Eucommia ulmoides Oliv. (EU), also known as Du-Zhong, is a medicinal herb commonly used in Asia to treat hypertension and diabetes. Despite evidence of the protective effects of EU against diabetes, its precise effects and mechanisms of action against advanced glycation end-products (AGEs) are unclear. In this study, we evaluated the effects of EU on AGEs-induced renal disease and explored the possible underlying mechanisms using streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice received EU extract (200 mg/kg) orally for 6 weeks. EU treatment did not change blood glucose and glycated hemoglobin (HbA1c) levels in diabetic mice. However, the EU-treated group showed a significant increase in the protein expression and activity of glyoxalase 1 (Glo1), which detoxifies the AGE precursor, methylglyoxal (MGO). EU significantly upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression but downregulated that of receptor for AGE (RAGE). Furthermore, histological and immunohistochemical analyses of kidney tissue showed that EU reduced periodic acid–Schiff (PAS)-positive staining, AGEs, and MGO accumulation in diabetic mice. Based on these findings, we concluded that EU ameliorated the renal damage in diabetic mice by inhibiting AGEs formation and RAGE expression and reducing oxidative stress, through the Glo1 and Nrf2 pathways.

Chronic low-grade inflammation may increase the risk of chronic disease, while diets rich in anti-inflammatory components may reduce it. To determine the anti-inflammatory properties of the traditional Korean diet (K-diet) that comprises high amounts of vegetables, fiber and phytochemicals, moderate amounts of legumes, and low amounts of animal fat, ten obese women aged 50–60 years were randomly assigned to the K-diet or control diet group. The control diet was a Westernized Korean diet commonly consumed in Korea, which is high in animal fat and protein. Subjects were housed in metabolic unit-like conditions during the 2-week intervention. Plasma was collected before and after the intervention to measure inflammatory cytokines using ELISA. The dietary inflammatory index (DII) was calculated based on nutrients and food intake. The DII score for the K-diet was lower than that of the control diet (−0.94 ± 1.39 vs. 1.04 ± 1.61, p < 0.001). In the K-diet group, anti-inflammatory interleukin (IL)-10 levels increased (4.45 ± 0.34 pg/mL vs. 5.94 ± 0.33 pg/mL, p = 0.0102), whereas pro-inflammatory nuclear factor kappa B (NF-κB) levels decreased (7.70 ± 0.62 pg/mL vs. 2.71 ± 0.49 pg/mL, p = 0.0015), but not in the control group. In the K-diet group, NF-κB levels negatively correlated with IL-10 levels (r = −0.794, p = 0.006). The K-diet has anti-inflammatory properties, and IL-10 and NF-κB are putative inflammatory markers for K-diet studies.

Over the last several decades, there has been a considerable growth in type 2 diabetes (T2DM) in Asians. A pathophysiological mechanism in Asian T2DM is closely linked to low insulin secretion, β-cell mass, and inability to compensate for insulin resistance. We hypothesized that genetic variants associated with lower β-cell mass and function and their combination with unhealthy lifestyle factors significantly raise T2DM risk among Asians. This hypothesis was explored with participants aged over 40. Participants were categorized into T2DM (case; n = 5383) and control (n = 53,318) groups. The genetic variants associated with a higher risk of T2DM were selected from a genome-wide association study in a city hospital-based cohort, and they were confirmed with a replicate study in Ansan/Ansung plus rural cohorts. The interacted genetic variants were identified with generalized multifactor dimensionality reduction analysis, and the polygenic risk score (PRS)-nutrient interactions were examined. The 8-SNP model was positively associated with T2DM risk by about 10 times, exhibiting a higher association than the 20-SNP model, including all T2DM-linked SNPs with p < 5 × 10⁻⁶. The SNPs in the models were primarily involved in pancreatic β-cell growth and survival. The PRS of the 8-SNP model interacted with three lifestyle factors: energy intake based on the estimated energy requirement (EER), Western-style diet (WSD), and smoking status. Fasting serum glucose concentrations were much higher in the participants with High-PRS in rather low EER intake and high-WSD compared to the High-EER and Low-WSD, respectively. They were shown to be higher in the participants with High-PRS in smokers than in non-smokers. In conclusion, the genetic impact of T2DM risk was mainly involved with regulating pancreatic β-cell mass and function, and the PRS interacted with lifestyles. These results highlight the interaction between genetic impacts and lifestyles in precision nutrition.