05). However, CAP-containing diet enhanced pH, cohesiveness, springiness, gumminess and chewiness of muscle (P < 0.05), thereby improving the muscle physical properties. The CAP100 group did not affect the muscle content of crude protein and crude fat (P > 0.05), nevertheless it increased the content of essential and non-essential amino acids (P < 0.05), which improved the nutritional value of grass carp muscle. The CAP30 group promoted the synthesis of proteins in grass carp by regulating rapamycin signaling pathway which increased the crude protein content in muscle. Meanwhile, the CAP30-containing diet upregulated the expression of genes myogenic factor 5 (Myf5), myogenic regulatory factor 4 (Mrf4), myogenin (MyoG), myogenic determining factor (MyoD) and myosin heavy chain (MyHC) proteins which participate in muscle growth and development of the muscle. Compared with the control group, the tenderness and the content of inosinic acid in the CAP100 group muscle were increased (P < 0.05), and the content of volatile compounds which regulate fishy smell was decreased in muscles in the CAP100 group (P < 0.05). Collectively, our results indicated that CAP improved the nutritional value and sensory properties of the muscle without affecting the growth performance and feed utilization of grass carp.

Decreased methylglyoxal-mediated protein glycation in the healthy aging mouse model of ectopic expression of UCP1 in skeletal muscle

Mice with ectopic expression of uncoupling protein-1 (UCP1) in skeletal muscle exhibit a healthy aging phenotype with increased longevity and resistance to impaired metabolic health. This may be achieved by decreasing protein glycation by the reactive metabolite, methylglyoxal (MG). We investigated protein glycation and oxidative damage in skeletal muscle of mice with UCP1 expression under control of the human skeletal actin promoter (HSA-mUCP1) at age 12 weeks (young) and 70 weeks (aged). We found both young and aged HSA-mUCP1 mice had decreased advanced glycation endproducts (AGEs) formed from MG, lysine-derived Nε(1-carboxyethyl)lysine (CEL) and arginine-derived hydroimidazolone, MG-H1, whereas protein glycation by glucose forming Nε-fructosyl-lysine (FL) was increased ca. 2-fold, compared to wildtype controls. There were related increases in FL-linked AGEs, Nε-carboxymethyl-lysine (CML) and 3-deoxylglucosone-derived hydroimidazolone 3DG-H, and minor changes in protein oxidative and nitration adducts. In aged HSA-mUCP1 mice, urinary MG-derived AGEs/FL ratio was decreased ca. 60% whereas there was no change in CML/FL ratio – a marker of oxidative damage. This suggests that, normalized for glycemic status, aged HSA-mUCP1 mice had a lower flux of whole body MG-derived AGE exposure compared to wildtype controls. Proteomics analysis of skeletal muscle revealed a shift to increased heat shock proteins and mechanoprotection and repair in HSA-mUCP1 mice. Decreased MG-derived AGE protein content in skeletal muscle of aged HSA-mUCP1 mice is therefore likely produced by increased proteolysis of MG-modified proteins and increased proteostasis surveillance of the skeletal muscle proteome. From this and previous transcriptomic studies, signaling involved in enhanced removal of MG-modified protein is likely increased HSPB1-directed HUWE1 ubiquitination through eIF2α-mediated, ATF5-induced increased expression of HSPB1. Decreased whole body exposure to MG-derived AGEs may be linked to increased weight specific physical activity of HSA-mUCP1 mice. Decreased formation and increased clearance of MG-derived AGEs may be associated with healthy aging in the HSA-mUCP1 mouse.

Monsoon Effect on Heavy Metal and Chemical Composition in Parastromateus niger of the Oman Sea: Health Risk Assessment of Fish Consumption.

This study aimed to evaluate the bioaccumulation of heavy metals (copper, zinc, and lead) and chemical compositions (fat, protein, moisture, and ash) in the Parastromateus niger muscle of the Oman Sea in pre-monsoon and post-monsoon. An atomic absorption spectrophotometer was used to determine heavy metal concentrations in fish muscle tissue. Chemical composition contents were measured using the Association of Official Analytical Chemists (AOAC) methods. Zinc was the most abundant heavy metal in two seasons (0.077 ± 0.005μg/g), followed by copper (0.033 ± 0.005μg/g) and lead (0.015 ± 0.005μg/g). The mean concentrations of all heavy metals of muscle in pre-monsoon were higher than in post-monsoon. The concentrations of Cu, Zn, and Pb were lower than the maximum permissible limits (MPL) of international standards for human consumption established by FAO, FAO/WHO, WHO, and MAFF. The protein and fat content in fish muscle collected in pre-monsoon was higher than in post-monsoon. A significant difference between protein, fat, moisture, and ash values was recorded in two seasons (P < 0.05). The human health risk of heavy metals was evaluated according to the United States Environmental Protection Agency (USEPA) standards. The estimated daily intake (EDI) of each heavy metal in two seasons was lower than the tolerable daily intake (TDI). THQ (target hazard quotient) and TTHQ (total target hazard quotient) values were lower than the threshold limit of 1.0, indicating a non-carcinogenic risk for consumers. TR (target carcinogenic risk) value for Pb was much lower than the unacceptable risk level (10-4); therefore, the consumption of muscles of Parastromateus niger did not significantly pose a human health risk.

The effect of aeromoniasis on protein and DNA content and histopathology of muscle and gill in adaptively immunized fish

The effect of aeromoniasis on protein and DNA content and histopathology of muscle and gill in adaptively immunized fish

ATF5 is a regulator of exercise-induced mitochondrial quality control in skeletal muscle

ObjectivesThe Mitochondrial Unfolded Protein Response (UPRmt) is a compartment-specific mitochondrial quality control (MQC) mechanism that uses the transcription factor ATF5 to induce the expression of protective enzymes to restore mitochondrial function. Acute exercise is a stressor that has the potential to temporarily disrupt organellar protein homeostasis, however, the roles of ATF5 and the UPRmt in maintaining basal mitochondrial content, function and exercise-induced MQC mechanisms in skeletal muscle are not known. MethodsATF5 KO and WT mice were examined at rest or after a bout of acute endurance exercise. We measured protein content in whole muscle, nuclear, cytosolic and mitochondrial fractions, in addition to mRNA transcript levels in whole muscle. Using isolated mitochondria, we quantified rates of oxygen consumption and ROS emission to observe the effects of the absence of ATF5 on organelle function. ResultsATF5 KO mice exhibited a larger and less functional muscle mitochondrial pool, most likely a culmination of enhanced biogenesis via increased PGC-1α expression, and attenuated mitophagy. The absence of ATF5 resulted in a reduction in antioxidant proteins and increases in mitochondrial ROS emission, cytosolic cytochrome c, and the expression of mitochondrial chaperones. KO muscle also displayed enhanced exercise-induced stress kinase signaling, but a blunted mitophagic and UPRmt gene expression response, complemented by significant increases in the basal mRNA abundance and nuclear localization of ATF4. Instead of promoting its nuclear translocation, acute exercise caused the enrichment of ATF5 in mitochondrial fractions. We also identified PGC-1α as an additional regulator of the basal expression of UPRmt genes. ConclusionThe transcription factor ATF5 retains a critical role in the maintenance of mitochondrial homeostasis and the appropriate response of muscle to acute exercise for the optimization of mitochondrial quality control.