Pancreatic autophagy and protein expression of insulin-related genes in type 2 diabetic rats with periodontitis

doi:10.12307/2022.926

Abstract

Abstract: BACKGROUND: Diabetes is prone to cause multiple organ diseases in the body. Periodontitis is one of the complications. The more severe the inflammation of periodontitis is, the less favorable it is for glycemic control.
OBJECTIVE: To investigate the effect of periodontitis on autophagy of pancreatic tissue in a rat model of type 2 diabetes mellitus.
METHODS: Forty 6-week-old male Sprague-Dawley rats were randomly divided into a control group and an experimental group, and rats in the experimental group were subdivided into three groups (n=10 per group): a diabetes group, a periodontitis group, and a diabetes+periodontitis group. High fat and high sugar feeding+intraperitoneal injection of streptozotocin was used to establish a diabetic model, and silk thread ligation was used to establish a periodontitis model. Enzyme-linked immune sorbent assay was used to detect the expression of inflammatory factors in rat serum. Real-time fluorescent quantitative PCR was used to detect the expression of autophagy and insulin secretion-related genes in rat pancreatic tissue. Western blot was used to detect the protein expression of autophagy-related in rat pancreatic tissue.
RESULTS AND CONCLUSION: The results of enzyme-linked immunosorbent assay showed that the expression of tumor necrosis factor α, interleukin 1β, and interleukin 6 was increased sequentially in the diabetes group, the periodontitis group, and the diabetes+periodontitis group compared with that in the control group (P < 0.05). The results of real-time fluorescent quantitative PCR showed that, compared with the control group, the mRNA expression of glucokinase and recombinant glucose transporter 2 was decreased in the diabetes group and the diabetes+periodontitis group, especially in the diabetes+periodontitis group (P < 0.05). At the same time, the mRNA expression of uncoupling protein 2, Beclin1, and LC3II was increased in the diabetes group and the diabetes+periodontitis group, and increased most in the diabetes+periodontitis group (P < 0.05). However, there was no significant difference between the periodontitis group and the control group (P > 0.05). The results of western blot showed that, compared with the control group, the expression of Beclin1, LC3II/LC3I was increased in the diabetes group and the diabetes+periodontitis group, and increased most in the diabetes+periodontitis group (P < 0.05). And there was no significant difference between the periodontitis group and the control group (P > 0.05). Therefore, it is speculated that type 2 diabetes mellitus with periodontitis may induce excessive autophagy of pancreatic islet cells, then impact the secretion function of insulin in islet cells, and finally aggravate the development of diabetes mellitus in the rat models.

Key words: diabetes, periodontitis, autophagy, insulin secretion, inflammatory factor

CLC Number:

Du Shasha, Cai Zhiguo, Yang Kun, Liu Qi. Pancreatic autophagy and protein expression of insulin-related genes in type 2 diabetic rats with periodontitis[J]. Chinese Journal of Tissue Engineering Research, 2022, 26(29): 4605-4610.

Figures/Tables 9

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