Subjects with IGT and NDD, but not isolated IFG, exhibit a greater arterial stiffness.

The liver plays a vital role in metabolism, detoxification, digestion, and the maintenance of homeostasis. During development, the vertebrate embryonic liver undergoes a series of morphogenic processes known as hepatogenesis. Hepatogenesis can be separated into three interrelated processes: endoderm specification, hepatoblast differentiation, and hepatic outgrowth. Throughout this process, signaling molecules and transcription factors initiate and regulate the coordination of cell proliferation, apoptosis, differentiation, intercellular adhesion, and cell migration. Hifs are already recognized to be essential in embryonic development, but their role in hepatogenesis remains unknown. Using the zebrafish embryo as a model organism, we report that the lack of Hif2-alpha but not Hif1-alpha blocks hepatic outgrowth. While Hif2-alpha is not involved in hepatoblast specification, this transcription factor regulates hepatocyte cell proliferation during hepatic outgrowth. Furthermore, we demonstrated that the lack of Hif2-alpha can reduce the expression of liver-enriched gene 1 (leg1), which encodes a secretory protein essential for hepatic outgrowth. Additionally, exogenous mRNA expression of leg1 can rescue the small liver phenotype of hif2-alpha morphants. We also showed that Hif2-alpha directly binds to the promoter region of leg1 to control leg1 expression. Interestingly, we discovered overrepresented, high-density Hif-binding sites in the potential upstream regulatory sequences of leg1 in teleosts but not in terrestrial mammals. We concluded that hif2-alpha is a key factor required for hepatic outgrowth and regulates leg1 expression in zebrafish embryos. We also proposed that the hif2-alpha-leg1 axis in liver development may have resulted from the adaptation of teleosts to their environment.

Objective 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. Methods A total of 4,555 patients aged ≥18 years were enrolled in this study. The sleep duration was classified into three groups: short (<7 h), normal (7–9 h), and long (≥9 h). The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate sleep quality, and poor sleep quality was defined as a global PSQI score of >5. Results 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. Conclusions Poor sleep quality was related to lower uric acid levels, whereas short sleep duration was associated with higher uric acid levels.

Hepassocin (HPS) is a hepatokine that regulates hepatocyte proliferation. It is known that HPS plays an important role in the development of nonalcoholic fatty liver diseases (NAFLD). Fatty acids, such as oleic acid (OLA), exhibit the ability to activate the signal transducer and activator of transcription‐3 (STAT3), and the binding site of STAT3 is found in the promoter region of HPS. However, the regulation of HPS by fatty acids is still obscure. To clarify the regulation of HPS, we detected the expression of HPS by western blots. In addition, a hepatic steatosis cell culture model was established by treatment of different fatty acids, including linoleic acid (LNA), oleic acid, palmitic acid, and stearic acid. The intracellular lipid accumulation was confirmed by oil red O staining. Blocking of STAT3 activity was achieved by the pretreatment of the STAT3 inhibitor, stattic. We found that activation of STAT3 by interleukin‐6 (IL‐6) was mediated in the regulation of HPS expression. Treatment of unsaturated fatty acids significantly induced intracellular lipid accumulation in HepG2 cells. Moreover, the expressions of HPS were increased in unsaturated fatty acid‐treated HepG2 cells, as compared with saturated fatty acid‐treated groups. Also, the expression of HPS induced by OLA was blocked by the inhibition of STAT3 activity. Furthermore, we found that deletion of HPS by small interfering ribonucleic acid transfection decreased the protective effect of OLA on cell viability. Taken together, we provided evidence that STAT3 plays an important role in the regulation of OLA‐induced HPS expression and the increased HPS may further participate in the development of NAFLD. In addition, the increase of HPS might be involved in the protective effect of OLA on cell viability.

Background: To assess the prevalence of urban-rural disparity in lower extremities amputation (LEA) among patients with diabetes and to explore whether patient-related or physician-related factors might have contributed to such disparity.Methods: This was a population-based study including patients with diabetes aged ≥55 years from 2009 to 2013. Among them, 9236 received LEA. Data were retrieved from Taiwan's National Health Insurance (NHI) claims. A multiple Poisson regression model was also employed to assess the urban-rural difference in LEA prevalence by simultaneously taking into account socio-demographic variables and density of practicing physicians. Results: Between 2009 and 2013, the annual prevalence of LEA declined from 30.4 to 20.5 per 10,000 patients. Compared to patients from urban areas, those who lived in sub-urban and rural areas suffered from a significantly elevated prevalence of LEA, with a prevalence rate ratio (PRR) of 1.47 (95% CI, 1.39-1.55) and 1.68 (95% CI, 1.56-1.82), respectively. The density of physicians who presumably provided diabetes care can barely explain the urbanrural disparity in LEA prevalence. Conclusions:Although the universal health insurance has largely removed financial barriers to health care, the urban-rural disparity in LEA prevalence still exists in Taiwan after nearly two decades of the NHI program.