Hyperglycemia is the most important factor leading to the complications of type 2 diabetes mellitus (T2DM). The primary condition for the treatment of T2DM is to change the glucose and lipid metabolism disorders in the liver and other insulin-sensitive tissues. The current study aims to unearth the potential molecular mechanism of inhibiting liver gluconeogenesis to provide a new theoretical basis for the treatment of T2DM. High glucose (HG) induction of HepG2 cells followed by treatment with sequence-similar family 3 member D (FAM3D). Dual specificity phosphatases 1 (DUSP1), zinc finger protein 36 (ZFP36), salt-induced kinase 1 (SIK1), p-SIK1, posphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) gene and protein expression level were detected by quantitative real-time polymerase chain reaction and western blot. The PEPCK and G6Pase activities were detected by enzyme linked immunosorbent assay.Glucose production assay to determine glucose content. The RNA binding protein immunoprecipitation assay was used to detect the binding of ZFP36 to SIK1. FAM3D facilitated the expression of DUSP1 but suppressed the expression of gluconeogenesis-related factors in an HG environment. The expression of ZFP36 was up-regulated in an HG environment. ZFP36 could reverse the inhibition of gluconeogenesis caused by FAM3D. HG-induced upregulation of ZFP36 was downregulated by overexpression of DUSP1. ZFP36 bound to SIK1, and downregulation of ZFP36 promoted SIK1 expression and inhibits gluconeogenesis. Our study demonstrated FAM3D inhibited gluconeogenesis through the DUSP1/ ZFP36/SIK1 axis in an HG environment, which provided a new theoretical basis for exploring the pathogenesis and treatment strategy of T2DM.

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The disability resource centers (DRCs) of world-class universities play a central role in achieving the goal of promoting inclusion and equity in higher education. To provide a reference for the development of inclusive education in China’s double first-class universities, the DRCs of the top 10 universities were selected as typical cases to analyze their experiences and dilemmas. Regarding service mechanisms, DRCs aimed to ensure equitable access so that students with disabilities (SWD) could fully and holistically participate in universities, thereby improving inclusion on campus. In addition, DRCs established official websites as a service platform and developed clear service procedures and grievances to ensure the quality of service. Regarding service content, DRCs emphasized enhancing the disability awareness of campus members and provided support and services for SWD in their study, life, and employment to ensure that SWD could receive high-quality higher education. However, DRCs also suffered from dilemmas of low service application rates, flawed service mechanisms, and controversial service quality. Accordingly, suggestions and implications are proposed to improve inclusion and equity in China’s double first-class universities, including establishing a collaborative disability service system with DRCs as the core, optimizing the service mechanism, and providing personalized and diversified support service content.

Aluminum exposure can lead to different degrees of damage to various organ systems of the body. It has been previously revealed that that aluminum exposure can damage the liver, causing liver dysfunction. However, the speci c mechanism remains unclear. This research aims to uncover the damaging effect of aluminum exposure on rat liver and to demonstrate the role of autophagy and apoptosis in this effect.Thirty-two Wistar rats were randomly divided into the control group (C group), low-dose aluminum exposure group (L group), middle-dose aluminum exposure group (M group), and high-dose aluminum exposure group (H group) (n = 8). The rats respectively received intraperitoneal injection of 0, 5, 10 and 20 mg/(kg•d) AlCl 3 solution for 4 w (5 times/w). After the experiment, changes in the ultrastructure and autolysosome in rat liver were observed; the liver function, apoptosis rate, as well as levels of apoptosisassociated proteins and autophagy-associated proteins were detected. The results indicated that aluminum exposure damaged rat liver function and structure and resulted in an increase of autolysosomes. TUNEL staining revealed an elevated number of apoptotic hepatocytes after aluminum exposure. Moreover, we found from Western blotting that the levels of autophagy-associated proteins Beclin1 and LC3-II increased; apoptotic protein Caspase-3 level elevated and Bcl-2/Bax ratio reduced. Our research suggested that aluminum exposure can lead to high autophagy and apoptosis levels of rat hepatocytes, accompanied by hepatocyte injury and impaired liver function. This study shows that autophagy and apoptosis pathways participate in aluminum toxication-induced hepatocyte injury.

Aluminum exposure can lead to different degrees of damage to various organ systems of the body. It has been previously revealed that that aluminum exposure can damage the liver, causing liver dysfunction. However, the specific mechanism remains unclear. This research aims to uncover the damaging effect of aluminum exposure on rat liver and to demonstrate the role of autophagy and apoptosis in this effect. Thirty-two Wistar rats were randomly divided into the control group (C group), low-dose aluminum exposure group (L group), middle-dose aluminum exposure group (M group), and high-dose aluminum exposure group (H group) (n = 8). The rats respectively received intraperitoneal injection of 0, 5, 10 and 20 mg/(kg·d) AlCl3 solution for 4 w (5 times/w). After the experiment, changes in the ultrastructure and autolysosome in rat liver were observed; the liver function, apoptosis rate, as well as levels of apoptosis-associated proteins and autophagy-associated proteins were detected. The results indicated that aluminum exposure damaged rat liver function and structure and resulted in an increase of autolysosomes. TUNEL staining revealed an elevated number of apoptotic hepatocytes after aluminum exposure. Moreover, we found from Western blotting that the levels of autophagy-associated proteins Beclin1 and LC3-II increased; apoptotic protein Caspase-3 level elevated and Bcl-2/Bax ratio reduced. Our research suggested that aluminum exposure can lead to high autophagy and apoptosis levels of rat hepatocytes, accompanied by hepatocyte injury and impaired liver function. This study shows that autophagy and apoptosis pathways participate in aluminum toxication-induced hepatocyte injury.