See the published version of this preprint at Chinese Medicine.
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Research
Fei Yin
chongqing university oftechnology
Corresponding Author
Jianhui Liu
Chongqing University of Technology
Corresponding Author
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This work is licensed under a CC BY 4.0 License. Read Full License
Background: Trilobatin, a natural compound, has been found to exhibit anti-diabetic properties in high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic mice. But up to now no research has been reported on the effect of trilobatin on insulin resistance in peripheral tissues. Herein, we determined the effects of trilobatin on insulin resistance in palmitate-treated C2C12 myotubes and ob/ob mice.
Methods: 8-10 weeks of male ob/ob mice and same background C57BL/6 mice were used to evaluate the role of trilobatin on insulin resistance; Protein expression and phosphorylation were measured by western blot; Glucose uptake was determined a fluorescent test.
Results: treatment with trilobatin prevented palmitate-induced insulin resistance by enhancing glucose uptake and the phosphorylation of insulin resistance substrate 1 (IRS1) and protein Kinase B, (PKB/AKT), recovered the translocation of GLUT4 from cytoplasm to membrane, but preincubation with LY294002, an inhibitor of PI3K, blocked the effects of trilobatin on glucose uptake and the distribution of GLUT4 in C2C12 myotubes. Furthermore, administration with trilobatin for 4 weeks significantly improved insulin resistance by decreasing fasting blood glucose and insulin in serum, enhancing the phosphorylation of IRS1 and AKT, and recovering the expression and translocation of GLUT4 in ob/ob mice.
Conclusions: IRS-AKT-GLUT4 signaling pathway might be involved in trilobatin ameliorating insulin resistance in skeletal muscle of obese animal models.
Keywords
glucose transporter 4 (GLUT4), insulin receptor substrate 1(IRS1), insulin resistance, protein kinase B (PKB/AKT), trilobatin
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CURRENT STATUS: Published
View the published article at Chinese Medicine.
Version 2
Posted 16 Sep, 2020
No community comments so far
Editorial decision: Accept
On 01 Oct, 2020
Review #1 received
Received 27 Sep, 2020
Reviewer #1 agreed
On 21 Sep, 2020
Reviewers invited
Invitations sent on 18 Sep, 2020
Editor assigned
On 15 Sep, 2020
Submission checks complete
On 14 Sep, 2020
Editor invited
On 14 Sep, 2020
No comments provided
Editorial decision: Major revision
On 04 Sep, 2020
Review #1 received
Received 03 Sep, 2020
Review #2 received
Received 29 Aug, 2020
Reviewer #2 agreed
On 25 Aug, 2020
Reviewer #1 agreed
On 24 Aug, 2020
Reviewers invited
Invitations sent on 10 Aug, 2020
Editor assigned
On 24 Jul, 2020
Submission checks complete
On 23 Jul, 2020
Editor invited
On 23 Jul, 2020
First submitted
On 22 Jul, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Clinical Pharmacology
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See the published version of this preprint at Chinese Medicine.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Fei Yin
chongqing university oftechnology
Corresponding Author
Jianhui Liu
Chongqing University of Technology
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Chinese Medicine.
Version 2
Posted 16 Sep, 2020
No community comments so far
Editorial decision: Accept
On 01 Oct, 2020
Review #1 received
Received 27 Sep, 2020
Reviewer #1 agreed
On 21 Sep, 2020
Reviewers invited
Invitations sent on 18 Sep, 2020
Editor assigned
On 15 Sep, 2020
Submission checks complete
On 14 Sep, 2020
Editor invited
On 14 Sep, 2020
No comments provided
Editorial decision: Major revision
On 04 Sep, 2020
Review #1 received
Received 03 Sep, 2020
Review #2 received
Received 29 Aug, 2020
Reviewer #2 agreed
On 25 Aug, 2020
Reviewer #1 agreed
On 24 Aug, 2020
Reviewers invited
Invitations sent on 10 Aug, 2020
Editor assigned
On 24 Jul, 2020
Submission checks complete
On 23 Jul, 2020
Editor invited
On 23 Jul, 2020
First submitted
On 22 Jul, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Clinical Pharmacology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Chinese Medicine.
Background: Trilobatin, a natural compound, has been found to exhibit anti-diabetic properties in high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic mice. But up to now no research has been reported on the effect of trilobatin on insulin resistance in peripheral tissues. Herein, we determined the effects of trilobatin on insulin resistance in palmitate-treated C2C12 myotubes and ob/ob mice.
Methods: 8-10 weeks of male ob/ob mice and same background C57BL/6 mice were used to evaluate the role of trilobatin on insulin resistance; Protein expression and phosphorylation were measured by western blot; Glucose uptake was determined a fluorescent test.
Results: treatment with trilobatin prevented palmitate-induced insulin resistance by enhancing glucose uptake and the phosphorylation of insulin resistance substrate 1 (IRS1) and protein Kinase B, (PKB/AKT), recovered the translocation of GLUT4 from cytoplasm to membrane, but preincubation with LY294002, an inhibitor of PI3K, blocked the effects of trilobatin on glucose uptake and the distribution of GLUT4 in C2C12 myotubes. Furthermore, administration with trilobatin for 4 weeks significantly improved insulin resistance by decreasing fasting blood glucose and insulin in serum, enhancing the phosphorylation of IRS1 and AKT, and recovering the expression and translocation of GLUT4 in ob/ob mice.
Conclusions: IRS-AKT-GLUT4 signaling pathway might be involved in trilobatin ameliorating insulin resistance in skeletal muscle of obese animal models.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
This is a list of supplementary files associated with this preprint. Click to download.
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