Diabetes mellitus (DM) and DM-related complications place a high socioeconomic burden on individuals and society. Updating nationwide information periodically is thus pivotal to preventing DM and improving its management in Taiwan. We used the National Health Insurance Research Database; disease diagnosis codes were assigned according to the International Classification of Diseases, 9th Revision, Clinical Modification. DM was defined as ≥3 outpatient visits or 1 hospitalization within a year. We excluded individuals with gestational DM, those with missing data, and those aged >100 years. Type 1 DM (T1DM) was defined based on information from the catastrophic illness registry. From 2005 to 2014, total population with DM increased by 66% and age-standardized prevalence in patients aged 20-79 years increased by 41%. The DM prevalence was generally higher in men; however, the prevalence was higher in women aged ≥65 years. The prevalence of DM was approximately 50% in those aged >80 years. DM incidence increased by 19%; the increase was most obvious in patients aged 20-39 years (p < 0.001). The standardized incidence of T1DM slightly decreased by 11% (p = 0.118) and standardized prevalence of T1DM increased from 0.04% to 0.05%. Number of T1DM accounted for 0.51-0.59% of the entire diabetic population during the observation period. DM prevalence is continually increasing, but the incidence only marginally increased from 2005 to 2014. Moreover, DM is a major problem in elderly people. The higher incidence of DM in men is consistent with the pandemic of overweight and obesity in men in Taiwan.

The intrinsic risk factors of rotator cuff disease (RCD) include degeneration, inflammation, oxidative stress, and circulation impairment. Both diabetes and hyperlipidemia are thought to increase these risk factors and therefore potentially enhance RCD development. However, few studies, and few longitudinal follow-up studies in particular, exist to prove this. Both diabetes and hyperlipidemia can increase a patient’s risk of developing RCD. Cohort study; Level of evidence, 3. A total of 498,678 participants, including 28,391 diagnosed with diabetes and 25,621 with hyperlipidemia in the year 2000, were followed for an 11-year period. Multivariate Cox proportional hazards models were used to explore the effect of (1) diabetes, (2) hyperlipidemia, (3) diabetes with/without insulin use, and (4) hyperlipidemia with/without statin use on the development of RCD. In the subgroup of patients with hyperlipidemia, multivariate Cox proportional hazards models were also performed to explore the relationship between statin use and RCD development. During an 11-year follow-up period, 26,664 patients developed RCD. The crude hazard ratio (HR) for RCD in patients with diabetes as compared with those without diabetes was 2.11 (95% CI, 2.02-2.20; P < .0001). The crude HR for RCD in patients with hyperlipidemia as compared with those without hyperlipidemia was 2.00 (95% CI, 1.92-2.08; P < .0001). Multivariate Cox proportional hazards analysis revealed that, in addition to older age and female sex, both diabetes and hyperlipidemia increased the risk of RCD (diabetes: HR, 1.47 [95% CI, 1.41-1.54]; P < .0001) (hyperlipidemia: HR, 1.48 [95% CI, 1.42-1.55]; P < .0001). An elevated risk still existed in patients with diabetes with/without insulin use (diabetes with insulin use: HR, 1.43 [95% CI, 1.35-1.51]; P < .0001) (diabetes without insulin use: HR, 1.64 [95% CI, 1.53-1.75]; P < .0001). An increased risk also existed in patients with hyperlipidemia with/without statin use (hyperlipidemia with statin use: HR, 1.16 [95% CI, 1.10-1.23]; P < .0001) (hyperlipidemia without statin use: HR, 2.01 [95% CI, 1.89-2.13]; P < .0001). In the subgroup of patients with hyperlipidemia, statin use was associated with a lower risk of developing RCD when compared with no statin use (rosuvastatin: HR, 0.41 [95% CI, 0.35-0.49]; P < .0001) (simvastatin: HR, 0.62 [95% CI, 0.54-0.71]; P < .0001) (other statins: HR, 0.66 [95% CI, 0.60-0.72]; P < .0001). The present longitudinal, population-based follow-up study showed that either diabetes or hyperlipidemia alone was an independent risk factor for RCD development. Statin use might provide protection against RCD in patients with hyperlipidemia.

Visfatin is an adipokine that is highly expressed in visceral fat. Plasma levels of visfatin have been reported to be higher in subjects with obesity and/or type 2 diabetes mellitus. However, the role of visfatin in endothelial dysfunction has been largely unexplored. We investigated the possible pathogenic role of visfatin in endothelial dysfunction, particularly focusing on its effect on inflammatory mediators. Primary human umbilical vein endothelial cells (HUVECs) pretreated with visfatin (1, 10 and 50 ng ml⁻¹) were used to study the relationship between visfatin and endothelium dysfunction. Expressions of adhesion molecules (ICAM-1, VCAM-1 and E-selectin) and cytokines (interleukin (IL)-6 and IL-8) affected by visfatin were investigated by enzyme-linked immunosorbent assay, flow cytometry and real-time PCR. Activity of nuclear factor (NF)-κB was examined by electrophoretic mobility shift assay. At a visfatin concentration of 50 ng ml⁻¹, significant increases in IL-6, IL-8, ICAM-1, VCAM-1 and E-selectin gene expression along with increased IL-6, IL-8 and sE-selectin protein levels in the conditioned medium were detected. Flow cytometry showed that the addition of visfatin significantly increased ICAM-1 expression and VCAM-1 expression (10 and 50 ng ml⁻¹, respectively). Electrophoretic mobility shift assay confirmed that visfatin increased the DNA-binding activity of NF-κB. In addition, pretreatment with visfatin (10 and 50 ng ml⁻¹) increased human monocyte cell line THP-1 adhesion to HUVECs. Our findings suggest that visfatin causes endothelial dysfunction by increasing inflammatory and adhesion molecule expression at least partly through the upregulation of NF-κB activity.