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Revistas
Asian Biomedicine
Volumen 14 (2020): Edición 6 (December 2020)
Acceso abierto
IRAK inhibitor can improve insulin sensitivity in insulin-resistant mice fed with a high-fat diet
Mostafa Allahyari
Mostafa Allahyari
,
Athena Rajaie
Athena Rajaie
y
Hossein Fallah
Hossein Fallah
| 31 dic 2020
Asian Biomedicine
Volumen 14 (2020): Edición 6 (December 2020)
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Article Category:
Original article
Publicado en línea:
31 dic 2020
Páginas:
253 - 260
DOI:
https://doi.org/10.1515/abm-2020-0034
Palabras clave
adipose tissue
,
diabetes mellitus
,
inflammation
,
insulin resistance
,
mice
,
inbred C57BL
,
thiazolidinediones
© 2020 Mostafa Allahyari et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Figure 1
Timeline of treatment of the mice. Mice were treated with their respective diets for 14 weeks. They were treated with the interventional drugs or controls for the final 2 weeks ahead of final measurements.
Figure 2
(A) Weight of the mice at the beginning (light gray) and the end (dark gray) of the study. The mice were treated for 2 weeks with IRAKi, pioglitazone (Pio), or a combination of both (IRAKi+Pio). Control mice received no treatment. (B) Weight gain (n = 8 mice in each group). ***P < 0.0001 compared with the control group (high-fat diet). ###P < 0.0001 compared with the sham group (high-fat diet, DMSO vehicle control treatment). *P < 0.05 compared with the standard diet group.
Figure 3
Serum levels of biochemical factors. Insulin resistance was developed in mice fed with the high-fat diet for 12 weeks, and then these mice were treated for 2 weeks with IRAKi, pioglitazone (Pio), or a combination of both (IRAKi+Pio). Glucose, triglyceride, and cholesterol were measured in serum of mice after 12 h fasting. **P < 0.001, ***P < 0.0001 compared with the control group. ##P < 0.001, ###P < 0.0001 compared with the sham group, ††P < 0.001 compared with the standard diet group (n = 8 mice per group).
Figure 4
Serum levels of insulin in fasting mice. Insulin resistance developed in mice fed with the high-fat diet for 12 weeks, and then these mice were treated for 2 weeks with the IRAKi, pioglitazone (Pio), or a combination of both (IRAKi+Pio). Blood serum insulin was then measured after 12 h fasting. **P < 0.001 compared with the control group, ##P < 0.001 compared with the sham group (n = 8 mice per group).
Figure 5
HOMA-IR index in mice after various treatments. Insulin resistance developed in mice fed with the high-fat diet for 12 weeks, and then these mice were treated for 2 weeks with the IRAKi, pioglitazone (Pio), or a combination of both (IRAKi+Pio). HOMA-IR was computed using a standard formula. ***P < 0.0001 compared with the control group. ###P < 0.0001 compared with the sham group. †P < 0.05 compared with the standard diet group (n = 8 mice per group).
Figure 6
IL-6 mRNA copy numbers in mice after various treatments. Insulin resistance developed in mice fed with the high-fat diet for 12 weeks, and then these mice were treated for 2 weeks with the IRAKi, pioglitazone (Pio), or a combination of both (IRAKi+Pio). qPCR assayed the level of IL-6 gene expression. *P < 0.05, **P < 0.01, ***P < 0.0001 compared with the control group. #P < 0.05, ##P < 0.001, ###P < 0.0001 compared with the sham group. ††P < 0.001 compared with the standard diet group. ‡‡P < 0.001 comparing IRAKi and IRAKi/Pio groups (n = 8 mice per group).
Primer sequences for qPCR
Direction
GAPDH
IL-6
Forward primer (5′–3′)
CCCATCACCATCTTCCAGGAGC
CCTCTGGTCTTCTGGAGTACC
Reverse primer (5′–3′)
CCAGTGAGCTTCCCGTTCAGC
ACTCCTTCTGTGACTCCAGC
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