Objective: Abdominal adipose is closely related to many endocrine and metabolic diseases. The aim of this study was to analyze the distribution of abdominal adipose tissue in a healthy population in northern China determined by abdominal computed tomography (CT).Methods: Data for this study were obtained from a multicenter, retrospective, cross-sectional study that collected abdominal CT scans of 1787 healthy individuals from 4 representative cities in northern China. Areas of visceral adipose tissue (VATA) and subcutaneous adipose tissue (SATA) were obtained by measuring CT images at the level of the 3rd lumbar vertebra. Visceral adipose tissue index (VATI) and subcutaneous adipose index (SATI) were obtained by normalizing the square of height to analyze the distribution of the above indexes and visceral obesity among different body mass index (BMI), gender and age.Results: The mean age of this healthy population was 45.3 ± 15.2 years and the mean BMI was 23.5 ± 3.2 kg/m², with 902 men and 885 women. Compared with women, men had a significantly higher median VATA (120.9 vs. 67.2 cm²), VATI (39.1 vs. 25.6 cm²/m²) and a significantly higher percentage of visceral adiposity (VATA ≥ 100 cm²) (60.8 vs. 30.4%), while women had significantly higher SATA (116.9 vs. 146.7 cm²) and SATI (38.8 vs. 55.8 cm²/m²) than men. Whether men or women, VATI was positively correlated with age. Interestingly, SATI was weakly positively correlated with age in women, while SATI was weakly negatively correlated with age in men. In persons with a normal BMI, the proportion of visceral adiposity increases with age, whereas in men with a normal BMI, the proportion of visceral adiposity decreases after the age of 60 years but remains >50%.Conclusions: The distribution of abdominal visceral and subcutaneous adipose tissue parameters measured by CT differed among gender, age, and BMI. Even men and women with normal BMI have a high proportion of visceral obesity.

Oxidative stress plays an important role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Baicalin has been shown to exert protective effects in various liver diseases. The mechanism of baicalin’s antioxidative effect in NAFLD is currently unclear. The aim of this study was to investigate the effects and mechanisms of baicalin on oxidative stress in a new tissue-engineered liver model of NAFLD. The 3D model of NAFLD was induced by a fat-supplemented medium (fatty acids, FFA group) for 8 days and baicalin was administered on the 5th day. CCK-8 assay showed that baicalin at concentrations below 100 μM had no obvious cytotoxicity. Baicalin inhibited apoptosis and lactate dehydrogenase release in the FFA group. Baicalin reduced the levels of reactive oxygen species and malondialdehyde induced by FFA, and increased superoxide dismutase and glutathione amounts. However, it did not upregulate nuclear erythroid 2-related factor 2 compared with the FFA group. Mitochondrial morphology was partially restored after baicalin treatment, and ATP5A expression and mitochondrial membrane potential were increased. The superoxide anion scavenging ability of baicalin was enhanced in a dose-dependent manner. In summary, baicalin reduces oxidative stress and protects the mitochondria to inhibit apoptosis in the 3D NAFLD model via its own antioxidant activity.

The kidneys are often involved in adverse effects and toxicity caused by exposure to foreign compounds, chemicals, and drugs. Early predictions of these influences are essential to facilitate new, safe drugs to enter the market. However, in current drug treatments, drug-induced nephrotoxicity accounts for 1/4 of reported serious adverse reactions, and 1/3 of them are attributable to antibiotics. Drug-induced nephrotoxicity is driven by multiple mechanisms, including altered glomerular hemodynamics, renal tubular cytotoxicity, inflammation, crystal nephropathy, and thrombotic microangiopathy. Although the functional proteins expressed by renal tubules that mediate drug sensitivity are well known, current in vitro 2D cell models do not faithfully replicate the morphology and intact renal tubule function, and therefore, they do not replicate in vivo nephrotoxicity. The kidney is delicate and complex, consisting of a filter unit and a tubular part, which together contain more than 20 different cell types. The tubular epithelium is highly polarized, and maintaining cellular polarity is essential for the optimal function and response to environmental signals. Cell polarity depends on the communication between cells, including paracrine and autocrine signals, as well as biomechanical and chemotaxis processes. These processes affect kidney cell proliferation, migration, and differentiation. For drug disposal research, the microenvironment is essential for predicting toxic reactions. This article reviews the mechanism of drug-induced kidney injury, the types of nephrotoxicity models (in vivo and in vitro models), and the research progress related to drug-induced nephrotoxicity in three-dimensional (3D) cellular culture models.