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R-spondin 1 (RSPO1) is a ligand for the intestinal stem cell (ISC) marker Lgr5 in the crypt, which functions to amplify canonical Wnt signaling to stimulate the division of ISCs. Despite the crucial role of recombinant human RSPO1 (rhRSPO1) in homeostasis and regeneration, little is known about RSPO1 among different species. Here, we cloned the porcine RSPO1 (pRSPO1) gene and obtained rpRSPO1 protein through the expression system of the recombinant

This work provided an interesting finding of lysine (Lys) control on skeletal muscle growth besides protein synthesis. According to the isobaric tag for relative and absolute quantitation and molecular docking analyses, we found both in

This experiment was conducted to study the effects of dietary supplementation with acidifiers on the growth performance, meat quality, and intestinal health of broiler chickens. A total of 648 male Arbor Acres broiler chickens at 1 d old were randomly divided into 6 groups, and each group consisted of 6 replicates with 18 broilers per replicate. The dietary treatments were as follows: negative control (NC, the basal diet), NC + antibiotic (enramycin, 8 mg/kg, positive control [PC]), NC + phosphoric acid (PA, 0.1, 0.2, and 0.3 g/kg), and NC + lactic acid (LA, 0.3 g/kg). The feeding trial lasted for 42 d. The results showed that the feed-to-gain ratio of the NC + acidifier groups was lower than that of the NC and PC groups from 1 to 42 d (P

Intestinal stem cells (ISCs) decode and coordinate various types of nutritional information from the diet to support the crypt-villus axis architecture, but how specific dietary molecules affect intestinal epithelial homeostasis remains unclear. In the current study, L-glutamate (Glu) supplementation in either a nitrogen-free diet (NFD) or a corn-soybean meal diet (CSMD) stimulated gut growth and ISC expansion in weaned piglets. Quantitative proteomics screening identified the canonical Wnt signalling pathway as a central regulator of intestinal epithelial development and ISC activity in vivo. Importantly, the Wnt transmembrane receptor Frizzled7 (FZD7) was upregulated in response to dietary Glu patterns, and its perturbations in intestinal organoids (IOs) treated with a specific inhibitor and in FZD7-KO IPEC-J2 cells disrupted the link between Glu inputs and β-catenin signalling and a subsequent reduction in cell viability. Furthermore, co-localization, coimmunoprecipitation (Co-IP), isothermal titration calorimetry (ITC), and microscale thermophoresis (MST) revealed that Glu served as a signalling molecule directly bound to FZD7. We propose that FZD7-mediated integration of the extracellular Glu signal controls ISC proliferation and differentiation, which provides new insights into the crosstalk of nutrients and ISCs.

This study was conducted to explore the regulatory role of methionine (Met) in feather follicle and feather development during the embryonic period of chicks. A total of 280 fertile eggs (40 eggs/group) were injected with 0, 5, 10, 20 mg of L-Met or DL-Met/per egg on embryonic day 9 (E9), and whole-body feather and skin tissues were collected on E15 and the day of hatching (DOH). The whole-body feather weight was determined to describe the feather growth, and the skin samples were subjected to hematoxylin and eosin staining and Western blotting for the evaluation of feather follicle development and the expressions of Wingless/Int (Wnt)/β-catenin signaling pathway proteins, respectively. The results showed that L- or DL-Met did not affect the embryo weight (P > 0.05), but increased the absolute and relative whole-body feather weights. Specifically, 5 and 10 mg of L-Met and 5, 10, and 20 mg of DL-Met significantly increased the absolute feather weight at E15 (P 0.05). The levels of L- and DL-Met were quadratically correlated with the absolute and relative feather weights of chicks on the DOH (P

1. This study investigated the pattern of feather follicle morphogenesis and the expression of the Wnt/β-catenin signalling pathway in the skin of yellow-feathered broiler chick embryos during feather development, using haematoxylin and eosin (HE) staining and Western blot assays, respectively. 2. The results showed that the skin displayed protrusions during embryonic days E7-E9, feather buds elongated during E10-E11 with anterior-posterior and proximal-distal asymmetries, and the epidermis invaginated to form the primary feather follicles (Pfs) at E12. At E13, the formation of the feather follicle and the epidermis at the base of the feather bud further invaginated into the dermis. By E15, Pf formation was essentially complete, and secondary feather follicles (Sfs) appeared. It was speculated that Pfs and Sfs developed independently and that Pfs occurred earlier than Sfs. 3. Quantitative measurements of Pf density reached a maximum at E15 and then decreased gradually. Sf density started to increase from E15. 4. Protein expression levels of β-catenin, TCF4, cyclin D1, and c-Myc were significantly increased during E8-E12 (P 0.05) and then decreased from E13 to the day of hatching (DOH) (P 0.05). The result of the β-catenin immunolocalisation signal intensity assay was consistent with the result of the Western blot assay. 5. Collectively, the results indicated that the Wnt/β-catenin signalling pathway is essential for promoting the development of feather follicles, especially during E7-E15.

Avian feathers have robust growth and regeneration capability and serve as a useful model for decoding hair morphogenesis and other developmental studies. However, the molecular signaling involved in regulating the development of feather follicles is unclear. The purpose of this study was to investigate the role of the Wnt/β-catenin pathway in regulating feather morphogenesis in embryonic chicks through in ovo injection of different doses of Dickkopf-1 (DKK1, a specific inhibitor of the target of the Wnt/β-catenin pathway). A total of 120 fertilized embryo eggs were randomly divided into 4 treatments, including a noninjection group (control group) and groups injected with 100 μL of phosphate-buffered saline (PBS)/egg (PBS control group), 100 μL of PBS/egg containing 600-ng DKK1/egg (600-ng DKK1 group), and 100-μL PBS/egg containing 1,200-ng DKK1/egg (1,200-ng DKK1 group). Feathers and skin tissues were sampled on embryonic (E) day 15 and the day of hatching to examine the feather mass, diameter and density of feather follicles, and the protein expression of the Wnt/β-catenin pathway. The results showed that, compared with CON and PBS treatment, the injection of DKK1 into the yolk sac of chick embryos had no significant effect on the hatching rate and embryo weight (P > 0.05), while it significantly decreased the relative mass of feathers in the whole body (P < 0.05). The high dose of DKK1 (1,200-ng DKK1/egg) decreased the relative mass of feathers on the back, chest, belly, neck, wings, head, and legs, which was more obvious than that in the 600-ng DKK1 group, which presented a dose-dependent effect. In addition, DKK1 injection significantly downregulated the protein expression levels of β-catenin, transcription factor 4, Cyclin D1, and c-Myc (P < 0.05). The immunofluorescence result of β-catenin was consistent with the Western blotting assay results. Altogether, these observations suggested that the Wnt/β-catenin signaling pathway is involved in regulating feather follicle development and feather growth during the embryonic development of chicks.

Heat stress induced by continuous high ambient temperatures or strenuous exercise in humans and animals leads to intestinal epithelial damage through the induction of intracellular stress response. However, the precise mechanisms involved in the regulation of intestinal epithelial cell injury, especially intestinal stem cells (ISCs), remain unclear. Thereby, in vitro a confluent monolayer of IPEC-J2 cells was exposed to the high temperatures (39, 40, and 41°C), the IPEC-J2 cell proliferation, apoptosis, differentiation, and barrier were determined, as well as the expression of GRP78, which is a marker protein of endoplasmic reticulum stress (ERS). The Wnt/β-catenin pathway-mediated regenerative response was validated using R-spondin 1 (Rspo1). And ex-vivo, three-dimensional cultured enteroids were developed from piglet jejunal crypt and employed to assess the ISC activity under heat exposure. The results showed that exposure to 41°C for 72 hr, rather than 39°C and 40°C, decreased IPEC-J2 cell viability, inhibited cell proliferation and differentiation, induced ERS and cell apoptosis, damaged barrier function and restricted the Wnt/β-catenin pathway. Nevertheless, Wnt/β-catenin reactivation via Rspo1 protects the intestinal epithelium from heat exposure-induced injury. Furthermore, exposure to 41°C for 24 hr reduced ISC activity, stimulated crypt-cell apoptosis, upregulated the expression of GRP78 and caspase-3, and downregulated the expression of β-catenin, Lgr5, Bmi1, Ki67, KRT20, ZO-1, occludin, and claudin-1. Taken together, we conclude that heat exposure induces ERS and downregulates the Wnt/β-catenin signaling pathway to disrupt epithelial integrity by inhibiting the intestinal epithelial cell proliferation and stem cell expansion.

Crop milk is the sole source of nutrition that sustains young pigeons (squabs) throughout growth and development. Protein accounts for approximately 55% of the nutrients in crop milk; however, its regulation mechanism remains unclear. In our study, three experiments were conducted to investigate the possible underlying mechanism of crop milk protein synthesis and nutritional interventions. Isobaric tagging for relative and absolute quantification (iTRAQ) analysis found that the Janus activated kinase (JAK)/signal transducers and activators of transcription (STAT) pathway was significantly up-regulated in breeding pigeons during lactation compared to non-breeding pigeons. Moreover, the serum prolactin (PRL) levels increased, and the protein expression of the PRL receptor (PRLR)/JAK2/STAT5 pathway was significantly up-regulated during lactation. The serum PRL, the PRLR/JAK2/STAT5 pathway, the crop milk protein synthesis, and the squab growth performance were inhibited by bromocriptine mesylate injection, a PRL-specific inhibitor. In addition, dietary supplementation with 0.30% dl-methionine or dl-methionine-dl-methionine (especially 0.30% dl-methionine-dl-methionine), significantly increased serum PRL levels and PRLR/JAK2/STAT5 activity, and improved the crop milk protein synthesis. In conclusion, our results demonstrated that the PRL-induced PRLR/JAK2/STAT5 signaling pathway plays a vital regulatory role in crop milk protein synthesis, and 0.30% dl-methionine-dl-methionine is superior to dl-methionine in promoting crop milk protein synthesis.

This study was conducted to explore the regulatory role of the target of rapamycin complex 1 (TORC1) signaling pathway in crop milk synthesis in breeding pigeons (Columba livia). Three groups of breeding pigeons in the lactation period (n = 30 pairs/group) were respectively injected with rapamycin (RAPA, a specific inhibitor of the target of rapamycin complex) at doses of 0 (vehicle, control), 0.6, or 1.2 mg/kg body weight (BW)/day via the wing vein for 7 days. The average daily feed intake (ADFI) and BW of the breeding pigeons and the BW of young squabs were respectively recorded throughout the experimental period. The breeding pigeons were sacrificed to collect their crop tissues, crop milk, and serum on the eighth day of the experiment. The results showed that neither 0.6 nor 1.2 mg/kg BW RAPA injection affected BW loss or ADFI in breeding pigeons (P > 0.05), while crop thickness and crop relative weight were significantly decreased (P < 0.05) in the 1.2 mg/kg BW rapamycin-injected group. Simultaneously, RAPA (especially at 1.2 mg/kg BW) decreased the crude protein, αs1-casein, αs2-casein, β-casein, and amino acid contents (Asp, Thr, Ser, Glu, Gly, Ala, Cys, Val, Met, Ile, Leu, Tyr, Lys, His, Arg, and Pro) of crop milk (P < 0.05) and the concentrations of albumin, total protein, and uric acid in the serum of breeding pigeons (P < 0.05). Additionally, the expression of TORC1 pathway-related proteins (TORC1, S6K1, S6, 4EBP1, and eIF4E) was downregulated in the crop tissues of breeding pigeons by 0.6 or 1.2 mg/kg BW/day RAPA injection (P < 0.05). Accordingly, the average daily gain (ADG) of young squabs declined, and the mortality rate increased significantly (P < 0.05). Together, the results showed that RAPA reduced protein and amino acid levels in the crop milk of breeding pigeons and retarded young squab growth, suggesting a crucial role of TORC1 in crop milk synthesis in breeding pigeons.

Feathers play a critical role in thermoregulation and directly influence poultry production. Poor feathering adversely affects living appearance and carcass quality, thus reducing profits. However, producers tend to ignore the importance of feather development and do not know the laws of feather growth and development. The objective of this study was to fit growth curves to describe the growth and development of feathers in yellow-feathered broilers during the embryonic and posthatching periods using different nonlinear functions (Gompertz, logistic and Bertalanffy). Feather mass and length were determined during the embryonic development and posthatching stages to identify which growth model most accurately described the feather growth pattern. The results showed that chick embryos began to grow feathers at approximately embryonic (E) day 10, and the feathers grew rapidly from E13 to E17. There was little change from E17 to the day of hatching (DOH). During the embryonic period, the Gompertz function (Y = 798.48e-203 431exp(-0.87t), Akaike's information criterion (AIC) = -0.950 × 103, Bayesian information criterion (BIC) = -0.711 × 103 and mean square error (MSE) = 559.308) provided the best fit for the feather growth curve compared with the other two functions. After hatching, feather mass and length changed little from the DOH to day (D) 14, increased rapidly from D21 to D91 and then grew slowly after D91. The first stage of feather molting occurred from 2 to 3 weeks of age when the down feathers were mostly shed and replaced with juvenile feathers, and the second stage occurred at approximately 13 to 15 weeks of age. The three nonlinear functions could overall fit the feather growth curve well, but the Bertalanffy model (Y = 116.88 × (1-0.86e-0.02t)3, AIC = 1.065 × 105, BIC = 1.077 × 105 and MSE = 11.308) showed the highest degree of fit among the models. Therefore, the Gompertz model exhibited the best goodness of fit for the feather growth curve during the embryonic development, while the Bertalanffy model was the most suitable model due to its accurate ability to predict the growth and development of feathers during the growth period, which is an important commercial characteristic of yellow-feathered chickens.

BACKGROUND: Intramuscular fat (IMF) and polyunsaturated fatty acids (PUFAs) have been thought to play a crucial role in improving meat quality. Considering the ability of pioglitazone hydrochloride (PGZ) to deposit fat, and the anti‐stress capability of chromium methionine (CrMet), we combined these compounds to produce higher quality meat in poultry. A total of 3000 female chickens were divided into four groups (five replicates, each with 150 chickens): control, control plus15 mg·kg⁻¹ PGZ, control plus 200 μg·kg⁻¹ CrMet, and control plus15 mg·kg⁻¹ PGZ plus 200 μg·kg⁻¹ CrMet. The experiment lasted for 28 days. RESULTS: Compared to the control group and the PGZ group, the average daily gain (ADG) was significantly increased in the PGZ plus CrMet group, whereas the feed‐to‐gain ratio (F/G) was decreased from 0 to 14 days. Meanwhile, the redness value of breast muscle and IMF of thigh muscle increased in the PGZ plus CrMet group compared with the control group and these detections in the PGZ plus CrMet group exhibited highest value among the four groups. The cooking loss decreased in the breast muscle and thigh muscle after PGZ combined with CrMet in diets. The percentages of C16:1, C18:2n‐6 and PUFAs increased in the PGZ plus CrMet group. The mRNA abundance of peroxisome proliferator activated receptor (PPAR) γ, PPAR coactivator 1 α, and fatty acid binding protein 3 was significantly enhanced with PGZ plus CrMet supplementation. CONCLUSION: Collectively, dietary supplementation with PGZ plus CrMet improved growth performance and meat quality by decreasing the cooking loss and increasing the IMF and PUFA levels. © 2019 Society of Chemical Industry

Selenium (Se), one of the indispensable nutrients for both human health and animal growth, participates in various physiological functions, such as antioxidant and immune responses and metabolism. The role of dietary Se, in its organic and inorganic forms, has been well documented in domestic animals. Furthermore, many feeding strategies for different animals have been developed to increase the Se concentration in animal products to address Se deficiency and even as a potential nutritional strategy to treat free radical-associated diseases. Nevertheless, studies on investigating the optimum addition of Se in feed, the long-term consequences of Se usage in food for animal nutrition, the mechanism of metallic Se nanoparticle (SeNP) transformation in vivo, and the nutritional effects of SeNPs on feed workers and the environment are urgently needed. Starting from the absorption and metabolism mechanism of Se, this review discusses the antioxidant role of Se in detail. Based on this characteristic, we further investigated the application of Se in animal health and described some unresolved issues and unanswered questions warranting further investigation. This review is expected to provide a theoretical reference for improving the quality of food animal meat as well as for the development of Se-based biological nutrition enhancement technology.

Enterotoxigenic E. coli causes severe infectious diarrhea with high morbidity and mortality in weanling pigs mainly through the production of heat-stable enterotoxins. Iturin A, originally isolated from the insect Hyalophora cecropia, exerts strong antibiotic activity against Gram-positive and Gram-negative bacteria. Thus, our study investigated whether iturin A could protect the intestinal epithelium from the insults of E. coli Rosetta containing the gene coding for heat-stable enterotoxin b (STb-Rosetta). Twenty-eight piglets were divided into four groups and were orally administered PBS (control), 0.16 g/kg BW iturin A, 2 × 109 CFU STb-Rosetta, and 0.16 g/kg BW iturin A + 2 × 109 CFU STb-Rosetta respectively for 8 days. The intestinal epithelial morphology and barrier function were assessed by H&E staining and Ussing chamber, and the growth advantage in enteroids derived from jejunal crypts of piglets in each group was used to evaluate the intestinal stem cell (ISC) activity. The results showed that iturin A increased the average daily gain (ADG) and average daily feed intake (ADFI) of piglets exposed to STb-Rosetta (P < 0.05). Meanwhile, STb-Rosetta-induced decrease in jejunum weight and damage to jejunal morphology and barrier function were significantly improved after iturin A supplementation (P < 0.05). Furthermore, the jejunal crypt cells from piglets in the iturin A + STb-Rosetta group had greater growth advantages of ISCs compared with the STb-Rosetta group, including enteroid forming efficiency, surface area, budding efficiency, and branching coefficient (P < 0.05). Our results indicate that iturin A protects against STb-Rosetta-induced intestinal mucosal injury, which provides an intervention strategy that regulates the function of ISCs in the high turnover-rate crypt-villous axis under ETEC infection. This study was supported by the National Natural Science Foundation of China (31872389, 32072777) and Basic and Applied Basic Research Foundation of Guangdong Province (2019B1515210021).

The intestine is the central organ of early weaning stress in piglets; however, the response of intestinal stem cells (ISCs) that drive epithelial renewal between the different breeds of piglets is not yet known. Therefore, this investigation was to explore the sensitivity of ISCs to early weaning stress. Taoyuan Black and Duroc piglets were slaughtered at 21 days of age (on the day of weaning) and 24 days of age (3 days after weaning) with 10 pigs, respectively. And the results showed that Taoyuan Black pigs are more tolerant to early weaning stress, while the mucosal mass of jejunum was significantly decreased in 24-day-old Duroc piglets compared with the 21-day-old Duroc piglets (P < 0.05). The weaning stress damaged the jejunal structure, decreased the expression of tight junction related proteins ZO-1, Occludin, and Claudin-1, and increased intestinal permeability in Duroc piglets (P < 0.05). The ex vivo intestinal organoids (IOs) derived from the jejunal crypt of Duroc piglets after weaning exhibited lower expansion efficiency (P < 0.05). Furthermore, the levels of proliferating cell marker PCNA, terminally differentiated cell marker KRT20, absorptive cell marker Villin, goblet cell marker MUC2, and Paneth cell marker lysozyme were significantly reduced in the jejunum, crypt, and jejunal organoids of 24-day-old Duroc (P < 0.05). ROS levels in the jejunum of Duroc piglets were increased along with the inhibition of the Nrf2 pathway compared with 21-day-old Duroc piglets (P < 0.05). Collectively, the Taoyuan Black pigs had stronger tolerance to weaning stress; however early weaning suppressed the Nrf2 pathway, decreased proliferation and differentiation activity of ISCs, and disrupted intestinal homeostasis in Duroc piglets.

Wnt/β-catenin pathways have an important role in porcine skeletal muscle growth. Nevertheless, the mechanism for how it respond to environmental stimulations, especially nutrients, has not been well-investigated. In this study, piglets and skeletal muscle satellite cells (MuSCs) were used to investigate the work process of the lysine (Lys) signal transmitted to β-catenin in governing skeletal muscle growth. Briefly, the piglets and MuSCs were divided into the control group, the Lys deficiency group, and the Lys rescue group, taken together with the specific inhibitor and target gene knockdown for further study. We found that the transmembrane frizzled7 (FZD7) receptor displayed the same changes with the Wnt/β-catenin pathway and positively correlated with Lys levels in skeletal muscle and MuSCs. Meanwhile, the molecular docking analyses showed that FZD7 and Lys form connections at Gly17, Phe18, Cys19, and Asp84. In contrast, FZD7 specific inhibitor Fz7-21-TFA suppressed Lys rescued MuSC viability (P< 0.05). The distribution of Ki67 and active β-catenin in the Lys rescue group were also decreased by FZD7 inhibitor (P< 0.05). Furthermore, the decreased FZD7 level caused Lys re-activated TCF4/LEF activity and the Wnt/β-catenin pathway suppression (P< 0.05). Additionally, FZD7 knockdown restricted C2C12 viability and proliferation ability (P< 0.05). Besides, FZD7 knockdown inhibited the Wnt/β-catenin pathway and Lys deficiency caused much more serious inhibition of the Wnt/β-catenin pathway (P< 0.05), and these restrictions fail to be rescued by re-supplemented Lys or Wnt3a (P< 0.05). Moreover, we titrated Lys solution into recombinant pig FZD7 (rpFZD7) protein solution by using isothermal titration calorimetry, and the heat release during titration demonstrated there was an interaction between Lys and rpFZD7. Collectively, these results indicated that Lys is not only a molecular block for protein synthesis, but is also a ligand that binds to FZD7, directly activating the Wnt/β-catenin pathway to stimulate MuSCs to promote skeletal muscle growth.

Scope The intestinal epithelium is nourished by various nutrients and subjected to persistent and widespread feed-derived mycotoxin stress. l-Carnosine (LC) possesses robust antioxidant activity; however, its role in protecting intestinal mucosa against deoxynivalenol (DON) is still unclear. Methods and results In this study, 300 mg kg-1 BW LC and 3 mg kg-1 BW DON are orally administered to mice either alone or in combination for 10 days to investigate the role of LC in protecting the intestine against DON. This study found that LC alleviates the growth retardation of mice and repairs the damaged jejunal structure and barrier functions under DON exposure. LC rescues the intestinal stem cells (ISCs), increases the growth advantage in enteroids derived from jejunal crypts of mice in each group ex vivo, improves the proliferation and apoptosis of intestinal cells, and promotes ISC differentiation into absorptive cells, goblet cells, and Paneth cells. Furthermore, LC activates Nrf2 signaling by binding to Keap1 to reverse the striking DON-induced increase in ROS levels. Conclusion The study findings unveil that LC potentiates the antioxidant capacity of ISCs by regulating the Keap1/Nrf2 signaling pathway, which contributes to the intestinal epithelial regeneration response to DON insult.

Intestinal stem cell (ISC)-driven intestinal homeostasis is subjected to dual regulation by dietary nutrients and toxins. Our study investigated the use of lauric acid (LA) to alleviate deoxynivalenol (DON)-induced intestinal epithelial damage. C57BL/6 mice in the control, LA, DON, and LA + DON groups were orally administered PBS, 10 mg/kg BW LA, 2 mg/kg BW DON, and 10 mg/kg BW LA + 2 mg/kg BW DON for 10 days. The results showed that LA increased the average daily gain and average daily feed intake of the mice exposed to DON. Moreover, the DON-triggered impairment of jejunal morphology and barrier function was significantly improved after LA supplementation. Moreover, LA rescued ISC proliferation, inhibited intestinal cell apoptosis, and promoted ISC differentiation into absorptive cells, goblet cells, and Paneth cells. The jejunum crypt cells from the mice in the LA group expanded into enteroids, resulting in a significantly greater enteroid area than that in the DON group. Furthermore, LA reversed the DON-mediated inhibition of the Akt/mTORC1/S6K1 signaling axis in the jejunum. Our results indicated that LA accelerates ISC regeneration to repair intestinal epithelial damage after DON insult by reactivating the Akt/mTORC1/S6K1 signaling pathway, which provides new implications for the function of LA in ISCs.

The intestinal epithelium is derived from intestinal stem cells (ISCs) and has direct contact with nutrients and toxins. However, whether methionine (Met) or a methionine hydroxyl analogue (2-hydroxy-4-(methylthio)butanoic acid (HMB)) can alleviate deoxynivalenol (DON)-induced intestinal injury remains unknown. Mice were treated orally with Met or HMB on days 1-11 and with DON on days 4-8. On day 12, the mice were sacrificed, and the jejunum was collected for crypt isolation and culture. Mouse enteroids were treated with DON and Met or HMB ex vivo. The results showed that Met and HMB increased the average daily feed intake and average daily gain of the mice. Met and HMB also improved the jejunal structure and barrier integrity and promoted ISC expansion, as indicated by the increased enteroid formation efficiency and area, under DON-induced injury conditions. In addition, DON-induced decreases in ISC activity were rescued Wnt/β-catenin signaling reactivation by Met or HMB in vivo and ex vivo. Collectively, our findings reveal that Met and HMB alleviated DON-induced intestinal injury by improving ISC expansion and reactivating Wnt/β-catenin signaling. Our study thus provides a nutritional intervention for intestinal diseases involving Wnt/β-catenin signaling.

Glutamate (Glu) is a critical nutritional regulator of intestinal epithelial homeostasis. In addition, intestinal stem cells (ISCs) at crypt bases are known to play important roles in maintaining the renewal and homeostasis of the intestinal epithelium, and the aspects of communication between Glu and ISCs are still unknown. Here, we identify Glu and mammalian target of rapamycin complex 1 (mTORC1) as essential regulators of ISC expansion. The results showed that extracellular Glu promoted ISC expansion, indicated by increased intestinal organoid forming efficiency and budding efficiency as well as cell proliferation marker Ki67 immunofluorescence and differentiation marker Keratin 20 (KRT20) expression. Moreover, the insulin receptor (IR) mediating phosphorylation of the insulin receptor substrate (IRS) and downstream signaling phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway was involved in this response in ISCs. As expected, Glu-induced mTORC1 signaling activation was observed in the intestinal porcine enterocyte cell line (IPEC-J2), and Glu activated the PI3K/Akt/mTORC1 pathway. Accordingly, PI3K inhibition partially suppressed Glu-induced mTORC1 activation. In addition, Glu increased the phosphorylation levels of IR and IRS, and inhibiting IR downregulated the IRS/PI3K/Akt pathway. Collectively, our findings first indicate that extracellular Glu activates mTORC1 via the IR/IRS/PI3K/Akt pathway and stimulates ISC expansion, providing a new perspective for regulating the growth and health of the intestinal epithelium.

Sex identification plays an important role in avian production. Hitherto, it is difficult to distinguish the sexes of monomorphic birds based on their external features. The chromo-helicase-DNA-binding genes contain CHD-W gene and CHD-Z gene, which are located on the W chromosome and Z chromosome, respectively. Since CHD-W gene is unique to females, the polymerase chain reaction can be used for sex identification. However, extracting DNA procedures for verifying the sex is tedious and expensive. To address these disadvantages, the objective of this study was to develop a simple DNA extraction assay to efficiently process blood, liver, and feather samples. The results showed that 2% dimethylsulfoxide was suitable for processing blood, and phosphate-buffered saline was suitable for processing liver and feather samples. The specific primers were designed, and the length of the targets is 474 bp on Z chromosome and 319 bp on W chromosome. The pigeons were identified as females based on the presence of two bands on the gel, and as males based on the presence of one band. Taken together, our results suggested that feather samples were more appropriate than blood or liver for sex identification of pigeons. Compared to the traditional DNA extraction, this method shortened the assay time and reduced the cost.

Mechanistic target of rapamycin complex 1 (mTORC1) coordinates cell growth and metabolism with environmental cues, such as amino acids, growth factors, and energy. Glutamate (Glu) is a primary metabolic fuel for the intestinal epithelium and extensively involves numerous physiological processes. Crypt intestinal stem cells (ISCs) driven intestinal epithelial renewal that needs a continuous energy supplement. However, the effects of Glu on the expansion of porcine ISCs and intestinal epithelial development remain unclear. Therefore, the objective of this study was to investigate the underlying mechanism that Glu promotes intestinal development. Firstly, a total of 14 weaned piglets (Duroc × Landrace × Large White) with similar body weight (BW) were randomly allocated into the control group, and the 1.0% Glu group with 7 replicates per group and 1 piglet per replicate. The experiment lasts for 21 days. The results showed that dietary Glu increased small intestinal weights, jejunal villus height, and the ratio of the villus height to the crypt depth. Moreover, dietary Glu promoted the proliferation and differentiation of intestinal epithelial cells. Subsequently, iTRAQ proteomics screening indicated that intestinal mTORC1 signaling may participate in Glu-stimulated intestinal epithelial development, which was confirmed by Western blotting. Meanwhile, the IR/IRS/PI3K/Akt pathway and EGFR/ERK pathway are the upstream of Glu-induced mTORC1 signaling activation, which verified in IPEC-J2 cell line and intestinal organoids. Furthermore, the in vivo and ex vivo crypt ISCs experiments showed that Glu accelerated ISC expansion as increased intestinal organoid forming efficiency and budding efficiency. Glu also promoted ISC self-renew and differentiated into various functional cells (enterocytes, goblet cells, enteroendocrine cells, Paneth cells). In summary, mTORC1 integrated Glu signal stimulated ISC expansion and ultimately promoted epithelial development.

Apoptosis is programmed cell death that can be stimulated by external stress or nutrition restrictions. Lysine (Lys) is an essential amino acid for pig growth, and the relationship between Lys deficiency caused apoptosis and inhibition of skeletal muscle growth remains unknown. The objective of this study was to investigate whether apoptosis could be regulated by Lys supplementation and the potential mechanism. In current work, 30 male Duroc × Landrace × Large weaned piglets were divided randomly into 3 groups: control group (Lys 1.30%), Lys deficiency group (Lys 0.86%), and Lys rescue group (Lys 0.86%, 0-14d; 1.30%,15–28 d). The experiment lasted for 28 days, and on the morning of 29 d, piglets were slaughtered to collect samples. Isobaric tag for relative and absolute quantification (iTRAQ) proteomics analysis of the longissimus dorsi muscle showed that Janus family tyrosine kinase (JAK)-signal transducer and activator of transcription (STAT) pathway was involved in Lys deficiency-induced apoptosis and inhibited skeletal muscle growth. Meanwhile, western blotting results of the longissimus dorsi muscle demonstrated that Lys deficiency caused apoptosis (P < 0.05) with the JAK2-STAT3 pathway inhibition (P < 0.05). Interestingly, apoptosis was suppressed (P < 0.05), and the JAK2-STAT3 pathway was reactivated (P < 0.05) after Lys re-supplementation in longissimus dorsi muscle. In addition, results of satellite cells (SCs) isolated from the longissimus dorsi muscle of 5-day-old Landrace piglets showed that Lys deficiency-induced apoptosis (P < 0.05) was mediated by the JAK2-STAT3 pathway inhibition (P < 0.05). Moreover, the JAK2-STAT3 pathway was reactivated (P < 0.05) by Lys re-supplementation and suppressed apoptosis in SCs (P < 0.05), and this effect was blocked (P < 0.05) after SCs treated with AG-490 (a specific inhibitor of JAK2). Collectively, Lys inhibited apoptosis in SCs to govern skeletal muscle growth via the JAK2-STAT3 pathway.

The intestinal health of chick embryos is vital for their life-long growth, and exogenous nutrition intervention may provide sufficient nutrition for embryonic development. In the present study, we investigated the effect of in ovo injection of L-methionine (L-Met) on the intestinal structure and barrier function of chick embryos. There were 4 groups of treatments: the control (CON) group injected with phosphate-buffered saline (PBS) and the other 3 groups injected with 5, 10, and 20 mg L-Met/egg, respectively. The injection was performed on embryonic day 9 (E9), and intestinal samples were collected on the day of hatching for analysis. The results showed that, compared with the CON group, the groups administered an in ovo injection of L-Met increased relative weights of the duodenum, jejunum, and ileum (P

Apoptosis is programmed cell death that can be stimulated by external stress or nutrition restrictions. However, the precise mechanism of apoptosis in skeletal muscle remains unknown. The objective of this study was to investigate whether apoptosis could be regulated by lysine (Lys) supplementation and the potential mechanism. In this study, an isobaric tag for relative and absolute quantification (iTRAQ) proteomics analysis of the longissimus dorsi muscle from piglets showed that the Janus family tyrosine kinase (JAK)-signal transducer and activator of transcription (STAT) pathway was involved in Lys deficiency-induced apoptosis and inhibited skeletal muscle growth. Meanwhile, western blotting results demonstrated that Lys deficiency led to apoptosis in the longissimus dorsi muscle with the JAK2-STAT3 pathway inhibition. Interestingly, apoptosis was suppressed, and the JAK2-STAT3 pathway was reactivated after Lys re-supplementation. In addition, the results showed that Lys deficiency-induced apoptosis in satellite cells (SCs) was mediated by the JAK2-STAT3 pathway inhibition. Moreover, the JAK2-STAT3 pathway was reactivated by Lys re-supplementation and suppressed cell apoptosis, and this effect was inhibited after treatment with Tyrphostin B42 (AG 490). In conclusion, we found that Lys inhibits apoptosis in SCs to govern skeletal muscle growth via the JAK2-STAT3 pathway.

Enterotoxigenic Escherichia coli causes severe infectious diarrhea with high morbidity and mortality in newborn and weanling pigs mainly through the production of heat-stable enterotoxins (STs). However, the precise regulatory mechanisms involved in ST-induced intestinal epithelium injury remain unclear. Consequently, we conducted the experiments in vivo (mice), ex vivo (mouse and porcine enteroids), and in vitro (MODE-K and IPEC-J2 cells) to explore the effect of STp (one type of STa) on the integrity of the intestinal epithelium. The results showed that acute STp exposure led to small intestinal edema, disrupted intestinal integrity, induced crypt cell expansion into spheroids, and downregulated Wnt/β-catenin activity in the mice. Following a similar trend, the enteroid-budding efficiency and the expression of Active β-catenin, β-catenin, Lgr5, PCNA, and KRT20 were significantly decreased after STp treatment, as determined ex vivo. In addition, STp inhibited cell proliferation, induced cell apoptosis, destroyed cell barriers, and reduced Wnt/β-catenin activity by downregulating its membrane receptor Frizzled7 (FZD7). In contrast, Wnt/β-catenin reactivation protected the IPEC-J2 cells from STp-induced injury. Taking these findings together, we conclude that STp inhibits intestinal stem cell expansion to disrupt the integrity of the intestinal mucosa through the downregulation of the Wnt/β-catenin signaling pathway.

The study aimed to investigate the effects of pioglitazone hydrochloride (PGZ) and resveratrol (RES) on yellow-feathered broiler chickens. A total of 500 broiler chickens were randomly divided into four groups and fed a basic diet (control group) or a basic diet supplemented with 15 mg/kg PGZ, 400 mg/kg RES, or 15 mg/kg PGZ plus 400 mg/kg RES for 28 days. Compared with the control group, the PGZ and PGZ plus RES groups presented a significantly higher average daily gain and a decreased feed-to-gain ratio. Increases in the dressing percentage, semi-eviscerated yield, muscle intramuscular fat content, and C18:1n-9c, C18:3n-6, C20:3n-3, and monounsaturated fatty acid (MUFA) percentages were found in the PGZ plus RES group. Moreover, the diet supplemented with RES or PGZ plus RES increased the activities of catalase, glutathione peroxidase, and superoxide dismutase, and decreased the levels of reactive oxygen species of thigh muscle. Additionally, the mRNA abundance of peroxisome proliferator-activated receptor &gamma, coactivator 1&alpha, fatty acid-binding protein 3, nuclear factor erythroid-2-related factor 2, and superoxide dismutase 1 was increased in the PGZ plus RES group. In conclusion, this study suggested that dietary supplementation of PGZ combined with RES improved the growth performance, the muscle intramuscular fat content, and antioxidant ability of yellow-feathered broiler chickens.

l-Glutamate (Glu) is a nutritionally functional amino acid for pigs. In addition, intestinal stem cells (ISCs) maintain epithelial renewal and homeostasis by dynamically regulating proliferation and differentiation to cope with environmental cues. The rapid renewal of the intestinal epithelium requires a continuous supply of energy sources such as Glu. However, the effects of Glu on ISCs and epithelial renewal are poorly understood. In this study, we found that dietary Glu accelerated intestinal epithelial renewal and gut growth. The epidermal growth factor receptor (EGFR)/extracellular regulated protein kinase (ERK) pathway and mechanistic target of rapamycin complex 1 (mTORC1) signaling were involved in this response in piglets. Subsequent cellular assessment suggested that the EGFR/ERK pathway was upstream of Glu-induced mTORC1 signaling activation. Furthermore, we found that Glu activated the EGFR/ERK pathway and promoted ISC proliferation and differentiation in porcine intestinal organoids. Collectively, our findings suggest that Glu drives intestinal epithelial renewal by increasing ISC activity via the EGFR/ERK/mTORC1 pathway. The present study provides direct evidence that mTORC1 is activated by extracellular Glu through EGFR and that Glu acts as a nutritionally functional amino acid for piglets to maintain intestinal growth and health.

Wnt/β-catenin plays a crucial role in skeletal muscle growth, but its specific mechanism still unclear. In this study, due to the distinct role of lysine in pig industry, we provided it as an entry point to investigate the role of Wnt/β-catenin in governing skeletal muscle growth. Firstly, total 18 weaned piglets were divided into three groups: control group, lysine deficiency group and lysine re-supplementation group (lysine levels added from 0.83% to 1.31% at 14 d). After 28 d experiment, all pigs were slaughtered to measure the change of Wnt/β-catenin in skeletal muscle. Secondly, satellite cell (SC) was isolated and cultured with Wnt activator, such as Wnt3a and WRN (Wnt3a, R-spondin1, Noggin) after lysine deficiency for 48 h to investigate cell proliferation and differentiation ability and the level of Wnt/β-catenin in different conditions. The results showed that compared with the control group, lysine deficiency significantly reduced longissimus dorsi muscle weight and Pax7 positive SC, and inhibited Wnt/β-catenin (P < 0.05). Fortunately, these restrictions were rescued to the control levels by lysine re-supplementation (P > 0.05). Meanwhile, compared with the lysine deficiency group, the MTT and western blotting assay showed cell proliferation ability was significantly increased with re-activated Wnt/β-catenin by re-supplemented lysine, Wnt3a or WRN (P < 0.05), respectively. Moreover, under the condition of cell differentiation, compared with the control group, cell fusion index was significantly decreased in the lysine deficiency group (P < 0.05), whereas it was significantly increased with lysine re-supplementation group, Wnt3a or WRN respective supplementation group in comparison with the lysine deficiency group (P < 0.05). In addition, compared with the lysine deficiency group, the protein levels of myogenic regulatory factors and Wnt/β-catenin pathway were also re-activated by re-supplemented lysine, Wnt3a or WRN (P < 0.05). Collectively, we found Wnt/β-catenin activation is required for porcine SC proliferation and differentiation to promote skeletal muscle growth.

As the first limiting amino acid, lysine (Lys) has been thought to promote muscle fiber hypertrophy by increasing protein synthesis. However, the functions of Lys seem far more complex than that. Despite the fact that satellite cells (SCs) play an important role in skeletal muscle growth, the communication between Lys and SCs remains unclear. In this study, we investigated whether SCs participate directly in Lys-induced skeletal muscle growth and whether the mammalian target of rapamycin complex 1 (mTORC1) pathway was activated both in vivo and in vitro to mediate SC functions in response to Lys supplementation. Subsequently, the skeletal muscle growth of piglets was controlled by dietary Lys supplementation. Isobaric tag for relative and absolute quantitation (iTRAQ) analysis showed activated SCs were required for longissimus dorsi muscle growth, and this effect was accompanied by mTORC1 pathway upregulation. Furthermore, SC proliferation was governed by medium Lys concentrations, and the mTORC1 pathway was significantly enhanced in vitro. After verifying that rapamycin inhibits the mTORC1 pathway and suppresses SC proliferation, we conclude that Lys is not only a molecular building block for protein synthesis but also a signal that activates SCs to manipulate muscle growth via the mTORC1 pathway.

This study aimed to investigate the effects of dietary supplementation with dl-methionine (dl-Met) and dl-methionyl-dl-methionine (dl-Met-Met) in breeding pigeons on the carcass characteristics, meat quality and antioxidant activity of squabs. A total of 324 pairs of breeding pigeons were selected and allotted to 9 treatments in a completely randomized design, and the birds were fed dietary treatments for 45 d, including a Met-deficient basal diet (BD, crude protein = 15%, Met = 0.25%) and BD + 0.15%, 0.30%, 0.45%, or 0.60% dl-Met or dl-Met-Met diets. Compared with the diet fed to the BD group, dietary dl-Met or dl-Met-Met supplementation effectively increased the carcass yield, semieviscerated yield, eviscerated yield, breast muscle yield, thigh muscle yield, a* value, catalase activity, total superoxide dismutase activity and glutathione peroxidase activity, but decreased the L* value, malonaldehyde concentration, drip loss and cooking loss of squabs (p &lt, 0.05). The relative bioavailability values of dl-Met-Met relative to those of dl-Met were 467% and 376% based on carcass yield and breast muscle yield, respectively (p &lt, 0.001). Moreover, dl-Met-Met was more effective than dl-Met in decreasing the drip loss and improving the antioxidant activity of the breast and thigh muscles of squabs (p &lt, 0.05). As a source of Met, dl-Met-Met, rather than dl-Met, was more beneficial to squabs.

This work was designed to investigate the synergistic effects of pioglitazone hydrochloride (PGZ) and chromium methionine (CrMet) on meat quality, muscle fatty acid profile, and antioxidant ability of pigs. Pigs in four groups were fed a basic diet or basic diet supplemented with 15 mg/kg of PGZ, 200 μg/kg of CrMet, or 15 mg/kg of PGZ + 200 μg/kg of CrMet. In comparison to the control group, the average daily feed intake, feed/gain ratio, and serum high-density lipoprotein level decreased in the PGZ + CrMet group. Dietary PGZ + CrMet supplementation increased carcass dressing percentage, intramuscular fat, and marbling score. The percentages of C18:1ω-9c, C18:2ω-6c, C18:3ω-3, and polyunsaturated fatty acid (PUFA) in the longissimus thoracis muscle were increased in the PGZ + CrMet group. Greater superoxide dismutase and glutathione peroxidase activities were observed in the PGZ + CrMet group compared to the control group. Collectively, these findings suggested that feed with PGZ and CrMet improved the growth performance and meat quality, especially for PUFA proportions and antioxidant ability.

The type of myofiber is important for porcine meat quality. Meanwhile, the nt/Ca2+ pathway has been showed multiple roles in skeletal muscle formation; however, the distinct mechanism is still unclear. In this study, the weaned piglets and satellite cells were designed into the control group, lysine deficiency group and lysine rescue group to investigate the function of Wnt/Ca2+ pathway in governing skeletal muscle typing. After we confirm the growth of weaned piglets was controlled by lysine, the isobaric tag for relative and absolute quantification (iTRAQ) analysis of skeletal muscle detected that Wnt/Ca2+ pathway was involved in the transition of fast and slow fiber. Then, we found the ratio of type I myofiber in Semimembranous (fast muscle) was significantly increased after lysine deficiency (P < 0.05), and decreased by lysine rescue (P < 0.05). In contrast, the ratio of type I myofiber in Semitendinous muscle (slow muscle) was significantly decreased in the lysine deficiency group, and increased in the lysine rescue group (P < 0.05). Furthermore, the Wnt/Ca2+ pathway was significantly increased in Semimembranous muscle, while decreased in Semitendinous muscle with lysine deficiency, and this phenomenon was inversed after lysine rescue (P < 0.05). Meanwhile, the Wnt/Ca2+ pathway was stronger in satellite cells isolated from Semitendinous muscle (StSCs) than that of Semimembranous satellite cell (SmSCs) (P < 0.05). And we also found the StSCs enter in differentiation is more easily than SmSCs (P < 0.05). Besides, the ratio of type I myofiber originated from StSCs showed greater than StSCs (P < 0.05). In summary, we conclude that satellite cells participate in the Wnt/Ca2+ pathway controlled porcine myofiber determination.

The experiment was conducted to study whether insulin receptor substance 1 (IRS1) / Protein kinase B (Akt)/target of the rapamycin (TOR) signalling pathway activation stimulates crop milk protein synthesis in the domestic pigeon (Columba livia). Crop milk was collected from ten 1-d-old squabs and analysed for nutrient content. During the non-breeding period and the first day of lactation, blood samples were collected from 5 pairs of breeding pigeons and the levels of prolactin and insulin were determined. Crop samples were collected from 5 pairs of breeders at d 14 and 16 of the incubation period and d 1, 3 and 7 of the lactation period. Crop samples were evaluated for changes in crop weight and thickness and changes in the expression patterns of IRS1/Akt/TOR signalling pathway-related proteins. The results demonstrated that prolactin induces a gradual increase in the relative weight and thickness of the crop, with crops reaching a maximum size at the third day of lactation. Pigeon crop milk contains 64.1% crude protein and 29.7% crude fat based on dry weight. Serum prolactin and insulin levels in the lactation period were significantly higher than those in the non-breeding period. Compared with non-breeding pigeons, the expression of the phosphorylated IRS1 phosphorylated Akt, phosphorylated TOR, phosphorylated ribosomal protein S6 kinase, phosphorylated S6, phosphorylated eukaryotic initiation factor 4E binding protein 1 and eukaryotic initiation factor 4E were significantly up-regulated in the crop of pigeons in the lactation period. In conclusion, prolactin might induce changes in crop tissue and form the physiological structure for crop milk synthesis. Furthermore, the synthesis of crop milk protein is regulated by activation of the IRS1/Akt/TOR signalling pathway.

The micronutrient, zinc, plays a vital role in modulating cellular signaling recognition and enhancing intestinal barrier function. However, the precise mechanisms underlying the zinc regulation of intestinal stem cell (ISC) renewal and regeneration ability, which drive intestinal epithelial turnover to maintain the intestinal barrier, under physiological and pathological conditions are unknown. In this study, we used in vivo mouse plus ex vivo enteroid model to investigate thoroughly the protection efficacy of zinc L-aspartate (Zn-Asp) on intestinal mucosal integrity exposed to deoxynivalenol (DON). The results showed that 10 rather than 20 mg/kg body weight (BW) Zn-Asp (calculation in zinc) significantly increased the jejunum mass and ameliorated mucosa injury caused by 2 mg/kg BW DON treatment, including improvement of the intestinal morphology and barrier, as well as enteroid-forming and -budding efficiency, which was expanded from crypt cells isolated from jejunum of mice in each group. The repair process stimulated by Zn-Asp was also accompanied by increased fluorescence signal intensity of KRT20 and Villin; increased numbers of MUC2+, CAG+, LYZ+, BrdU+ and Ki67+ cells in mouse jejunum; and protein expression of Ki67 and PCNA in the jejunum, crypt and enteroid. Simultaneously, Zn-Asp increased ISC activity to promote intestinal epithelial renewal even under physiological conditions. These results were further verified in ex vivo enteroid culture experiments, which were treated with 100 μmol/L Zn-Asp (calculation in zinc) and 100 ng/mL DON for 72 h. Furthermore, we demonstrated that Zn-Asp improved intestinal integrity or accelerated wound healing along with Wnt/β-catenin signaling upregulation or reactivation. Our findings indicate Zn-Asp, especially Zn, enhances ISC activity to maintain the intestinal integrity by activating the Wnt/β-catenin signaling, which sheds some light upon effective preventive strategies for intestinal injury induced by mycotoxin based on ISCs with exogenous zinc preparations in the proper drugs, health foods or qualified feed.

Background Muscle fat content and fatty acid composition play an important role in poultry flavor and taste. To investigate the effects of pioglitazone hydrochloride (PGZ) on growth performance and thigh muscle quality in yellow-feathered chickens, 360 female chickens were randomly divided into three groups and treated with three doses of PGZ (0, 7.5, and 15 mg kg-1 ) for 28 days. Each group had six replicates of 20 chickens. Results The results showed that dietary supplementation with 15 mg kg-1 PGZ increased average daily feed intake (ADFI) and the average daily gain (ADG) from 0 to 14 days. Furthermore, the triglyceride (TG) level was decreased by 15 mg kg-1 PGZ, whereas the eviscerated yield was increased. The relative weight of the heart and kidneys showed a linear increase with dietary PGZ supplementation, and the drip loss of the thigh muscle was significantly decreased by 15 mg kg-1 PGZ supplementation. Moreover, a* value, intramuscular fat (IMF), and polyunsaturated fatty acids (PUFAs) showed a linear increase, and pH24 h and drip loss showed a quadratic influence with the levels of PGZ supplementation. In particular, the PUFA proportion was increased by 7.63% and 9.14% in the 7.5 mg kg-1 PGZ and 15 mg kg-1 PGZ groups, respectively. Additionally, 15 mg kg-1 of PGZ increased the total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-PX ) activity. Conclusion In summary, 15 mg kg-1 PGZ has substantial effects on growth performance and meat quality, particularly by decreasing drip loss and increasing IMF content, PUFA proportions, and antioxidant ability. © 2019 Society of Chemical Industry.

Lysine (Lys) is an essential amino acid for mammals in promoting protein synthesis and skeletal muscle growth. However, the underlying mechanism by which Lys governs muscle growth remains unknown. Lys is not only a material for protein synthesis but also a signaling molecule. Cell migration is a fundamental process for satellite cells (SCs) to promote muscle fiber hypertrophy and thus increase muscle mass. Nevertheless, the communication between Lys and SC has not yet attracted sufficient attention. In this study, we investigated whether Lys directly stimulates SC migration and whether this effect is mediated via the focal adhesion kinase (FAK) pathway. The results of a cell wound-healing assay and transwell assays indicated a significant inhibition of migration ability by Lys deficiency. In addition, the phosphorylation of FAK, paxillin and protein kinase B (Akt) was significantly suppressed, as were the level of integrin β3. Fortunately, we found that increasing Lys levels from deficiency to sufficiency rescued the migration ability to the control level. Moreover, compared with those in the Lys-deficiency group, the proteins in the FAK pathways were reactivated in the Lys-resupplementation group. In conclusion, these findings indicate that the FAK pathway mediates Lys-induced SC migration.