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Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and <t>AS160</t> phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 <t>S318,</t> and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.
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Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and <t>AS160</t> phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 <t>S318,</t> and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.
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Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

The fabrication and photothermal responsive behavior of the NIR-responsive dynamic wrinkled PDMS/CNTs-PPy composites. (A) The process and principle of in-situ generation of Ppy wrinkle-patterned surface. (B) Conductive atomic force microscopy (C-AFM) current mapping of PDMS/CNTs (left) and PDMS/CNTs-Ppy (right) nanocomposites. (C) It presents AFM characterization of the PDMS/CNTs-PPy composites at different time points, showing the evolution of the surface morphology from smooth to a disordered labyrinthine wrinkle pattern through 2D topography, phase, and 3D morphology images. (D–F) The evolution of width, height, and surface roughness of Ppy film with polymerization time (t), respectively. (G) Hydrophobicity change before (left) and after (right) Ppy coating. (H) Schematic of surface morphology change under NIR ON/OFF cycling. (I) Temperature profiles under NIR irradiation in different media. (J) Temperature profiles in phosphate-buffered saline (PBS) under NIR irradiation, comparing PDMS/CNTs-Ppy, PDMS/CNTs, and pristine PDMS. (K) Temperature profiles for composites with different CNT content (0, 0.025, 0.05, 0.075, and 0.1%). (L) Temperature profiles at varying NIR power densities for the 0.05 wt% CNT composite. (M) Equilibrium temperatures at different power densities. (N) Temperature cycling stability test (10 min ON/OFF intervals) under ∼1.33 W cm −2 NIR irradiation. Note: Unless specified (e.g., J-L), experiments used the 0.05 % CNT composite and ∼1.33 W cm −2 NIR power density. Data are mean ± S.D. (n = 5).

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: The fabrication and photothermal responsive behavior of the NIR-responsive dynamic wrinkled PDMS/CNTs-PPy composites. (A) The process and principle of in-situ generation of Ppy wrinkle-patterned surface. (B) Conductive atomic force microscopy (C-AFM) current mapping of PDMS/CNTs (left) and PDMS/CNTs-Ppy (right) nanocomposites. (C) It presents AFM characterization of the PDMS/CNTs-PPy composites at different time points, showing the evolution of the surface morphology from smooth to a disordered labyrinthine wrinkle pattern through 2D topography, phase, and 3D morphology images. (D–F) The evolution of width, height, and surface roughness of Ppy film with polymerization time (t), respectively. (G) Hydrophobicity change before (left) and after (right) Ppy coating. (H) Schematic of surface morphology change under NIR ON/OFF cycling. (I) Temperature profiles under NIR irradiation in different media. (J) Temperature profiles in phosphate-buffered saline (PBS) under NIR irradiation, comparing PDMS/CNTs-Ppy, PDMS/CNTs, and pristine PDMS. (K) Temperature profiles for composites with different CNT content (0, 0.025, 0.05, 0.075, and 0.1%). (L) Temperature profiles at varying NIR power densities for the 0.05 wt% CNT composite. (M) Equilibrium temperatures at different power densities. (N) Temperature cycling stability test (10 min ON/OFF intervals) under ∼1.33 W cm −2 NIR irradiation. Note: Unless specified (e.g., J-L), experiments used the 0.05 % CNT composite and ∼1.33 W cm −2 NIR power density. Data are mean ± S.D. (n = 5).

Article Snippet: Fabrication of the PDMS/CNTs substrate : A polydimethylsiloxane (PDMS) substrate was prepared by combining the base and curing agent (Sylgard 184, Dow Corning) at a predetermined weight ratio of 10:1.

Techniques: In Situ, Microscopy, Irradiation, Saline

The biocompatibility and functional characteristics of different surfaces. Live/dead staining (A) and CCK8 OD value (B) of C2C12 cells cultured on TCP, PDMS/CNTs, and PDMS/CNTs-Ppy. (C) Calcium transient of CMs on different surfaces at day 5 of culture. (D)Expression of cardiac-specific proteins of α-actinin (green) and CX-43 (red) in the CMs on non-electroactive PDMS/CNTs-PLA and electroactive PDMS/CNTs-Ppy. (E) and (F) Immunofluorescence intensity statistics were calculated based on CX-43 and α-actinin immunostaining images. (G)Heatmap of DEGs between PDMS/CNTs-Ppy and PDMS/CNTs-PLA after hierarchical cluster analysis (n = 3 rats per group). (H) PCA plot of proteomics data in these two groups. (I) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus PDMS/CNTs-PLA. (J) Volcano plot of protein expression in PDMS/CNTs-Ppy and PDMS/CNTs-PLA. (K) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus PDMS/CNTs-PLA). (L) Network of the muscle differentiation-related GO enriched from all DEGs with a fold change >2.0. The data were expressed as mean ± S.D. (n = 3).

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: The biocompatibility and functional characteristics of different surfaces. Live/dead staining (A) and CCK8 OD value (B) of C2C12 cells cultured on TCP, PDMS/CNTs, and PDMS/CNTs-Ppy. (C) Calcium transient of CMs on different surfaces at day 5 of culture. (D)Expression of cardiac-specific proteins of α-actinin (green) and CX-43 (red) in the CMs on non-electroactive PDMS/CNTs-PLA and electroactive PDMS/CNTs-Ppy. (E) and (F) Immunofluorescence intensity statistics were calculated based on CX-43 and α-actinin immunostaining images. (G)Heatmap of DEGs between PDMS/CNTs-Ppy and PDMS/CNTs-PLA after hierarchical cluster analysis (n = 3 rats per group). (H) PCA plot of proteomics data in these two groups. (I) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus PDMS/CNTs-PLA. (J) Volcano plot of protein expression in PDMS/CNTs-Ppy and PDMS/CNTs-PLA. (K) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus PDMS/CNTs-PLA). (L) Network of the muscle differentiation-related GO enriched from all DEGs with a fold change >2.0. The data were expressed as mean ± S.D. (n = 3).

Article Snippet: Fabrication of the PDMS/CNTs substrate : A polydimethylsiloxane (PDMS) substrate was prepared by combining the base and curing agent (Sylgard 184, Dow Corning) at a predetermined weight ratio of 10:1.

Techniques: Functional Assay, Staining, Cell Culture, Expressing, Immunofluorescence, Immunostaining

Biological activity and adhesion status of cells on PDMS/CNTs-Ppy before and after NIR irradiation. (A) Live/dead assay of C2C12 cells before (up) and after (down) cell detachment (green, live cells; red, dead cells). (B) Changes in cell morphology before (left) and after (right) NIR irradiation by SEM. (C) Immunofluorescence staining of F-actin (red) and vinculin (green). (D) Immunofluorescence staining of γ-H2AX (green). (E) Fluorescence intensity statistics were calculated based on Vinculin immunofluorescence images. (F) Fluorescence intensity statistics were calculated based on γ-H2AX immunofluorescence images. (G) Heatmap of DEGs between PDMS/CNTs-Ppy and TCP-Ppy after hierarchical cluster analysis. (H) PCA plot of proteomics data in these two groups. (I) Volcano plot of protein expression in PDMS/CNTs-Ppy and TCP-Ppy. (J) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (K) GO terms enriched from up-regulation DEGs associated with C2C12 adhesion and differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (L) GO terms enriched from down-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (M) Network of the cell adhesion-related GO enriched from all DEGs with a fold change>2.0. The data were expressed as mean ± S.D. (n = 3); ns means no significance.

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: Biological activity and adhesion status of cells on PDMS/CNTs-Ppy before and after NIR irradiation. (A) Live/dead assay of C2C12 cells before (up) and after (down) cell detachment (green, live cells; red, dead cells). (B) Changes in cell morphology before (left) and after (right) NIR irradiation by SEM. (C) Immunofluorescence staining of F-actin (red) and vinculin (green). (D) Immunofluorescence staining of γ-H2AX (green). (E) Fluorescence intensity statistics were calculated based on Vinculin immunofluorescence images. (F) Fluorescence intensity statistics were calculated based on γ-H2AX immunofluorescence images. (G) Heatmap of DEGs between PDMS/CNTs-Ppy and TCP-Ppy after hierarchical cluster analysis. (H) PCA plot of proteomics data in these two groups. (I) Volcano plot of protein expression in PDMS/CNTs-Ppy and TCP-Ppy. (J) GO terms enriched from up-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (K) GO terms enriched from up-regulation DEGs associated with C2C12 adhesion and differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (L) GO terms enriched from down-regulation DEGs associated with C2C12 differentiation (PDMS/CNTs-Ppy versus TCP-Ppy). (M) Network of the cell adhesion-related GO enriched from all DEGs with a fold change>2.0. The data were expressed as mean ± S.D. (n = 3); ns means no significance.

Article Snippet: Fabrication of the PDMS/CNTs substrate : A polydimethylsiloxane (PDMS) substrate was prepared by combining the base and curing agent (Sylgard 184, Dow Corning) at a predetermined weight ratio of 10:1.

Techniques: Activity Assay, Irradiation, Live Dead Assay, Immunofluorescence, Staining, Fluorescence, Expressing

High integrity of cell sheets acquired by the NIR response dynamic wrinkle system. (A) Schematic illustrating the process of obtaining cell sheets, controlled remotely with on-off NIR light. (B) Immunofluorescence images of F-actin (red) and vinculin (green) in C2C12 and L6 cells. (C) Immunofluorescence images of C2C12 and L6 cell suspensions. (D) Bulk cell sheets obtained from the PDMS/CNTs-Ppy surface. (E) Viability test of cells transferred onto PDMS/CNTs-Ppy after transfer from the PDMS/CNTs-Ppy surface: Calcein-AM (green, live), EthD-1 (red, dead). (F) Immunofluorescence images of F-actin (red) and vinculin (green) in C2C12 and L6 cells before cell sheet detachment. (G) Corresponding images after detachment. (H) Immunofluorescence images of F-actin (red) and fibronectin (green) in C2C12 cell sheets. (I) Immunofluorescence images of ZO-1 (green) in C2C12 cell sheets.

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: High integrity of cell sheets acquired by the NIR response dynamic wrinkle system. (A) Schematic illustrating the process of obtaining cell sheets, controlled remotely with on-off NIR light. (B) Immunofluorescence images of F-actin (red) and vinculin (green) in C2C12 and L6 cells. (C) Immunofluorescence images of C2C12 and L6 cell suspensions. (D) Bulk cell sheets obtained from the PDMS/CNTs-Ppy surface. (E) Viability test of cells transferred onto PDMS/CNTs-Ppy after transfer from the PDMS/CNTs-Ppy surface: Calcein-AM (green, live), EthD-1 (red, dead). (F) Immunofluorescence images of F-actin (red) and vinculin (green) in C2C12 and L6 cells before cell sheet detachment. (G) Corresponding images after detachment. (H) Immunofluorescence images of F-actin (red) and fibronectin (green) in C2C12 cell sheets. (I) Immunofluorescence images of ZO-1 (green) in C2C12 cell sheets.

Article Snippet: Fabrication of the PDMS/CNTs substrate : A polydimethylsiloxane (PDMS) substrate was prepared by combining the base and curing agent (Sylgard 184, Dow Corning) at a predetermined weight ratio of 10:1.

Techniques: Immunofluorescence

Schematic diagram showing the mechanism of VML tissue repair. L6 cell sheets obtained from the PDMS/CNTs-Ppy conductive wrinkled cell culture platform are transplanted into the VML site for skeletal muscle repair. The microstructured, electroactive substrate pre-primes the L6 cells, while preserving cell-cell connections, cell-ECM interactions, and a high-density, high-activity cell sheet. Consequently, the L6 cell sheets promote myogenic differentiation, maintain electromechanical coupling, reduce inflammation, and enhance neovascularisation, enabling rapid functional repair at the injury site.

Journal: Bioactive Materials

Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

doi: 10.1016/j.bioactmat.2026.01.046

Figure Lengend Snippet: Schematic diagram showing the mechanism of VML tissue repair. L6 cell sheets obtained from the PDMS/CNTs-Ppy conductive wrinkled cell culture platform are transplanted into the VML site for skeletal muscle repair. The microstructured, electroactive substrate pre-primes the L6 cells, while preserving cell-cell connections, cell-ECM interactions, and a high-density, high-activity cell sheet. Consequently, the L6 cell sheets promote myogenic differentiation, maintain electromechanical coupling, reduce inflammation, and enhance neovascularisation, enabling rapid functional repair at the injury site.

Article Snippet: Fabrication of the PDMS/CNTs substrate : A polydimethylsiloxane (PDMS) substrate was prepared by combining the base and curing agent (Sylgard 184, Dow Corning) at a predetermined weight ratio of 10:1.

Techniques: Cell Culture, Preserving, Activity Assay, Cell Characterization, Functional Assay