Evaluating the global impact of low physical activity on type 2 diabetes: Insights from the global burden of disease 2019 study.

AIM: We aimed to assess the global implications of low physical activity (LPA) on type 2 diabetes mellitus (T2DM) by utilizing data from the Global Burden of Disease (GBD) 2019. METHODS: The analysis was conducted by examining the age-standardized disability-adjusted life years (DALYs) rates over a 30-year period. To assess the trends, we utilized estimated annual percentage changes (EAPCs). RESULTS: The study revealed a notable increase in the burden of DALYs attributable to T2DM resulting from LPA, with an EAPC of 0.84 (95% confidence interval 0.78-0.89). Among the regions examined, Oceania showed the highest burden, whereas Eastern Europe exhibited the lowest burden. Specifically, within the Central Asia region, a considerable increase in T2DM-LPA DALYs was observed, with an EAPC of 3.18 (95% confidence interval 3.01-3.36). The burden associated with T2DM-LPA DALYs was found to be similar between genders and increased across all age groups, peaking in the 80-84 years. Furthermore, there was a clear association between the socio-demographic index (SDI) and the age-standardized DALYs rate. Regions categorized as low-middle and middle SDI experienced a substantial rise in burden. CONCLUSION: This study highlights a substantial increase in the T2DM-LPA DALYs in low-middle and middle SDI regions, as well as among individuals aged 80-84 years. These findings emphasize the importance of implementing comprehensive global health interventions that promote physical activity, particularly targeting high-risk populations and regions.

A Case Report of MODY3 Combined with Intestinal Neuroendocrine Tumor.

Maturity-onset diabetes of the young 3 (MODY3) is an autosomal dominant monogenic diabetes mellitus characterized by defective ß-cell function and non-insulin-dependent early-onset diabetes mellitus. The facts that patients with MODY3 are often misdiagnosed as type 1 and type 2 diabetes mellitus and genetic diagnosis is expensive, make its diagnosis very challenging. In this study, we reported a case of MODY3, which was verified to be caused by a mutation in hepatocyte nuclear factor 1α gene (c.598C>T, p.Arg200Trp). In addition, the patient had a neuroendocrine tumor simultaneously, and a KMT2D gene mutation (c.5587C>G, p.Pro1863Ala) might be associated with this leson.

Ginkgo biloba Extract 50 (GBE50) Ameliorates Insulin Resistance, Hepatic Steatosis and Liver Injury in High Fat Diet-Fed Mice.

BACKGROUND: Ginkgo biloba extract 50 (GBE50) has a variety of pharmacological functions such as anti-inflammatory, antioxidant and maintenance of glucose and lipid metabolism homeostasis. However, the therapeutic effects and mechanisms of GBE50 on non-alcoholic fatty liver disease (NAFLD) remain unknown. Therefore, in this study, we evaluated the therapeutic effects of GBE50 in NAFLD by using a high-fat diet (HFD) mice model. METHODS: C57BL/6J mice were fed a HFD diet for 15 weeks and were given respectively 25, 50, and 100 mg/kg GBE50 daily by gavage from 3 to 15 weeks. After the administration, blood samples and liver tissues were collected for biochemical detection, histological measurement, immunohistochemistry and Western blot, respectively. RESULTS: We found that GBE50 treatment could ameliorate insulin resistance (IR), glucose intolerance, lipid accumulation, hepatic steatosis and liver injury in HFD-fed mice. Further mechanism exploration discovered that the hepatoprotective effects of GBE50 on NAFLD may be related to the strengthening of IRS-1 signal activation and the weakening of NF-κB, Akt and endoplasmic reticulum stress signals activation. CONCLUSION: GBE50 is a potentially powerful therapeutic agent for the treatment of NAFLD.

miR-503/Apelin-12 mediates high glucose-induced microvascular endothelial cells injury via JNK and p38MAPK signaling pathway.

INTRODUCTION: Diabetic patients are often accompanied by complications of diabetic vascular disease, which could lead to heart failure or stroke. In this work, we explored the role of miR-503/Apelin-12 in diabetic angiopathy (DA) in vitro. METHODS: ELISA and qPCR were applied to assess the expression of miR-503 and Apelin-12 in high glucose (HG)-treated microvascular endothelial cells (HMEC-1). The effects of miR-503 on apoptosis, inflammation and oxidative stress were assessed by flow cytometry, western blotting, qPCR, and ELISA. The interaction between miR-503 and Apelin-12 was evaluated by dual-luciferase reporter assay, qPCR and ELISA, respectively. Western blotting was performed to examine the function of miR-503/Apelin-12 on JNK and p38MAPK activation. RESULTS: MiR-503 was markedly increased and Apelin-12 was decreased in HG-treated HMEC-1 cells. MiR-503 inhibitor significantly assuaged apoptosis, inflammation and oxidative stress in HMEC-1 cells. MiR-503 could specifically bind to the 3'UTR of Apelin and inversely downregulate Apelin-12 expression. Furthermore, Apelin-12 suppressed apoptosis, inflammation and oxidative stress. Inhibition of Apelin-12 could partially reverse the decrease of p-JNK and p-p38 expression levels induced by miR-503 suppression. CONCLUSION: In HG-induced microvascular cells injury, miR-503/Apelin-12 enhances inflammation and oxidative stress by regulating JNK and p38MAPK pathway, suggesting a potential therapeutic target for DA.

Relationships between serum Omentin-1 levels and bone mineral density in older men with osteoporosis.

OBJECTIVE: To investigate the correlation between serum Omentin-1 levels and the presence of osteoporosis in older men. METHODS: Serum Omentin-1, bone turnover biochemical markers, and bone mineral density (BMD) were determined in 45 older men with osteoporosis or 45 older men without osteoporosis (65-70 years old). RESULTS: Omentin-1 levels were increased in older men with osteoporosis, and the differences remained significant after controlling for fat mass. Omentin-1 was negatively correlated with BMD. In a multiple linear stepwise regression analysis, Omentin-1, lean mass, but not fat mass, were independent predictors of BMD for the combined group. Significant negative correlations between Omentin-1 and bone-specific alkaline phosphatase (BAP) and bone cross-linked N-telopeptides of type Ⅰ collagen (NTX) were found. Omentin-1 was also independently associated with BMD and bone turnover markers in older men with osteoporosis and control groups that were considered separately. CONCLUSIONS: Omentin-1 is an independent predictor of BMD in older men with osteoporosis, and it is negatively correlated with bone turnover biochemical markers. It is suggested that Omentin-1 may exert a negative effect on bone mass through the regulation of the osteoblast differentiation in the older men with osteoporosis.