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. 2022 Apr 11;10(1):29-32.
doi: 10.1016/j.gendis.2022.03.017. eCollection 2023 Jan.

Irisin regulates pancreatic lipases through PPARγ-PGCα-FNDC5 pathway

Affiliations

Irisin regulates pancreatic lipases through PPARγ-PGCα-FNDC5 pathway

Horwitz Avital et al. Genes Dis. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interests.

Figures

Fig. 1
Figure 1
Irisin/FNDC5 is involved in pancreatic lipase regulation via the PPARγ-PGC1α pathway in response to nutrient flux. (A) Western blot analysis of protein levels normalized to actin in AR42J-B13 cells (control and OE-PPARγ) treated with exogenous irisin (60 ng/mL, 4 h). (B) RT-PCR analysis of transcript levels normalized to S18 in AR42J-B13 cells (control and OE-PPARγ) treated with exogenous irisin (60 ng/mL, 4 h). (C) Secreted PL protein levels in AR42J-B13 cells (control and OE-PPARγ) treated with exogenous irisin (60 ng/ml, 4 h). (D) Western blot analysis of secreted PLRP2 protein levels in AR42J-B13 cells (control and OE-PPARγ) treated with exogenous irisin (60 ng/mL, 4 h). (E) Western blot analysis of secreted PL protein levels in primary exocrine pancreas acinar cells were treated with exogenous irisin (60 ng/mL, 4 h). (F) Western blot analysis of secreted PLRP2 protein levels in primary exocrine pancreas acinar cells were treated with exogenous irisin (60 ng/mL, 4 h). (G) Western blot analysis of protein levels normalized to actin in AR42J-B13 cells (control and OE-PPARγ) treated with rosiglitazone (100 nM, 24 h). (H) RT-PCR analysis of transcript levels normalized to S18 in AR42J-B13 cells (control and OE-PPARγ) treated with rosiglitazone (100 nM, 24 h). (I) Western blot analysis of secreted PL protein levels in AR42J-B13 cells (control and OE-PPARγ) treated with rosiglitazone (100 nM, 24 h). (J) Western blot analysis of secreted PLRP2 protein levels in AR42J-B13 cells (control and OE-PPARγ) treated with rosiglitazone (100 nM, 24 h). (K) Immunohistochemistry staining of PGC1α (red) and DAPI nucleus staining (blue) of AR42J-B13 acinar cells following treatment with rosiglitazone (24 h) or irisin (4 h). (L) Immunohistochemistry staining of PGC1α (red) and DAPI nucleus staining (blue) of OE-PPARγ AR42J-B13 acinar cells following treatment with rosiglitazone (24 h) or irisin (4 h). (M) Immunofluorescent staining of PPARγ (green) and DAPI nucleus staining (blue) of AR42J-B13 acinar cells following treatment with rosiglitazone (24 h) or irisin (4 h). (N) Immunofluorescent staining of PPARγ (green) and DAPI nucleus staining (blue) of OE-PPARγ AR42J-B13 acinar cells following treatment with rosiglitazone (24 h) or irisin (4 h). Photos were taken using Olympus fluorescent microscope at × 60 magnification (1 μm scale). (O) Western blot analysis of protein levels normalized to actin in AR42J-B13 cells treated with fatty acid (Pal, Ole, 500 μM) for 24 h. (P) RT-PCR analysis of transcript levels normalized to S18 in AR42J-B13 cells treated with fatty acid (Pal, Ole, 500 μM) for 24 h. (Q) Western blot analysis of secreted PL protein levels in AR42J-B13 cells treated with fatty acid Pal, Ole, 500 μM) for 24 h (R) Western blot analysis of secreted PLRP2 protein levels in AR42J-B13 cells treated with fatty acid (Pal, Ole, 500 μM) for 24 h. (S) Western blot analysis of protein levels normalized to actin in AR42J-B13 cells treated with Pal (500 μM, 24 h), exogenous irisin (60 ng/mL, 4 h) or combed treatments. (T) RT-PCR analysis of transcript levels normalized to S18 in AR42J-B13 cells treated with Pal (500 μM, 24 h), exogenous irisin (60 ng/mL, 4 h) or combed treatments. (U) Western blot analysis of secreted PL protein levels in AR42J-B13 cells treated with Pal (500 μM, 24 h), exogenous irisin (60 ng/mL, 4 h) or combed treatments. (V) Western blot analysis of secreted PLRP2 protein levels in AR42J-B13 cells treated with Pal (500 μM, 24 h), exogenous irisin (60 ng/mL, 4 h) or combed treatments. Results of RT-PCR and Western blot are expressed in the graphs as mean ± SE of 3–4 independent experiments (n = 3). Immunofluorescence staining was performed in quadruplet for each experiment, and quantification of PPARγ and PGC1α nuclear localization was performed on 200–250 cells for each treatment (randomly chosen). Asterisks represent statistical difference from control. ∗P < 0.05.

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