Changes of insulin receptors in high fat and high glucose diet mice with insulin resistance

ABSTRACT

This study aimed to observe the expression of insulin-signaling molecules in different organs of mice with insulin resistance (IR). Firstly, mice were fed a high-fat and high-sugar diet (HF group) to establish an IR model, and the controls (NF group) were fed with a normal diet. Next, the weight, fasting blood glucose (FBG), serum insulin and insulin tolerance were detected. Pathological changes of liver tissues were observed by H&E staining. The expressions of INSR, IRS-1 and IRS-2 in the liver, skeletal muscle and ovary were measured by qRT-PCR and western blotting. As a result, compared with the NF group, the HF group mice had increased weight, FBG, insulin and IR index after 6-week of feeding as well as a worse performance in the insulin tolerance test and H&E staining showed fatty liver-like changes after 12-week of feeding, exhibited lower expression of INSR, IRS-1 and IRS-2 in the liver of mice at 6 and 12 weeks. The expression of INSR and IRS-1 in skeletal muscle tissues exhibited the same trend, while those in ovary organs showed the opposite trend. These results suggested that the insulin signaling alters in the liver, skeletal muscle and ovary organs with the progress of IR.

KEYWORDS:

• insulin resistance
• liver
• ovary
• insulin signalling
• skeletal muscle

Disclosure statement

No potential conflict of interest was reported by the authors.

Authors’ contributions

Chen Lei and Jing Wang designed the study. Xin Li and Yuan-yuan Mao collected and analysed the data. Jian-qun Yan write the article. All authors have read and approved the submitted article.

Data availability statement

The data that support the findings of this study are openly available in ‘figshare’ at doi:10.6084/m9.figshare.22679746.

Additional information

Funding

This work was supported by Key Science and technology project in Ningxia (2020BFG02011); First-Class Discipline Construction Founded Project of NingXia Medical University and the School of Clinical Medicine(NXYLXK2017A05).