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. 2018 Oct;16(4):3345-3352.
doi: 10.3892/etm.2018.6615. Epub 2018 Aug 17.

Sericin enhances the insulin-PI3K/AKT signaling pathway in the liver of a type 2 diabetes rat model

Chengjun Song  1 , Donghui Liu  1 , Songhe Yang  1 , Luyang Cheng  2 , Enhong Xing  3 , Zhihong Chen  1
Affiliations

Sericin enhances the insulin-PI3K/AKT signaling pathway in the liver of a type 2 diabetes rat model

Chengjun Song et al. Exp Ther Med. 2018 Oct.

Abstract

The aim of the current study was to investigate the regulatory effect of sericin on the hepatic insulin-phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in a type 2 diabetes rat model. Male Sprague Dawley rats were randomly divided into four groups: Control group, diabetic model group, high-dose sericin group and low-dose sericin group, with 12 rats in each group. Fasting blood glucose was detected by the glucose oxidase method, and hepatic glycogen was determined by periodic acid-Schiff staining. The morphology of the liver was observed by hematoxylin and eosin staining. Immunohistochemical staining, western blotting and reverse transcription-quantitative polymerase chain reaction were used to determine the protein and mRNA expression levels of insulin receptor (IR), IR substrate-1 (IRS-1), PI3K and AKT. Compared with the control group, the blood glucose of the diabetic model group was significantly increased (P<0.05). The glycogen content and the expression levels of IR, IRS-1, PI3K and AKT in the diabetic model group were significantly lower (P<0.05), and the liver morphological structure of the diabetic model group exhibited obvious pathological changes compared with the control group. Compared with the diabetic model group, the blood glucose of the high- and low-dose sericin groups was significantly reduced, while the glycogen content and the expression levels of IR, IRS-1, PI3K and AKT in the sericin treatment groups were significantly increased (P<0.05). Additionally, the liver pathological changes of high-dose and low-dose sericin groups were markedly reduced. Sericin may enhance the signaling transduction effect of insulin by upregulating the expression levels of key factors (IR, IRS-1, PI3K and AKT) in the liver insulin-PI3K/AKT signaling pathway, thus promoting glucose transport and liver glycogen synthesis, and further reducing blood glucose.

Keywords: insulin; liver; phosphoinositide 3-kinase/protein kinase B signaling pathway; sericin; type 2 diabetes mellitus.

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Figures

Figure 1.
Figure 1.
Analysis of liver morphology. Changes in liver morphology in the control group, diabetic model group, high-dose sericin group and low-dose sericin group were observed with hematoxylin and eosin staining. Representative images are presented. Magnification, ×200.
Figure 2.
Figure 2.
Analysis of liver glycogen content and blood glucose level. (A) Liver glycogen content was evaluated by periodic acid-Schiff staining. Representative images are presented. Magnification, ×200. (B) Quantification of liver glycogen content. (C) Blood glucose level in each group. *P<0.05 vs. control group; #P<0.05 vs. diabetic model group; &P<0.05 vs. low-dose sericin group.
Figure 3.
Figure 3.
Analysis of IR, IRS-1, PI3K and AKT protein expression by immunohistochemical staining. (A) IR, IRS-1, PI3K and AKT protein expression in the rat livers of each group was detected by immunohistochemical staining (magnification, ×200). (B) Quantification of immunohistochemical staining in each group. *P<0.05 vs. control group; #P<0.05 vs. diabetic model group; &P<0.05 vs. low-dose sericin group. IR, insulin receptor; IRS-1, IR substrate-1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Figure 4.
Figure 4.
Analysis of IR, IRS-1, PI3K and AKT protein expression levels by western blotting. (A) Expression of IR, IRS-1, PI3K and AKT proteins in the rat livers of each group was detected by western blot analysis. (B) Quantification of protein expression in each group. *P<0.05 vs. control group; #P<0.05 vs. diabetic model group; &P<0.05 vs. low-dose sericin group. IR, insulin receptor; IRS-1, IR substrate-1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Figure 5.
Figure 5.
Analysis of IR, IRS-1, PI3K and AKT mRNA expression levels. The expression of (A) IR, (B) AKT and (C) IRS-1 and PI3K mRNA in the rat livers of each group was detected by reverse transcription-quantitative polymerase chain reaction. *P<0.05 vs. control group; #P<0.05 vs. diabetic model group. IR, insulin receptor; IRS-1, IR substrate-1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
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