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The current study was performed to investigate whether dietary β-hydroxy-β-methylbutyrate (HMB) could regulate liver injury in a lipopolysaccharide- (LPS-) challenged piglet model and to determine the mechanisms involved. Thirty piglets ( 21 ± 2 days old , 5.86 ± 0.18 kg body weight) were randomly divided into the control (a basal diet, saline injection), LPS (a basal diet), or LPS+HMB (a basal diet + 0.60% HMB-Ca) group. After 15 d of treatment with LPS and/or HMB, blood and liver samples were obtained. The results showed that in LPS-injected piglets, HMB supplementation ameliorated liver histomorphological abnormalities induced by LPS challenge. Compared to the control group, the activities of serum aspartate aminotransferase and alkaline phosphatase were increased in the LPS-injected piglets ( P < 0.05 ). The LPS challenge also downregulated the mRNA expression of L-PFK, ACO, L-CPT-1, ICDH β, and AMPKα1/2 and upregulated the mRNA expression of PCNA, caspase 3, TNF-α, TLR4, MyD88, NOD1, and NF-κB p65 ( P < 0.05 ). However, these adverse effects of the LPS challenge were reversed by HMB supplementation ( P < 0.05 ). These results indicate that HMB may exert protective effects against LPS-induced liver injury, and the underlying mechanisms might involve the improvement of hepatic energy metabolism via regulating AMPK signaling pathway and the reduction of liver inflammation via modulating TLR4 and NOD signaling pathways.

Background Oxidative stress is a key factor that influences piglets’ health. Taurine plays an imperative role in keeping the biological system from damage. This study was conducted to investigate the protective effect of taurine against muscle injury due to the secondary effect of diquat toxicity. Results Our study found that taurine effectively and dose-dependently alleviated the diquat toxicity induced rise of feed/gain, with a concurrent improvement of carcass lean percentage. The plasma content of taurine was considerably increased in a dose-dependent manner. Consequently, dietary taurine efficiently improved the activity of plasma antioxidant enzymes. Furthermore, taurine attenuated muscle damage by restoring mitochondrial micromorphology, suppressing protein degradation and reducing the percentage of apoptotic cells in the skeletal muscle. Taurine supplementation also suppressed the genes expression levels of the antioxidant-, mitochondrial biogenesis-, and muscle atrophy-related genes in the skeletal muscle of piglets with oxidative stress. Conclusions These results showed that the dose of 0.60% taurine supplementation in the diet could attenuate skeletal muscle injury induced by diquat toxicity. It is suggested that taurine could be a potential nutritional intervention strategy to improve growth performance.

The aim of this study was to investigate the alteration in growth performance and lipid metabolism during the development of yellow fat in pigs. A total of 30 pigs (9.23 ± 0.21 kg) were assigned to three treatments: (1) low fish oil (LFO), basal diet + 2% fresh fish oil; (2) high fish oil (HFO), basal diet + 8% fresh fish oil; and (3) oxidized fish oil (OFO), basal diet + 8% OFO (peroxide value = 250 meqO2kg−1). Pigs fed HFO and OFO diets showed yellow staining of fat and decreased growth performance, including average daily gain, average daily feed intake, and final body weight (P

Free radical-induced oxidative stress contributes to the development of metabolic syndromes (Mets), including overweight, hyperglycemia, insulin resistance and pro-inflammatory state. Most free radicals are generated from the mitochondrial electron transport chain; under physiological conditions, their levels are maintained by efficient antioxidant systems. A variety of transcription factors have been identified and characterized that control gene expression in response to oxidative stress status. Natural antioxidant compounds have been largely studied for their strong antioxidant capacities. This review discusses the recent progress in oxidative stress and mitochondrial dysfunction in Mets and highlights the anti-Mets, anti-oxidative, and anti-inflammatory effect of polyphenols as potential nutritional therapy.

Mitochondrial dysfunction in skeletal muscle has emerged as key to the development of obesity and its related metabolic disorders. Leucine (Leu) is an essential amino acid that has been reported to increase mitochondrial biogenesis in muscle cells, as has its metabolite β-hydroxy-β-methylbutyrate (HMB). However, two questions-which one is more potent and what is the cellular mechanisms of the action of Leu and HMB-remain to be answered. Therefore we aimed to investigate the effects of Leu and HMB on mitochondrial function in C2 C12 myotubes and analyze the underlying molecular mechanism.The effects of Leu and HMB on mitochondrial mass, mitochondrial respiration capacity, and the expression of genes related to mitochondrial biogenesis were evaluated in C2 C12 myotubes. Differentiated myotubes were treated with Leu (0.5 mM) or HMB (50 μM) with or without PPARβ/δ antagonist (GSK3787, 1 μM) and CDK4 antagonist (LY2835219, 1.5 μM), respectively, for 24 h. The results indicated that treatment with Leu or HMB significantly increased mitochondrial mass, mitochondrial respiration capacity, and the messenger RNA expression of genes associated with mitochondrial biogenesis (P0.05). In addition, these positive effects of Leu or HMB on these parameters were attenuated by GSK3787 and LY2835219 treatments (P0.05).Our results provide evidence indicating that as with Leu, HMB alone could increase mitochondrial biogenesis and function via regulation of PPARβ/δ and CDK4 pathways. Moreover, HMB seems to be more potent than Leu in the positive regulation of mitochondrial biogenesis and function in C2 C12 myotubes because the dosage used for HMB was much lower than that for Leu.

This study aimed at investigating the effects of dietary xylo-oligosaccharide (XOS) on intestinal functions (i.e., intestinal morphology, tight junctions, gut microbiota and metabolism) and growth performance in weaned piglets. 19 weaned piglets were randomly divided into two groups (n = 9/10): a control group (basic diet) and a XOS treated group in which piglets were fed 0.01% XOS for 28 days. Growth performance, blood cells and biochemical parameters, serum cytokines, intestinal morphology, tight junctions, gut microbiota, and the metabolic profiles of the gut digesta were analyzed. The results showed that dietary supplementation with XOS had little effects on growth performance, blood cells and biochemical parameters, and intestinal morphology. However, the inflammatory status and intestinal barrier were improved in XOS-fed piglets evidenced by the reduction of IFN-γ and upregulation of ZO-1. Microbiota analysis showed that XOS enhanced α-diversity and affected the relative abundances of Lactobacillus, Streptococcus, and Turicibacter at the genus level. The alterations in the microbiota might be further involved in carbohydrate metabolism, cell motility, cellular processes and signaling, lipid metabolism, and metabolism of other amino acids by functional prediction. A metabolomics study identified three differentiated metabolites, including coenzyme Q6, zizyphine A, and pentadecanal, which might be produced by the microbiota and further affect host metabolism. In conclusion, dietary XOS improved the inflammatory status, gut barrier, and microbiota communities, which might be used as a potential feed additive to prevent gut dysfunction caused by weaning in the pig industry.

This study aimed to investigate the effects of leucine (Leu) and its metabolites (α-ketoisocaproate (KIC) and β-hydroxy-β-methylbutyrate (HMB)) on muscle protein metabolism in growing pigs fed low-protein diets. 32 pigs (Large White × Landrace, 9.55 ± 0.19 kg) were divided into four groups (basal diet, L-Leu, KIC-Ca, HMB-Ca). Results showed that compared to the control, dietary supplementation of KIC and excess Leu significantly decreased the weight of soleus muscle (SM, P 0.05). In conclusion, HMB, but not KIC or excess Leu, might act as a nutrient signal to stimulate positive protein balance especially in muscles of oxidative fiber-types of growing pigs fed low-protein diets, and these effects might be associated with the Akt signaling.

The aim of this study was to investigate the effects of dietary β-hydroxy-β-methylbutyrate (HMB) on lipopolysaccharide (LPS)-induced muscle atrophy and to investigate the mechanisms involved. Sixty pigs (21 ± 2 days old, 5.86 ± 0.18 kg body weight) were used in a 2 × 3 factorial design and the main factors included diet (0, 0.60%, or 1.20% HMB) and immunological challenge (LPS or saline). After 15 d of treatment with LPS and/or HMB, growth performance, blood parameters, and muscle protein degradation rate were measured. The results showed that in LPS-injected pigs, 0.60% HMB supplementation increased the average daily gain and average daily feed intake and decreased the feed : gain ratio (P < 0.05), with a concurrent increase of lean percentage. Moreover, 0.60% HMB supplementation decreased the serum concentrations of blood urea nitrogen, IL-1β, and TNF-α and the rate of protein degradation as well as cell apoptosis in selected muscles (P < 0.05). In addition, dietary HMB supplementation (0.60%) regulated the expression of genes involved in mitochondrial biogenesis and increased the phosphorylation of Akt and Forkhead Box O3a (FoxO3a) in selected muscles, accompanied by decreased protein expression of muscle RING finger 1 and muscle atrophy F-box. These results indicate that HMB may exert protective effects against LPS-induced muscle atrophy by normalizing the Akt/FoxO3a axis that regulates ubiquitin proteolysis and by improving mitochondrial biogenesis.

Lipid metabolism is an important and complex biochemical process involved in the storage of energy and maintenance of normal biological functions. Leucine, a branched amino acid, has anti-obesity effects on glucose tolerance, lipid metabolism, and insulin sensitivity. Leucine also modulates mitochondrial dysfunction, representing a new strategy to target aging, neurodegenerative disease, obesity, diabetes, and cardiovascular disease. Although various studies have been carried out, much uncertainty still exists and further studies are required to fully elucidate the relationship between leucine and lipid metabolism. This review offers an up-to-date report on leucine, as key roles in both lipid metabolism and energy homeostasis in vivo and in vitro by acceleration of fatty acid oxidation, lipolysis, activation of the adenosine 5′-monophosphate-activated protein kinase (AMPK)–silent information regulator of transcription 1 (SIRT1)–proliferator-activated receptor γ coactivator-1α (PGC-1α) pathway, synthesis, and/or secretion of adipokines and stability of the gut microbiota.

Background: Intestinal barrier contributes as an important role in maintaining intestinal homeostasis. Oxidative stress can cause critical damages in intestinal integrity of animals. Objectives: This study was conducted to investigate the alleviated effect of taurine against small intestine (duodenum, jejunum, ileum) injury induced by oxidative stress. Methods: The piglet model of diquat-induced oxidative stress was employed. In addition, analysis of intestinal morphology, reverse transcription PCR (RT-PCR), and Western blot were used in this study. Results: Compared with the control group (CON), diquat-induced oxidative stress triggers immune response; the content of immunoglobulin M (IgM) and immunoglobulin G (IgG) was significantly changed, but 0.60% taurine supplementation could restore the level of serum immunoglobulin. Oxidative stress induces serious damage in intestinal morphology structure and tight junction barrier. Compared with the CON, the villus height of intestine was significantly decreased, the crypt depth and villus height/crypt depth (V/C) were also decreased, and 0.60% taurine supplementation could restore impaired morphology and even improve crypt depth and V/C of the jejunum and ileum. Compared with the CON, oxidative stress markedly increased the messenger RNA (mRNA) expression level of claudin-1 and occludin in the duodenum, and the value of occludin was significantly decreased in the jejunum of the diquat group (DIQ). Relative to the DIQ, 0.60% taurine supplementation increased the mRNA expression level of claudin-1, occludin, and ZO-1 in the ileum. Compared with the CON, the expression of claudin-1 protein was significantly upregulated, and occludin and ZO-1 protein were both downregulated in the small intestine of DIQ. Conclusion: Taurine exerts protective effects by regulating immune response and restores the intestinal tight junction barrier when piglets suffer from oxidative stress.

The effects and roles of branched-chain amino acid (BCAAs) ratios in lipid metabolism in adipose tissues of pigs are still unkown. We used pigs (Large White × Landrace, 35 ± 2 d) to investigate the effects of varying BCAA ratios (Leu: Ile: Val = 1:1:1, 1:0.75:0.75, 1:0.51:0.63, 1:0.25:0.25) on growth, carcass traits, and fat metabolism in adipose tissues. Results showed that as the ratio declined, the weight of total fat mass reduced while the adiponectin concentrations increased (P

Background: The effects and roles of the leucine (Leu) metabolite β-hydroxy-β-methylbutyrate (HMB) in lipid metabolism in adipose tissues of pigs are still unknown. Objectives: This study was conducted to investigate the effects of excess Leu versus HMB on growth, carcass traits, and lipid metabolism in adipose tissues of growing pigs. Methods and results: Compared to control, the Leu/HMB group significantly increased/reduced weight of total fat mass, respectively, with a concurrent increase of serum adiponectin concentration (P < 0.05). Moreover, dietary HMB supplementation regulated the expression of genes involved in adipose tissue function, accompanied by increases/decreases in the phosphorylation of AMPKα/mTOR in perirenal adipose tissue, respectively (P < 0.05). Serum IL-15 concentration and the mRNA abundance of IL-15, PGC-1α, and NRF-1 were also increased in the HMB group (P < 0.05). Conclusions: HMB supplementation can regulate adipose tissue function including fatty acid oxidation, lipolysis, and adipokine secretion. These effects may be partly mediated by AMPKα-mTOR pathway and associated with mitochondrial biogenesis, the AMPK-PGC-1α axis, and myokines secreted by muscle tissues.

Simple Summary This study shows the transcription profiles and the functional network in lncRNA and mRNA in the subcutaneous adipose tissue of Ningxiang piglets in four stages of development (piglets, nursery pigs, early fattening, and late fattening). A total of 2872 novel lncRNAs have now been determined. A total of 10,084 DEmRNAs and 931 DElncRNAs were determined. Interestingly, most DEmRNAs were up-regulated in the piglet stage and, in contrast, DElncRNAs were up-regulated in the late fattening stage. A complicated interaction between mRNAs and lncRNAs was determined via STEM and WGCNA, demonstrating that lncRNAs are an essential regulatory component in mRNAs. Modules 2 and 5 shows a similar mode of transcriptions for both mRNA and lncRNA, which are mainly involved in steroid biosynthesis, glycosphingolipid biosynthesis, metabolic pathways, and glycerolipid metabolism. The transcription levels of mRNAs and lncRNAs for both modules were higher in the early and late fattening stage. This may be explained by the active fatty acids, sterols, steroids, and lipid-related metabolic activity in the subcutaneous adipose tissue during the early and late fattening stage. Abstract Ningxiang pigs, a Chinese bred pig known for its tender meat and high quality unsaturated fatty acids. This study discovers the transcription profiles and functional networks in long non-coding RNA (lncRNA) and messenger RNA (mRNA) in subcutaneous adipose tissue. Subcutaneous adipose tissue was collected from piglet, nursery pig, early fattening, and late fattening stage of Ningxiang piglets, and lncRNA and mRNA transcription of each stage was profiled. A total of 339,204,926 (piglet), 315,609,246 (nursery), 266,798,202 (early fattening), and 343,740,308 (late fattening) clean reads were generated, and 2872 novel lncRNAs were identified. Additionally, 10,084 differential mRNAs (DEmRNAs) and 931 differential lncRNAs were determined. Most DEmRNAs were up-regulated in the piglet stage, while they were down-regulated in late fattening stage. A complicated interaction between mRNAs and lncRNAs was identified via STEM and WGCNA, demonstrated that lncRNAs are a significant regulatory component in mRNAs. The findings showed that modules 2 and 5 have a similar mode of transcription for both mRNA and lncRNA, and were mainly participated in steroid biosynthesis, glycosphingolipid biosynthesis, metabolic pathways, and glycerolipid metabolism. The mRNAs and lncRNAs transcription levels of both modules was higher in the early and late fattening stage, which may be due to the active activity of the metabolism in relation to fatty acids, sterols, steroids, and lipids in the subcutaneous adipose tissue during the early and late fattening stage. These findings could be expected to result in further research of the functional properties of lncRNA from subcutaneous adipose tissue at different stages of development in Ningxiang pigs.

// Yehui Duan 1, 2 , Fengna Li 1, 4 , Wenlong Wang 3 , Qiuping Guo 1, 2 , Chaoyue Wen 3 and Yulong Yin 1, 3 1 Laboratory of Animal Nutritional Physiology and Metabolic Process, Institute of Subtropical Agriculture Chinese Academy of Sciences, Key Laboratory of Agro-Ecological Processes in Subtropical Region, Hunan Provincial Engineering Research Center for Healthy Livestock and Poultry Production, Scientific Observing and Experimental Station of Animal Nutrition and Feed Science in South-Central, Ministry of Agriculture, Changsha, China 2 University of Chinese Academy of Sciences, Beijing, China 3 Laboratory of Animal Nutrition and Human Health, School of Biology, Hunan Normal University, Changsha, Hunan, China 4 Hunan Co-Innovation Center of Animal Production Safety, CICAPS, Hunan Collaborative Innovation Center for Utilization of Botanical Functional Ingredients, Changsha, Hunan, China Correspondence to: Yulong Yin, email: yinyulong@isa.ac.cn Fengna Li, email: lifengna@isa.ac.cn Keywords: branched-chain amino acids; energy axis; growing pigs; muscle fiber type Received: May 04, 2017 Accepted: September 05, 2017 Published: October 31, 2017 ABSTRACT There mainly exists four major myosin heavy chains (MyHC) (i.e., I, IIa, IIx, and IIb) in growing pigs. The current study aimed to explore the effects of low-protein diets supplemented with varying branched-chain amino acids (BCAAs) on muscle fiber characteristics and the AMPK-SIRT1-PGC-1α axis in skeletal muscles. Forty growing pigs (9.85 ± 0.35 kg) were allotted to 5 groups and fed with diets supplemented with varying leucine: isoleucine: valine ratios: 1:0.51:0.63 (20% crude protein, CP), 1:1:1 (17% CP), 1:0.75:0.75 (17% CP), 1:0.51:0.63 (17% CP), and 1:0.25:0.25 (17% CP), respectively. The skeletal muscles of different muscle fiber composition, that is, longissimus dorsi muscle (LM, a fast-twitch glycolytic muscle) , biceps femoris muscle (BM, a mixed slow- and fast-twitch oxido-glycolytic muscle), and psoas major muscle (PM, a slow-twitch oxidative muscle) were collected and analyzed. Results showed that relative to the control group (1:0.51:0.63, 20% CP), the low-protein diets with the leucine: isoleucine: valine ratio ranging from 1:0.75:0.75 to 1:0.25:0.25 especially augmented the mRNA and protein abundance of MyHC I fibers in BM and lowered the mRNA abundance of MyHC IIb particularly in LM ( P < 0.05), with a concurrent increase in the activation of AMPK and the mRNA abundance of SIRT and PGC-1α in BM ( P < 0.05). The results reveal that low-protein diets supplemented with optimal BCAA ratio, i.e. 1:0.75:0.75-1:0.25:0.25, induce muscle more oxidative especially in oxido-glycolytic skeletal muscle of growing pigs. These effects are likely associated with the activation of the AMPK-SIRT1-PGC-1α axis.

This study was conducted to determine the effect of low-protein diets on protein and energy metabolism in skeletal muscle, and to elucidate the underlying mechanism. A total of 18 growing pigs (average initial body weight = 36.47 kg) were individually penned and assigned to three treatments; each treatment was fed one of three diets containing either 18%, 15%, or 12% CP. The results showed that reducing dietary CP contents decreased (P0.05) the weight of half Longissimus dorsi (LD) muscle and serum concentration of insulin-like growth factor 1 (IGF-1). Compared with the 18% and 15% CP treatments, the 12% CP treatment suppressed (P0.05) the components of mammalian target of rapamycin complex 1 (mTORC1) pathway, but upregulated (P0.05) the mRNA levels for proteolysis-related genes, and concomitantly caused an increase (P0.05) in the percentage of apoptotic cells in LD muscle. Along with lower (P0.05) AMP/ATP ratio and greater (P0.05) energy charge value in LD muscle of the 12% CP treatment, there was a concurrent decrease (P0.05) in the proteins for AMP-activated protein kinase α (AMPKα) pathway. Likewise, these results were also observed in the Biceps femoris muscle with slightly different degree of impacts. These results indicate that the retardation effect of low-protein supply on muscle growth of growing pigs could be likely regulated by inhibiting IGF-1/mTORC1 protein synthesis cascade, along with strong alterations in energy status and AMPKα pathway.

Obesity has been considered to be a chronic disease that requires medical prevention and treatment. Intriguingly, many factors, including adipose tissue dysfunction, mitochondrial dysfunction, alterations in the muscle fiber phenotype and in the gut microbiota composition, have been identified to be involved in the development of obesity and its associated metabolic disorders (in particular type 2 diabetes mellitus). In this narrative review, we will discuss our current understanding of the relationships of these factors and obesity development, and provide a summary of potential treatments to manage obesity. Level of Evidence Level V, narrative review.

// Qian Jiang 1, 2, * , Gang Liu 1, 3, * , Xiuqi Wang 4 , Yongqing Hou 5 , Yehui Duan 1, 2 , Guoyao Wu 1, 6, 7 , Yulong Yin 1, 3, 8 and Kang Yao 1, 3, 8 1 Key Laboratory of Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, Hunan Provincial Engineering Research Center for Healthy Livestock and Poultry Production, Scientific Observing and Experimental Station of Animal Nutrition and Feed Science in South-Central, Ministry of Agriculture, Changsha 410125, China 2 University of Chinese Academy of Sciences, Beijing 100039, China 3 Hunan Collaborative Innovation Center for Utilization of Botanical Functional Ingredients, Hunan Collaborative Innovation Center of Animal Production Safety, Changsha 410128, China 4 College of Animal Science, South China Agricultural University/National Engineering Research Center for Breeding Swine Industry, Guangzhou 510642, Guangdong Province, China 5 Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, 430023 Wuhan, China 6 Department of Animal Science, Texas A&M University, College Station, TX 77843, USA 7 Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan Polytechnic University, Wuhan 430023, China 8 College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China * These authors have contributed equally to this research Correspondence to: Kang Yao, email: yaokang@isa.ac.cn Keywords: alpha-ketoglutarate, oxidative damage, cell apoptosis, mitochondrial respiration, intestinal porcine epithelial cells Received: May 05, 2017 Accepted: June 19, 2017 Published: August 24, 2017 ABSTRACT Alpha-ketoglutarate, a key intermediate in the Krebs cycle, has been reported to benefit intestinal health. We tested whether alpha-ketoglutarate can protect intestinal cells against hydrogen peroxide induced damage and aimed to reveal the underlying mechanism. Intestinal porcine epithelial cell line J2 were cultured in Dulbecco’s Modified Eagle Medium-High glucose with or without alpha-ketoglutarate and hydrogen peroxide. Cell viability, proliferation, mitochondrial respiration, mitochondrial membrane potential, antioxidant function, apoptosis and mitochondrial-dependent apoptotic pathways were determined. Our experiments demonstrated that, first, exposure to 100μM hydrogen peroxide decreased cell viability, DNA synthesis, mitochondrial respiration and antioxidant function, and increased apoptosis. Second, 2mM alpha-ketoglutarate addition attenuated hydrogen peroxide-induced cell cycle arrest, and improved cell viability, DNA synthesis, mitochondrial respiration and antioxidant function. Third, alpha-ketoglutarate enhanced tricarboxylic acid cycle activity, mitochondrial respiration, and decrease the intracellular content of reactive oxygen species. Finally, alpha-ketoglutarate stabilized the mitochondrial membrane potential, increased the ratio of Bcl-2/Bax, decreased the release of cytochrome c and activation of caspase-3, thereby prevented cell apoptosis. Altogether, we proposed that alpha-ketoglutarate protects intestinal cells against hydrogen peroxide-induced damage partly via mitochondria dependent pathway.

Mammalian skeletal muscles are composed of two major fibre types (I and II) that differ in terms of size, metabolism and contractile properties. In general, slow-twitch type I fibres are rich in mitochondria and have a greater insulin sensitivity than fast-twitch type II skeletal muscles. Although not widely appreciated, a forced induction of the slow skeletal muscle phenotype may inhibit the progress of obesity and diabetes. This potentially forms the basis for targeting slow/oxidative myofibers in the treatment of obesity. In this context, a better understanding of the molecular basis of fibre-type specification and plasticity may help to identify potential therapeutic targets for obesity and diabetes.

Skeletal muscle and adipose tissue are the two largest organs in the body. Skeletal muscle is an effector organ, and adipose tissue is an organ that stores energy; in addition, they are endocrine organs that secrete cytokines, namely myokines and adipokines, respectively. Myokines consist of myostatin, interleukin (IL)-8, IL-15, irisin, fibroblast growth factor 21, and myonectin; adipokines include leptin, adiponectin, resistin, chemerin, and visfatin. Furthermore, certain cytokines, such as IL-6 and tumor necrosis factor-α, are released by both skeletal muscle and adipose tissue and exhibit a bioactive effect; thus, they are called adipo-myokines. Recently, novel myokines or adipokines were identified through the secretomic technique, which has expanded our knowledge on the previously unknown functions of skeletal muscle and adipose tissue and provide a new avenue of investigation for obesity treatment or animal production. This review focuses on the roles of and crosstalk between myokines and adipokines in skeletal muscle and adipose tissue that modulate the molecular events in the metabolic homeostasis of the whole body.

Weaning affects intestinal development in mammals, and pigs are often used as an animal model for analyzing the metabolism and physiology of differentiating middle villus intestinal epithelial cells (DIECs). To assess the impact of weaning on the proteomes of DIECs, we weaned piglets on day 14 and collected their jejunum on days 0, 1, 3, 5, and 7 after weaning. Levels of proteins associated with (a) Golgi vesicle transport and protein glycosylation; (b) monosaccharide, lipid, phospholipid, and nucleotide metabolism; and (c) Krebs cycle and respiratory electron transport chain were decreased in DIECs after weaning. These results indicate that weaning decreases nutrient metabolism in DIECs. Moreover, these results suggest that dietary interventions (e.g., supplementation with functional amino acids) are required to counter these changes.

This study was conducted to compare the effects of Eucommia ulmoides leaves (EL) in different forms (EL extract, fermented EL, and EL powder) with antibiotics on growth performance, intestinal morphology, and the microbiota composition and diversity of weanling piglets. Compared to the control group, the antibiotics and EL extract significantly increased the average daily gain and decreased the feed: gain ratio as well as the diarrhea rate (P < 0.05). The EL extract significantly decreased the crypt depth and increased the ratio of villus height to crypt depth (P < 0.05), while the fermented EL group did the opposite (P < 0.05). The crypt depth in the antibiotics group was of similar value to the EL extract group, and was lower than the fermented EL and EL powder groups (P < 0.05). Compared to the control and antibiotics groups, the jejunul claudin-3 mRNA expression and the concentrations of total VFA, Chao 1, and ACE were significantly augmented in the EL extract group of piglets (P < 0.05). The EL extract groups also showed elevated Shannon (P < 0.05) and Simpson (P = 0.07) values relative to the control and antibiotics groups. At the phylum level, the EL extract group exhibited a reduced abundance of Bacteroidetes and an enhanced abundance of Firmicutes. At the genus level, the abundance of Prevotella was augmented in the EL extract group. Moreover, compared with the antibiotic group, the acetate concentration was enhanced in the EL extract and fermented EL groups. Overall, dietary supplementation with the EL extract, but not the fermented EL or EL powder, improved growth performance, jejunul morphology and function, as well as changed colonic microbial composition and diversity, which might be an alternative to confer protection against weanling stress in weanling piglets.

The aim of this study was to explore the effects of β-hydroxy-β-methylbutyrate (HMB) on intestinal function of lipopolysaccharide (LPS)-challenged piglets.Forty weaned piglets were used in a 2 × 2 factorial design. The major factors were challenge (saline or LPS) and diet (basal diet or 0.6% HMB-Ca diet). After 15 d of treatment with LPS or HMB, blood and intestine samples were obtained.The results showed that in LPS-injected pigs, HMB supplementation significantly increased jejunal villus height and ileal villus height-to-crypt depth ratio and decreased ileal crypt depth (P0.05). HMB also improved intestinal function indicated by elevated activities of intestinal mucosal disaccharidase and tricarboxylic acid cycle key enzymes. Furthermore, HMB significantly downregulated mRNA expression of Sirt1 in jejunum and mRNA expression of AMPKα1 and Sirt1 in ileum (P0.05), with a concurrent decrease of AMPKα phosphorylation in jejunum and ileum. Microbiota analysis indicated that HMB supplementation significantly increased α-diversity and affected relative abundances of Romboutsia and Sarcina at the genus level, accompanied by increased concentrations of all short-chain fatty acids except propionate in the terminate ileum of LPS-injected piglets.Dietary HMB supplementation could improve intestinal integrity, function, microbiota communities, and short-chain fatty acid concentrations in LPS-challenged piglets, suggesting its potential usage as a feed additive in weaned piglets to alleviate intestinal dysfunction triggered by immune stress.

Obesity increases the risk of developing insulin resistance and diabetes and is a major public health concern. Our previous study shows that dietary β-hydroxy-β-methylbutyrate (HMB) improves lipid metabolism in a pig model. However, it remains unclear whether HMB blocks obesity through gut microbiota. In this study, we found that HMB reduced body weight, alleviated the whitening of brown adipose tissue, and improved insulin resistance in mice fed a high-fat diet (HFD). High-throughput pyrosequencing of the 16S rRNA demonstrated that HMB administration significantly reversed the gut microbiota dysbiosis in HFD-fed mice, including the diversity of gut microbiota and relative abundances of Bacteroidetes and Firmicutes. Moreover, microbiota transplantation from HMB-treated mice attenuated HFD-induced lipid metabolic disorders. Furthermore, HFD-fed mice showed lower short-chain fatty acids, whereas administration of HMB increased the propionic acid production. Correlation analysis identified a significant correlation between propionic acid production and the relative Bacteroidetes abundance. Sodium propionate treatment also attenuated HFD-induced lipid metabolic disorders. Collectively, our results indicated that HMB might be used as a probiotic agent to reverse HFD-induced obesity, and the potential mechanism was associated with reprogramming gut microbiota and metabolism, especially Bacteroidetes-mediated propionic acid production. In future studies, more efforts should be made to confirm and expand the beneficial effects of HMB to human models.-Duan, Y., Zhong, Y., Xiao, H., Zheng, C., Song, B., Wang, W., Guo, Q., Li, Y., Han, H., Gao, J., Xu, K., Li, T., Yin, Y., Li, F., Yin, J., Kong, X. Gut microbiota mediates the protective effects of dietary β-hydroxy-β-methylbutyrate (HMB) against obesity induced by high-fat diets.

Obesity develops from an imbalance of energy homeostasis and is associated with chronic low-grade inflammation in white adipose tissues (WAT). Inflammation is involved in the pathophysiology of many obesity-induced disorders including insulin resistance and diabetes. Increasing evidence has shown that dietary leucine supplementation positively affects the parameters associated with obesity and obesity-related metabolic disorders. The beneficial effects include increased loss of body weight, reduced WAT inflammation, improved lipid and glucose metabolism, enhanced mitochondrial function, and preserved lean body mass. Although these beneficial effects have not been clearly established, dietary leucine supplementation, either alone or as part of a therapeutic regimen, may be a good nutritional tool in the prevention and management of obesity and obesity-induced metabolic disorders.

Branched-chain amino acids (BCAA), including leucine (Leu), isoleucine (Ile), and valine (Val), play critical roles in energy homeostasis and lipid metabolism in addition to their other functions, such as in protein metabolism. This study investigated the effects of different dietary BCAA ratios on the intramuscular fat (IMF) content and fatty acid composition in different location of skeletal muscles, including the longissimus dorsi (LD), biceps femoris (BF), and psoas major (PM) muscles of growing pigs, and also examined the mRNA expression levels of genes involved in lipid metabolism in these muscle tissues. The experiment was performed on 40 growing pigs (Large White × Landrace) with a similar initial weight (9.85 ± 0.35 kg). The pigs were randomly assigned to one of five diets: diet A was a positive control and contained 20 % crude protein (CP) with a Leu:Ile:Val ratio of 1:0.51:0.63 according to the recommendation of the National Research Council (NRC); for diets B to E, the CP level was reduced to 17 %, and the Leu:Ile:Val ratios were 1:1:1, 1:0.75:0.75, 1:0.51:0.63, and 1:0.25:0.25, respectively. No significant difference was observed in the average feed intake and feed efficiency of the pigs fed the low protein diet (17 % CP) with BCAA treatments relative to the positive control. However, there was a tendency for increased feed efficiency of the 1:0.75:0.75 group compared with the 1:1:1 group (P = 0.09). The BCAA ratio of 1:0.75:0.75 (17 % CP) increased the IMF content of BF muscle (P

This experiment was conducted to investigate the effects of branched-chain amino acids (BCAA) supplemented in protein-restricted diets on the growth performance and the expression profile of amino acid transporters and energy metabolism related regulators in the white adipose tissue (WAT) of different regional depots including dorsal subcutaneous adipose (DSA) and abdominal subcutaneous adipose (ASA). A total of 24 crossbred barrows (7.40 ± 0.70 kg) were randomly divided into 4 groups and were fed the following isocaloric diets for 33 days: 1) a recommended adequate protein diet (AP, 20% CP, as a positive control); 2) a low protein diet (LP, 17% CP); 3) the LP diet supplemented with BCAA (LP + B, 17% CP) to reach the same level of the AP diet group; 4) the LP diet supplemented with 2 times the amount of BCAA (LP + 2B, 17% CP). The daily gain and daily feed intake of the LP diet group were the lowest among all the treatments (P 0.05). Moreover, BCAA supplementation down-regulated the expression levels of amino acid transporters including L-type amino acid transporter 1 and sodium-coupled neutral amino acid transporter 2 in DSA, but up-regulated the expression level of L-type amino acid transporter 4 in ASA (P

This study was conducted to determine the alterations of inflammatory cytokines, energy metabolic regulators, and muscle fiber type in the LM of the piglets postweaning. Crossbred piglets (Landrace × Large White) weaned at 14 d age were randomly selected from 8 litters and slaughtered at 0 (W0), 1 (W1), 3 (W3), 5 (W5), or 7 (W7) days postweaning. The glycogen content, free glucose concentration, and enzyme activities, including ATPase (Na/K, Ca/Mg), creatine kinase, and lactic dehydrogenase (LDH), were detected in the skeletal muscle tissue. Concentrations of proinflammatory cytokines, including IL-1β, IL-6, and tumor necrosis factor-α (TNF-α), and anti-inflammatory cytokines, including IL-10 and transforming growth factor-β1 (TGF-β1), were measured in serum. The mRNA abundance of the above cytokines, energy metabolic regulators, and muscle fiber type related genes were determined via real-time quantitative PCR analysis. The adenosine monophosphate-activated protein kinase α (AMPKα) signaling was measured by Western blot analysis. Our results showed ATPase activities were lower on W7 d but LDH activity was higher on W3 d after weaning ( < 0.05). Serum TNF-α concentration was markedly increased on W1 d, then returned to the value of preweaning ( < 0.05), and almost all the values of inflammatory cytokines were reduced to a low point on W5 d after weaning. Additionally, the IL-6 mRNA abundance was upregulated during W3 to W7 d, but cytokine TNF-α was upregulated just on W7 d ( < 0.05). The mRNA abundance of AMPKα and uncoupling protein (UCP) 3 were both higher on W1 and W3 d, and UCP2 was higher on W7 d postweaning ( < 0.05). Myosin heavy chain (MyHC) I and MyHC IIx-type fibers were enhanced on W1 d, then returned to the value of preweaning, and the MyHC IIb-type fiber was significantly increased on W5 and W7 d ( < 0.05). Meanwhile, the value of P-AMPKα/T-AMPKα increased on W3 d postweaning ( < 0.05) compared with that on W0 d. These results indicate that weaning stress induced inflammation in skeletal muscle tissue during at least 7 d postweaning. It upregulated the expression of proinflammatory cytokines, which then stimulated the AMPKα and UCP involved in energy metabolism events, accompanied by significant alterations in muscle fiber type.

The metabolic roles of mitochondria go far beyond serving exclusively as the major producer of ATP in tissues and cells. Evidence has shown that mitochondria may function as a key regulator of skeletal muscle fiber types and overall well-being. Maintaining skeletal muscle mitochondrial content and function is important for sustaining health throughout the lifespan. Of great importance, β-hydroxy-β-methylbutyrate (HMB, a metabolite of L-leucine) has been proposed to enhance the protein deposition and efficiency of mitochondrial biogenesis in skeletal muscle, as well as muscle strength in both exercise and clinical settings. Specifically, dietary supplementation with HMB increases the gene expression of peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α), which represents an upstream inducer of genes of mitochondrial metabolism, coordinates the expression of both nuclear- and mitochondrion-encoded genes in mitochondrial biogenesis. Additionally, PGC-1α plays a key role in the transformation of skeletal muscle fiber type, leading to a shift toward type I muscle fibers that are rich in mitochondria and have a high capacity for oxidative metabolism. As a nitrogen-free metabolite, HMB holds great promise to improve skeletal muscle mass and function, as well as whole-body health and well-being of animals and humans.

Here, we investigated the roles and mechanisms of flavonoids from mulberry leaves (FML) on lipid metabolism in high fat diet (HFD)-fed mice. ICR mice were fed either a control diet (Con) or HFD with or without FML (240 mg/kg/day) by oral gavage for six weeks. FML administration improved lipid accumulation, alleviated liver steatosis and the whitening of brown adipose tissue, and improved gut microbiota composition in HFD-fed mice. Microbiota transplantation from FML-treated mice alleviated HFD-induced lipid metabolic disorders. Moreover, FML administration restored the production of acetic acid in HFD-fed mice. Correlation analysis identified a significant correlation between the relative abundances of Bacteroidetes and the production of acetic acid, and between the production of acetic acid and the weight of selected adipose tissues. Overall, our results demonstrated that in HFD-fed mice, the lipid metabolism improvement induced by FML administration might be mediated by gut microbiota, especially Bacteroidetes-triggered acetic acid production.

In recent years, chronic overnutrition, such as consumption of a high-fat diet (HFD), has been increasingly viewed as a significant modifiable risk factor for diseases such as diabetes and certain types of cancer. However, the mechanisms by which HFDs exert adverse effects on human health remains poorly understood. Here, this paper will review the recent scientific literature about HFD-induced inflammation and subsequent development of diseases and cancer, with an emphasis on mechanisms involved. Given the expanding global epidemic of excessive HFD intake, understanding the impacts of a HFD on these medical conditions, gaining great insights into possible underlying mechanisms, and developing effective therapeutic strategies are of great importance.

The objective of the study was to investigate the effect of feeding reduced CP, AA-supplemented diets on meat quality in growing and finishing pigs as well as the related mechanism. In experiment 1, 18 growing pigs (36.5 kg BW) were assigned randomly and fed 1 of 3 corn-soybean meal diets containing either 18% CP (normal protein, NP), 15% CP (low protein, LP), or 12% CP (very low protein, VLP). In experiment 2, 18 finishing pigs (62.3 kg BW) were allotted randomly into 1 of the following diets: 16% CP (NP), 13% CP (LP), or 10% CP (VLP). In both experiments, the LP and VLP diets were supplemented with crystalline AA to achieve equal content of standardized ileal digestible lysine, methionine, threonine, and tryptophan. At the end of each experiment, all pigs were slaughtered to collect longissimus dorsi muscle (LM) samples. Samples were used for determining meat quality, intramuscular fat (IMF) content, fatty acid composition, free AA profile, and expression of genes for myosin heavy chain isoforms. Results showed that growing and finishing pigs fed the LP diets increased (P < 0.05) redness value of LM, while finishing pigs fed the LP and VLP diets decreased (P < 0.05) the shear force values. Compared with the NP diet, growing and finishing pigs fed lower CP diets had higher (P < 0.05) contents of IMF and MUFA, and lower (P < 0.05) contents of PUFA. Besides, higher (P < 0.05) expression levels of type I and/or IIa muscle fibers were observed in LP diet-fed growing and finishing pigs, and greater concentrations of taurine and tasty AA in VLP diet-fed growing and finishing pigs. Taken together, our results indicate that low-protein diets could positively affect meat quality of growing and finishing pigs, and likely through regulation of IMF content and fatty acid composition, fiber characteristics, and free AA profile in the muscle.

The aim of this study was to investigate the effects of different branched-chain amino acid (BCAA) ratios on intestinal cell proliferation and protein metabolism.This in vivo study was conducted in growing pigs (average initial body weight = 9.85 ± 0.35 kg) exposed to different leucine, isoleucine, and valine (Leu:Ile:Val) ratios (1:1:1, 1:0.75:0.75, 1:0.51:0.63, and 1:0.25:0.25) in 17% crude protein (CP) diets for 45 d to determine intestinal morphology, cell proliferation, and amino acid transporter mRNA expression. This in vitro study was performed in porcine jejunal epithelial cell line to investigate the effects of different BCAA ratios (0, 1:0.25:0.25, 1:0.5:0.5, and 1:1:1) on cell proliferation, AA transporter expression. and protein turnover.Relative to the positive control (Leu:Ile:Val = 1:0.51:0.63, 20% CP), the 1:0.75:0.75 group (17% CP) significantly increased the jejunal villus height, the percentage of proliferating cell nuclear antigen-positive cells and decreased the ileal crypt depth (P 0.05). Moreover, most AA concentrations and AA transporter expression in the jejunal and ileal mucosa in 17% CP diets were increased to the levels similar to those in the positive control. Additionally, this in vitro study showed that the BCAA ratio of 1:0.25:0.25 significantly increased intestinal cell proliferation, mRNA expression of AA transporters, AA concentrations, and protein turnover (P 0.05).These findings suggest that optimal BCAA ratio (in vivo = 1:0.75:0.75; in vitro = 1:0.25:0.25) would improve intestinal morphology and cell proliferation, increase intestinal AA absorption through mediating expression of intestinal AA transporters, and promote intestinal protein turnover. The findings yield new insights into the use of BCAAs in humans and animals.

Leucine (Leu) and its metabolites α-ketoisocaproate (KIC) and β-hydroxy-β-methyl butyrate (HMB) are potent regulators of protein turnover. The aim of this study was to compare the inhibitory effects of Leu, KIC, and HMB on protein degradation and to investigate the mechanisms involved. The results showed that the inhibitory effect of HMB (0.38 ± 0.04) was more potent than that of Leu (0.76 ± 0.04) and KIC (0.56 ± 0.04, P < 0.01), and was significantly abolished in the presence of LY294002 (1.48 ± 0.02) and rapamycin (1.96 ± 0.02, P < 0.01). In the presence of insulin, the inhibitory effect of HMB (0.34 ± 0.03) was still more effective than that of Leu (0.60 ± 0.04) and KIC (0.57 ± 0.08, P < 0.05). Interestingly, LY294002 treatment markedly attenuated the effect of HMB, while rapamycin treatment failed to exert the same effect. Thus, HMB appears to be more potent than Leu and KIC in inhibiting protein degradation in the absence or presence of insulin, and this inhibitory effect may be dependent on PI3K/Akt signaling pathway regardless of insulin, and mTOR signaling was only involved in this effect of HMB in the absence of insulin.

This study evaluated the effect of branched-chain amino acid (BCAA) supplementation in low-protein diets on lipid metabolism in dorsal subcutaneous adipose (DSA), abdominal subcutaneous adipose (ASA), and perirenal adipose (PRA) tissues. A total of 24 piglets were allotted to four treatments, and each group was fed the adequate protein (AP) diet, low-protein (LP) diet, LP diet supplemented with BCAA (LP + B), or LP diet supplemented with twice BCAA (LP + 2B). Serum concentrations of leptin in the BCAA-supplemented treatments were higher (P0.01) than in the AP treatment, but lower (P0.01) than in the LP treatment. In DSA, the mRNA and protein levels for lipogenic-related genes were highest in the LP treatment and lowest in the LP + 2B treatment. However, in ASA and PRA, the expression levels for those genes were significantly elevated in the LP + 2B treatment. In conclusion, BCAA supplementation could alter the body fat condition, and this effect was likely modulated by the expression of lipid metabolic regulators in DSA, ASA, and PRA in a depot-specific manner.

The aim of this work was to study the lipid metabolism and energy status of skeletal muscle of pigs as affected by dietary protein restriction. Eighteen growing pigs were distributed into three treatments, and each group was fed one of three levels (20, 17, and 14%) of crude protein (CP) diets. Our results showed that pigs fed the 20% CP had greater (P < 0.05) gain:feed and muscle weight than those fed the 14% CP, but no differences between the 20 and 17% CP treatments. Additionally, protein restriction tended to increase (P = 0.07) the content of intramuscular fat (IMF) and up-regulated (P < 0.05) expression of lipogenic-related genes. Energy status was changed and, concomitantly, AMP-activated protein kinase α pathway was inhibited by reducing the dietary protein level. These results indicate protein restriction could be useful to improve IMF content of pigs through regulating lipid metabolism and associated energy utilization in muscle.

Revealing the expression patterns of genes involved in protein metabolism as affected by diets would be useful for further clarifying the importance of the balance among the branched-chain amino acids (BCAAs), which include leucine (Leu), isoleucine (Ile), and valine (Val). Therefore, we used growing pigs to explore the effects of different dietary BCAA ratios on muscle protein metabolism. The Leu:Ile:Val ratio was 1:0.51:0.63 (20% crude protein, CP), 1:1:1 (17% CP), 1:0.75:0.75 (17% CP), 1:0.51:0.63 (17% CP), and 1:0.25:0.25 (17% CP), respectively. Results showed that compared with the control group, low-protein diets with the BCAA ratio ranging from 1:0.75:0.75 to 1:0.25:0.25 elevated muscle free amino acid (AA) concentrations and AA transporter expression, significantly activated the mammalian target of rapamycin complex 1 pathway, and decreased serum urea nitrogen content and the mRNA expression of genes related to muscle protein degradation (P0.05). In conclusion, these results indicated that maintaining the dietary Leu:Ile:Val ratio within 1:0.25:0.25-1:0.75:0.75 in low-protein diets (17% CP) would facilitate the absorption and utilization of free AA and result in improved protein metabolism and muscle growth.

Liver metabolism is affected by nutrients. The aim of this study was to explore the effects of low-protein diets (17% crude protein, CP) supplemented with branched-chain amino acids (BCAAs), including leucine (Leu), isoleucine (Ile) and valine (Val), on hepatic amino acid profile and lipid metabolism in growing pigs. The ratio of Leu : Ile : Val in all groups was 1 : 0.51 : 0.63 (20% crude protein, CP), 1 : 1 : 1 (17% CP), 1 : 0.75 : 0.75 (17% CP), 1 : 0.51 : 0.63 (17% CP) and 1 : 0.25 : 0.25 (17% CP) respectively. Results revealed that compared to the positive control group (1 : 0.51 : 0.63, 20% CP), the low-protein diets significantly augmented the concentrations of most essential amino acids and non-essential amino acids (p

Branched-chain amino acids (BCAAs), including leucine (Leu), isoleucine (Ile), and valine (Val), are key regulators of protein synthesis in muscle. The aim of this study was to investigate the effect of different BCAA ratios (Leu:Ile:Val) on the proliferation, differentiation, and expression levels of the regulators related to protein metabolism of C2 C12 myocytes.Studies were conducted in C2C12 myocytes exposed to different BCAA ratios (Leu: Ile: Val = 0, 1:0.25:0.25, 1:1:1).The ratio of 1:0.25:0.25 increased cell viability and promoted cell cycle progression from G0/G1 phase to S phase, which was an indicator of proliferation enhancement (P 0.05). Moreover, this optimal ratio (1:0.25:0.25) promoted the differentiation of myocytes into myotubes by upregulating myogenin and interleukin-15 gene expression, and differently regulated the expression of L-type amino acid transporter 1 and 4 and system ASC amino acid transporters 2. Furthermore, the ratio stimulated mTOR expression at the mRNA and phosphorylated protein levels, as well as ribosomal protein S6 kinase and regulatory-associated protein of mTOR (raptor). In contrast, the optimal ratio decreased the amount of ubiquitin ligase muscle-specific RING finger 1 and muscle atrophy F-box during proliferation and differentiation (P 0.05). No change was observed in the expression of key genes related to energy metabolism except for uncoupling protein 3 (P 0.05).The results suggested that appropriate BCAA ratios could enhance proliferation and differentiation of the C2 C12 myocytes, also mediate the key regulators related to protein metabolism including the mTORC1 pathway. A proper utilization of balanced BCAA ratio in food would be beneficial to human and animal nutrition.

Adult humans do not possess active brown adipose tissue (BAT). If certain white depots could develop brownish characteristics, it could help to reduce the adverse effects of white adipose tissue (WAT) and to improve metabolic health [1]. WAT is principally devoid of uncoupling protein 1 (UCP-1) at thermoneutrality, whereas BAT demonstrates small but significant UCP-1 gene expression at thermoneutrality. The molecular signature that identifies brown and brownlike adipocytes is UCP-1. Pragmatically, browning is defined as any significantly increased UCP-1 expression at the mRNA level occurring in what are normally regarded as WAT depots [2].

Alpha-ketoglutarate (AKG), a key intermediate in the Krebs cycle, has been reported to promote protein synthesis through activating mechanistic targeting of rapamycin (mTOR) in enterocytes. The study tested the hypothesis that AKG may enhance growth and milk protein synthesis in porcine mammary epithelial cells (PMECs). PMECs were cultured for 96 h in Dulbecco’s modified Eagle’s-F12 Ham medium (DMEM-F12) containing prolactin (2 µg/ml) and AKG (0 or 1.5 mM). At the end of 96-h culture, the abundance of apoptosis-related proteins (caspase-3, caspase-9), milk-specific proteins (α-lactalbumin and β-casein), mTOR signaling proteins (mTOR, p-mTOR, PERK, p-PERK, eIF2a, P70S6K and p-P70S6K), and endoplasmic reticulum stress (ERS)-associated proteins (BiP and CHOP) in PMEC were determined. Addition of AKG dose-dependently enhanced cell viability in the absence or presence of prolactin, with optimal concentrations of AKG being at 1.0 and 1.5 mM, respectively. In the presence of prolactin, addition of 1.5 mM AKG: (1) decreased (P

A total of 96 barrows (48 pure-bred Bama mini-pigs representing fatty genotype, and 48 Landrace pigs representing lean genotype) were randomly assigned to either a low- or adequate-protein treatment diet. The experimental period commenced at 5 weeks of age and extended to the finishing period. After euthanasia, blood and skeletal muscle samples were collected from pigs at the nursery, growing, and finishing phases. Our results indicate that the concentrations of free AAs in the plasma and muscle decreased as the age of the pigs increased. In addition, a strain × growth phase interaction (P < 0.05) was observed for the free AA pool in the plasma and muscle. The low-protein diet upregulated (P < 0.05) the mRNA levels for T1R1/T1R3 involved in glutamate binding, but downregulated (P < 0.05) the mRNA levels for PAT1, PAT2, and ASCT2, which transport neutral AAs into muscles. Bama mini-pigs had higher (P < 0.05) mRNA levels for LAT1, SNAT2, and EAAC1, but a lower (P < 0.05) mRNA level for PepT1, compared with Landrace pigs. Collectively, our findings indicate that adequate provision of dietary protein plays an important role in regulating profiles of free AA pools and expression of key AA/peptide transporters/transceptors in a genotype- and tissue-specific manner.

Background To 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. Results Results showed that growing-finishing pigs fed the MP or AP diet improved (P

Energy metabolism is a basic and general process, by which the body acquires and uses energy to maintain normal function, and taurine plays a vital role in energy metabolism. Taurine deficiency may cause a weak energy metabolism and energy metabolism dysfunction. Taurine biosynthetic ability is limited, and its supplementation in the diet can strengthen energy metabolism in muscle performance, cardiac function, liver activity, and adipose tissue. Combining taurine with other drugs may have a superior effect in energy metabolism. In many metabolic disorders, taurine, or the combination of taurine with other drugs, also functions as a repair treatment for damaged tissues, and acts as a promoter for the balance of energy metabolism. The present study discusses the potential roles of taurine in energy metabolism.

Leucine (Leu) is a nutritionally essential branched-chain amino acid (BCAA) in animal nutrition. It is usually one of the most abundant amino acids in high-quality protein foods. Leu increases protein synthesis through activation of the mammalian target of rapamycin (mTOR) signaling pathway in skeletal muscle, adipose tissue and placental cells. Leu promotes energy metabolism (glucose uptake, mitochondrial biogenesis, and fatty acid oxidation) to provide energy for protein synthesis, while inhibiting protein degradation. Approximately 80 % of Leu is normally used for protein synthesis, while the remainder is converted to α-ketoisocaproate (α-KIC) and β-hydroxy-β-methylbutyrate (HMB) in skeletal muscle. Therefore, it has been hypothesized that some of the functions of Leu are modulated by its metabolites. Both α-KIC and HMB have recently received considerable attention as nutritional supplements used to increase protein synthesis, inhibit protein degradation, and regulate energy homeostasis in a variety of in vitro and in vivo models. Leu and its metabolites hold great promise to enhance the growth and health of animals (including humans, birds and fish).