Studies have shown that diabetes mellitus increased brachial-ankle pulse-wave velocity (baPWV), but the impact of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) remains controversial. Our objective was to investigate the impact of the different glycemic states on baPWV in a relatively healthy Chinese population. We enrolled 4938 subjects in the health examination center of the National Cheng Kung University Hospital from October 2006 to August 2009 after excluding those who were under medications for diabetes, hypertension, or hyperlipidemia or had a history of cardiovascular disease. The baPWV values to assess arterial stiffness were calculated as the distance traveled by the pulse wave divided by the time taken to travel the distance. The participants were classified into normal glucose tolerance (NGT; n = 3777), isolated IFG (n = 221), IGT (n = 726), and newly diagnosed diabetes (NDD; n = 214) groups. The mean values of baPWV were 1284.9 ± 205.2, 1379.6 ± 226.8, 1408.1 ± 251.7, and 1500.8 ± 282.5 cm/sec in NGT, isolated IFG, IGT, and NDD groups, respectively. The isolated IFG, IGT, and NDD groups had a higher baPWV value as compared with the NGT group. In a multiple linear regression test, both IGT and NDD groups, but not the isolated IFG group, had significantly higher baPWV values after adjustment for age, sex, body mass index, waist to hip ratio, smoking, alcohol consumption, habitual exercise, systolic blood pressure, and lipid profiles. Subjects with IGT and NDD, but not isolated IFG, exhibit a greater arterial stiffness.

To date, the association between sleep duration or sleep quality and hyperuricemia has remained unclear. In addition, sleep duration and quality were not considered concomitantly in previous studies. Thus, this study was aimed toward an examination of the association of sleep duration and quality with uric acid level in a Taiwanese population. A total of 4,555 patients aged ≥18 years were enrolled in this study. The sleep duration was classified into three groups: short (5. Poor sleepers were younger and had lower body mass index, blood pressure, uric acid, blood sugar, cholesterol, creatinine level, shorter sleep duration, and engaged in less exercise but had a higher white blood cell count and prevalence of smoking as compared to good sleepers. There were also differences in body mass index, blood pressure, uric acid, blood sugar, lipid profiles, and sleep quality among subjects with different sleep durations. After adjusting for other variables, poor sleep quality was associated with lower uric acid levels. In addition, short sleep duration was positively associated with higher uric acid levels. Poor sleep quality was related to lower uric acid levels, whereas short sleep duration was associated with higher uric acid levels.

Liver fibrosis is associated with liver-related outcomes, yet often remains underdiagnosed in primary care settings. Hyperuricemia is associated with non-alcoholic fatty liver disease (NAFLD), but the relationship between hyperuricemia and liver fibrosis remains unclear. Data on individuals without NAFLD is also limited. We investigated the association between hyperuricemia and liver fibrosis in subjects with and without NAFLD. This study recruited 11,690 relevant participants from a health-checkup center. NAFLD was based on ultrasonography. Hyperuricemia was defined as serum uric acid > 6.0 mg/dL in women and >7.0 mg/dL in men. Significant liver fibrosis was diagnosed with the aspartate aminotransferase to platelet ratio index ≥0.5. The following were positively associated with significant liver fibrosis: hyperuricemia (p = 0.001), age ≥ 65 years (p < 0.001), male gender (p < 0.001), obesity (p = 0.009), hypertension (p = 0.002), diabetes (p < 0.001), and NAFLD (p < 0.001) in the logistic regression. The positive association of hyperuricemia with significant liver fibrosis remained in subjects with NAFLD (p = 0.001), but not in subjects without NAFLD. In conclusion, hyperuricemia increased the associated risk of significant liver fibrosis. The positively associated risk existed in subjects with NAFLD, but not in those without it.

Sugar substitutes have been recommended to be used for weight and glycemic control. However, numerous studies indicate that consumption of artificial sweeteners exerts adverse effects on glycemic homeostasis. Although sucralose is among the most extensively utilized sweeteners in food products, the effects and detailed mechanisms of sucralose on insulin sensitivity remain ambiguous. In this study, we found that bolus administration of sucralose by oral gavage enhanced insulin secretion to decrease plasma glucose levels in mice. In addition, mice were randomly allocated into three groups, chow diet, high-fat diet (HFD), and HFD supplemented with sucralose (HFSUC), to investigate the effects of long-term consumption of sucralose on glucose homeostasis. In contrast to the effects of sucralose with bolus administration, the supplement of sucralose augmented HFD-induced insulin resistance and glucose intolerance, determined by glucose and insulin tolerance tests. In addition, we found that administration of extracellular signal-regulated kinase (ERK)-1/2 inhibitor reversed the effects of sucralose on glucose intolerance and insulin resistance in mice. Moreover, blockade of taste receptor type 1 member 3 (T1R3) by lactisole or pretreatment of endoplasmic reticulum stress inhibitors diminished sucralose-induced insulin resistance in HepG2 cells. Taken together, sucralose augmented HFD-induced insulin resistance in mice, and interrupted insulin signals through a T1R3-ERK1/2-dependent pathway in the liver.