Fig. 1

Major isoform of total AMPKɑ protein in goose liver NF and OF represent the control group and the overfeeding group, respectively"

Fig. 2

Subcellular localization of tAMPKɑ1 A. The content of tAMPKɑ1 in whole cell samples, cytoplasmic samples, nuclear samples, and isolated mitochondrial samples of primary goose hepatocytes was detected by WB (n=2). VDAC, Lamin B1, and GAPDH were used as marker proteins for mitochondria, nucleus, and cytoplasm, respectively. B. Co-localization of tAMPKɑ1 with mitochondria in primary goose hepatocytes. Red (Mito-tracker Red) indicates mitochondria, green indicates tAMPKɑ1, blue (DAPI) indicates the nucleus, yellow (co-localization of red and green) indicates tAMPKɑ1 molecules bound to mitochondria. C. Immunoblot images of mitochondrial proteins isolated from goose liver treated with different concentrations of trypsin"

Fig. 3

The protein abundance of wAMPKα1 and mAMPKα1 in fatty liver and normal liver of goose A. Immunoblot images showing the protein abundance of p-wAMPKα1 and t-wAMPKα1 in whole cell lysates of fatty liver and normal liver of goose, n=3; B, C. The quantification of the protein abundance of p-wAMPKα1 and t-wAMPKα1 in whole cell lysates of fatty liver and normal liver of goose after immunoblot analysis; D. Immunoblot images showing the protein abundance of p-mAMPKα1 and t-mAMPKα1 in mitochondrial fractions of fatty liver and normal liver of goose, n=3; E, F. The quantification of the protein abundance of p-mAMPKα1 and t-mAMPKα1 in mitochondrial fractions of fatty liver and normal liver of goose. * indicates P < 0.05, ** indicates P < 0.01, the same as below"

Fig. 4

The effect of glucose and palmitic acid treatment on the protein abundance of wAMPKα1 and mAMPKα1 in goose primary hepatocytes A. Immunoblot images showing the effect of glucose treatment on the protein abundance of t/p-wAMPKα1 and t/p-mAMPKα1 in primary goose hepatocytes. VDAC and Tubulin serve as loading controls for mitochondrial and whole cell lysates, respectively; B. Quantification of the protein abundance of p-wAMPKα1 and p-mAMPKα1 in glucose-treated and control groups of primary goose hepatocytes after immunoblot analysis, n=3; C. Quantification of the protein abundance of t-wAMPKα1 and t-mAMPKα1 in glucose-treated and control groups of primary goose hepatocytes after immunoblot analysis, n=3; D. Immunoblot images showing the effect of palmitic acid treatment on the protein abundance of t/p-wAMPKα1 and t/p-mAMPKα1 in primary goose hepatocytes; E. Quantification of the protein abundance of p-wAMPKα1 and p-mAMPKα1 in palmitic acid-treated and control groups of primary goose hepatocytes after immunoblot analysis, n=3; F. Quantification of the protein abundance of t-wAMPKα1 and t-mAMPKα1 in palmitic acid-treated and control groups of primary goose hepatocytes after immunoblot analysis, n=3"

Fig. 5

The effect of mitoAIP overexpression on the abundance of AMPKα1 and its substrates ACC1 and ULK1 proteins A. Representative immunoblot images showing the effect of overexpressing mitoAIP on the protein abundance of AMPKα1 and its substrates ACC1 and ULK1 in whole cell lysates. β-Actin serves as the loading control for whole cell lysates; B. Quantification of the protein abundance of relevant proteins from the immunoblot images, n=6; C. Representative immunoblot images showing the effect of overexpressing mitoAIP on the protein abundance of AMPKα1 and its substrates ACC1 and ULK1 in mitochondrial fractions. VDAC serves as the loading control for mitochondrial fractions; D. Quantification of the protein abundance of relevant proteins from the immunoblot images, n=6; E. Representative immunoblot images showing the effect of overexpressing mitoAIP on the protein abundance of AMPKα1 and its substrates ACC1 and ULK1 in whole cell lysates under conditions where AMPKα1 is activated by AICAR; F. Quantification of the protein abundance of relevant proteins from the immunoblot images, n=6; G. Representative immunoblot images showing the effect of overexpressing pmitoAIP on the protein abundance of AMPKα1 and its substrates ACC1 and ULK1 in mitochondrial fractions under conditions where AMPKα1 is activated by AICAR; H. Quantification of the protein abundance of relevant proteins from the immunoblot images, n=6. Tom20-mChF denotes empty vector, while Tom20-mChF-AIP denotes mitoAIP overexpression vector. The significance of differences between the mean values of the Tom20-mChF group and the Tom20-mChF+AICAR group, as well as between the Tom20-mChF+AICAR group and the Tom20-mChF-AIP+AICAR group, was evaluated using the t-test method"

Fig. 6

The effect of overexpressing mitoAIP on indicators related to mitochondrial function A. The effect of overexpressing pmitoAIP on mitochondrial membrane potential was detected using flow cytometry and JC-1; B. Quantitative analysis of mitochondrial membrane potential, n=6; C. Immunofluorescence images of AML12 cells overexpressing pmitoAIP and mitoTimer; D. Quantitative analysis of immunofluorescence, n=3. Tom20-mChF and pcDNA3.1 denote empty vectors, while Tom20-mChF-AIP and Tom20-AIP denote mitoAIP overexpression vectors"

Fig. 7

The effect of overexpression of mitoAIP on fat content in AML12 cells A. Under the treatment with oleic acid, the representative images of Oil Red O staining for control group and overexpression group (400×); B. Quantification after Oil Red O staining, n=4. Tom20-mChF denotes empty vector, and Tom20-mChF-AIP denotes mitoAIP overexpression vector. OA represents oleic acid treatment"