Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the AdipoRon-mediated mitigation of lipotoxicity-induced injury in LMH cells. (A) Oil Red O staining results for LMH cells. (B) TG and TC contents in LMH cells. (C) GPT and GOT activity levels in LMH cells. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; TG, triglyceride; TC, total cholesterol; GPT, glutamic pyruvic transaminase; GOT, glutamic oxaloacetic transaminase. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Staining, Activity Assay, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the mRNA expression of lipid metabolism-related genes in LMH cells. (A) Lipid synthesis-related genes. (B) Fatty acid β-oxidation-related genes. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; ACC, acetyl-CoA carboxylase; SCD-1, stearyl coenzyme A dehydrogenase-1; ACOX-1, acyl-CoA oxidase 1; CPT-1, carnitine palmitoyltransferase 1. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the expression of key signaling molecules of adiponectin that regulate lipid metabolism in LMH cells. (A) Relative mRNA expression of AdipoR1, AdipoR2, and AMPK. (B) Protein expression of AdipoR1, AdipoR2, AMPK, and p-AMPK. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; AMPK, adenosine 5′-monophosphate-activated protein kinase. All data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on lipid components in LMH cells. (A) Z score plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The Z score plot normalizes differential lipid molecules across different samples by calculating Z score values. The calculation formula is z=(x-μ)/σ, where x represents a specific score, μ denotes the mean, and σ indicates the standard deviation. The horizontal axis displays Z score values, the vertical axis shows differential lipids, and the differently colored points indicate samples from different groups. (B) Heatmap plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents different experimental groups, whereas the vertical axis denotes the differentially expressed lipid molecules within each group. The expression level of each lipid is indicated by a color gradient, with darker shades reflecting greater statistical significance. Color blocks at different positions represent the relative expression levels of corresponding lipid molecules at those positions: red indicates high expression of the substance in that group, while blue indicates low expression. (C) KEGG pathway annotation classification diagram for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents the enrichment ratio for each pathway, while the vertical axis displays the names of the metabolic pathways. Colors indicate the magnitude of p values, with redder hues corresponding to smaller p values, signifying more significant enrichment. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; OA, oleic acid; PA, palmitic acid; TAG, triacylglycerol; PG, phosphatidylglycerol; PetOH, phosphatidylethanol; PE, phosphatidylethanolamine; PC, phosphatidylcholine; HexCer-NS, hexosylceramide nonhydroxyfatty acid-sphingosine; HexCer-AP, hexosylceramide alpha-hydroxy fatty acid-phytosphingosine; GlcADG, glucuronosyldiacylglycerol; Cer-AP, ceramide alpha-hydroxy fatty acid-phytosphingosine; ACar, acylcarnitine.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Standard Deviation, Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of AdipoRon intervention on the expression of key adiponectin signaling molecules that regulate lipid metabolism in mixed fatty acid (OA + PA)-treated LMH cells. (A) Relative mRNA expression of AdipoR1, AdipoR2, PPARα, and AMPK. (B) Protein expression of AdipoR1, AdipoR2, PPARα, and AMPK. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+LA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 20 μM AdipoRon-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+HA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 60 μM AdipoRon-treated group; OA, oleic acid; PA, palmitic acid; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; PPARα, peroxisome proliferator-activated receptor-α; AMPK, adenosine 5′-monophosphate-activated protein kinase. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the AdipoRon-mediated mitigation of lipotoxicity-induced injury in LMH cells. (A) Oil Red O staining results for LMH cells. (B) TG and TC contents in LMH cells. (C) GPT and GOT activity levels in LMH cells. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; TG, triglyceride; TC, total cholesterol; GPT, glutamic pyruvic transaminase; GOT, glutamic oxaloacetic transaminase. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Staining, Activity Assay, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the mRNA expression of lipid metabolism-related genes in LMH cells. (A) Lipid synthesis-related genes. (B) Fatty acid β-oxidation-related genes. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; ACC, acetyl-CoA carboxylase; SCD-1, stearyl coenzyme A dehydrogenase-1; ACOX-1, acyl-CoA oxidase 1; CPT-1, carnitine palmitoyltransferase 1. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the expression of key signaling molecules of adiponectin that regulate lipid metabolism in LMH cells. (A) Relative mRNA expression of AdipoR1, AdipoR2, and AMPK. (B) Protein expression of AdipoR1, AdipoR2, AMPK, and p-AMPK. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; AMPK, adenosine 5′-monophosphate-activated protein kinase. All data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on lipid components in LMH cells. (A) Z score plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The Z score plot normalizes differential lipid molecules across different samples by calculating Z score values. The calculation formula is z=(x-μ)/σ, where x represents a specific score, μ denotes the mean, and σ indicates the standard deviation. The horizontal axis displays Z score values, the vertical axis shows differential lipids, and the differently colored points indicate samples from different groups. (B) Heatmap plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents different experimental groups, whereas the vertical axis denotes the differentially expressed lipid molecules within each group. The expression level of each lipid is indicated by a color gradient, with darker shades reflecting greater statistical significance. Color blocks at different positions represent the relative expression levels of corresponding lipid molecules at those positions: red indicates high expression of the substance in that group, while blue indicates low expression. (C) KEGG pathway annotation classification diagram for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents the enrichment ratio for each pathway, while the vertical axis displays the names of the metabolic pathways. Colors indicate the magnitude of p values, with redder hues corresponding to smaller p values, signifying more significant enrichment. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; OA, oleic acid; PA, palmitic acid; TAG, triacylglycerol; PG, phosphatidylglycerol; PetOH, phosphatidylethanol; PE, phosphatidylethanolamine; PC, phosphatidylcholine; HexCer-NS, hexosylceramide nonhydroxyfatty acid-sphingosine; HexCer-AP, hexosylceramide alpha-hydroxy fatty acid-phytosphingosine; GlcADG, glucuronosyldiacylglycerol; Cer-AP, ceramide alpha-hydroxy fatty acid-phytosphingosine; ACar, acylcarnitine.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Standard Deviation, Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Schematic diagram illustrating the molecular mechanism through which AdipoRon mitigates mixed fatty acid (OA + PA)-induced lipotoxicity in LMH cells. AdipoRon activates AMPK and PPARα signaling by binding to AdipoR1 and AdipoR2 on the LMH cell membrane, thereby downregulating the expression of the lipid synthesis-related genes ACC, FAS, SCD-1, and SREBP-1 and upregulating the expression of the fatty acid oxidation-related genes ACOX-1 and CPT-1. It subsequently regulates SP, GP, ACar, and GL metabolism; reduces cellular levels of Cer, SM, TAG, and ACar; and maintains the metabolic homeostasis of PE and PC, as well as cell membrane structural integrity and functional stability. Finally, it mitigates lipotoxic injury induced by mixed fatty acids (OA + PA) in LMH cells. Abbreviations: AMPK, adenosine 5′-monophosphate-activated protein kinase; PPARα, peroxisome proliferator-activated receptor-α; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthetase; SCD-1, stearyl coenzyme A dehydrogenase-1; SREBP-1, sterol regulatory element-binding protein 1; ACOX-1, acyl-CoA oxidase 1; CPT-1, carnitine palmitoyltransferase 1; SP, sphingolipid; GP, glycerophospholipid; ACar, acylcarnitine; GL, glycerolipid; Cer, ceramide; SM, sphingomyelin; TAG, triacylglycerol; PE, phosphatidylethanolamine; PC, phosphatidylcholine; glycosphingolipids; OA, oleic acid; PA, palmitic acid; LMH, leghorn male hepatoma.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Binding Assay, Membrane, Expressing, Functional Assay

Journal: Journal of Animal Science and Biotechnology

Article Title: Vitamin A-activated PPARγ signaling enhances intramuscular fat accumulation by overriding AMPK-mediated inhibition in late-fattening beef cattle

doi: 10.1186/s40104-025-01343-1

Figure Lengend Snippet: Integrated transcriptomic profiling and proteomic verification reveal key adipogenic pathways underlying marbling grade differences (A1 vs. A4) in longissimus dorsi muscle of Woking black cattle. A Integrated RNA-seq and qPCR validation of differentially expressed genes (DEGs) between A1-grade (low marbling) and A4-grade (high marbling) groups. Left: hierarchical clustering heatmap of DEGs; middle: volcano plot showing 80 downregulated and 46 upregulated genes in A4 vs. A1 (cutoff: |log 2 FC| > 1.5, FDR < 0.05); right: selected DEGs with corresponding log₂FC and adjusted p -values. Bottom: qPCR and RNA-seq log 2 FC comparisons for seven DEGs. B KEGG pathway enrichment analysis of DEGs reveals significant activation of AMPK signaling, adipocytokine signaling, thermogenesis, and lipid metabolism-related pathways in A4-grade samples. C Gene Ontology (GO) enrichment analysis indicates A4-grade group exhibits significant changes in oxidoreductase activity, mitochondrial inner membrane components, and protein transport processes. D Western blot validation of key signaling proteins in longissimus dorsi tissue. E Protein expression levels of AMPK and phosphorylated AMPK in longissimus dorsi of control (CON) and vitamin A-supplemented (VA) cattle. Data are presented as the mean ± standard error; * P < 0.05

Article Snippet: AMPK inhibitor Compound C (HY-13418A, MedChem Express, Shanghai, China) and AMPK agonist AICAR (HY-13417, MedChem Express, Shanghai, China) were dissolved in DMSO at 10 mmol/L, filter-sterilized through 0.22-μm PVDF membranes, and applied to cell cultures from differentiation D7 at final concentrations of 10 μmol/L (Compound C) and 300 μmol/L (AICAR).

Techniques: RNA Sequencing, Biomarker Discovery, Activation Assay, Activity Assay, Membrane, Western Blot, Expressing, Control

Journal: Journal of Animal Science and Biotechnology

Article Title: Vitamin A-activated PPARγ signaling enhances intramuscular fat accumulation by overriding AMPK-mediated inhibition in late-fattening beef cattle

doi: 10.1186/s40104-025-01343-1

Figure Lengend Snippet: ATRA activates adipogenic pathways to promote triglyceride accumulation and marker expression in BSMCs of Woking black cattle. Analysis of signaling pathway-related protein expression, including energy sensing and synthesis signaling pathway proteins (AMPK, p-AMPK, mTOR, p-mTOR, PI3K, p-PI3K, AKT, p-AKT). Data are presented as the mean ± standard error. a–c Different lowercase indicate significant differences ( P < 0.05)

Article Snippet: AMPK inhibitor Compound C (HY-13418A, MedChem Express, Shanghai, China) and AMPK agonist AICAR (HY-13417, MedChem Express, Shanghai, China) were dissolved in DMSO at 10 mmol/L, filter-sterilized through 0.22-μm PVDF membranes, and applied to cell cultures from differentiation D7 at final concentrations of 10 μmol/L (Compound C) and 300 μmol/L (AICAR).

Techniques: Marker, Expressing

Journal: Journal of Animal Science and Biotechnology

Article Title: Vitamin A-activated PPARγ signaling enhances intramuscular fat accumulation by overriding AMPK-mediated inhibition in late-fattening beef cattle

doi: 10.1186/s40104-025-01343-1

Figure Lengend Snippet: Pharmacological modulation of AMPK activity reveals its exclusive mediating role in vitamin A-Induced adipogenesis in BSMCs of boking black cattle. A Triglyceride (TG) concentrations and the expression levels of AMPK, p-AMPK, C/EBPα, PPARγ, and FABP4 proteins in adipocytes treated with control (CON), ATRA, Compound C, or ATRA + Compound C. B Quantification of relative protein expression levels shown in ( A ). C TG concentrations and protein expression levels in adipocytes treated with CON, ATRA, AICAR, or ATRA + AICAR. D Quantification of relative protein expression levels shown in ( C ). Data are presented as means ± standard deviation. a–c Different lowercase indicate significant differences ( P < 0.05)

Article Snippet: AMPK inhibitor Compound C (HY-13418A, MedChem Express, Shanghai, China) and AMPK agonist AICAR (HY-13417, MedChem Express, Shanghai, China) were dissolved in DMSO at 10 mmol/L, filter-sterilized through 0.22-μm PVDF membranes, and applied to cell cultures from differentiation D7 at final concentrations of 10 μmol/L (Compound C) and 300 μmol/L (AICAR).

Techniques: Activity Assay, Expressing, Control, Standard Deviation

Journal: Journal of Advanced Research

Article Title: Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip

doi: 10.1016/j.jare.2025.04.023

Figure Lengend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: To investigate the role of the AMPK signaling pathway in the protection of the intestinal epithelial barrier from oxidative stress damage by SeNPs, AMPK activator AICAR (MedChemExpres; Cat# HY-13417) and AMPK inhibitor Dorsomorphin (MedChemExpres; Cat# HY-13418A) were introduced into the gut-on-a-chip, respectively.

Techniques: Staining, Activity Assay, In Vitro

Journal: Journal of Advanced Research

Article Title: Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip

doi: 10.1016/j.jare.2025.04.023

Figure Lengend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to attenuate oxidative stress-induced intestinal barrier dysfunction and mast cell overactivation in mice. A. Immunofluorescence analysis of p-AMPK (red), NLRP3 (yellow) and Nrf2 (green) in jejunum of mice with different treatments (Scale bar: 100 μm). B. Western blot analysis of pAMPK and Nrf2 expression levels in mice jejunum. C. Western blot analysis of NLRP3 and its downstream pyroptosis-related protein expression levels in mice jejunum. Data are expressed as mean ± S.E.M. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: To investigate the role of the AMPK signaling pathway in the protection of the intestinal epithelial barrier from oxidative stress damage by SeNPs, AMPK activator AICAR (MedChemExpres; Cat# HY-13417) and AMPK inhibitor Dorsomorphin (MedChemExpres; Cat# HY-13418A) were introduced into the gut-on-a-chip, respectively.

Techniques: Immunofluorescence, Western Blot, Expressing