Backgroud Diabetes mellitus is a common chronic disease and a severe public health issue. The incidence trends for type 1 diabetes (TIDM) and type 2 diabetes (T2DM) have rarely been studied on a global scale. We aimed to determine the temporal and geographical trends of diabetes globally. Methods Data on diabetes mellitus, including incidence, prevalence from 1990 to 2017 were obtained from the 2017 Global Burden of Disease study. We calculated the estimated annual percentage changes (EAPCs) in age-standardized incidence rate (ASIR) of diabetes mellitus according to sex, region, and disease type. Results The worldwide incident cases of diabetes mellitus has increased by 102.9% from 11,303,084 cases in 1990 to 22,935,630 cases in 2017 worldwide, while the ASIR increased from 234 /100,000 persons (95% UI, 219–249) to 285/100,000 persons (95% UI, 262–310) in this period [EAPC = 0.87, 95% confidence interval (CI):0.79–0.96]. The global ASIRs of T1DM and T2DM both demonstrated significant increase during 1990–2017, with EAPCs of 0.34 (95% CI,0.30–0.39) and 0.89 (95% CI,0.80–0.97), respectively. The ASIR trends also varied considerably by regions and countries. The increase in ASIR was greatest in high sociodemographic index regions (EAPC = 1.05, 95% CI:0.92–1.17) and lowest in low-SDI regions (EAPC = 0.79, 95% CI:0.71–0.88). Conclusions Both the number of incident cases and ASIR of diabetes mellitus increased significantly during 1990–2017 worldwide, but the temporal trends varied markedly across regions and countries.
Obesity has been demonstrated to be linked to atrial fibrillation (AF) with atrial enlargement and tissue fibrosis. Long-term high calorie intake is the main reason for the prevalence of obesity. To investigate the possible causes of AF, such as chronic high-fat diet (HFD), and to identify the underlying mechanisms, the present study analyzed a variety of structural and gap junctional electrophysiological alterations in the atria of female rats fed an HFD. After consistent HFD feeding of female rats for 12 weeks, hematoxylin and eosin (H&E) and Masson's staining, RT-qPCR, western blotting, immunofluorescence and TUNEL staining were performed. In our study, approximately 3/5 of the HFD-fed rats (HFD-OB, n=13) displayed a significant increase in body weight, while the other 2/5 did not (HFD-NOB, n=8). In addition, the atrial weight of the HFD-OB and HFD-NOB rats was markedly heavier, as compared to the rats fed a normal diet (CT, n=20). According to the plasma lipid levels, both HFD-OB and HFD-NOB rats exhibited dyslipidemia. Furthermore, H&E staining revealed broadened interstitial space and myocyte disarray in atria of the HFD-fed rats (i.e., HFD-OB and HFD-NOB rats). Expression levels of atrial fibrosis relevant factors, transforming growth factor-β1 and matrix metalloproteinase-2, were significantly upregulated in the HFD-fed rat atria. In addition, we found a gap junction remodeling with distinct alterations in expression and distribution of connexin 40 (Cx40) and Cx43 in the HFD-fed rat atria. Moreover, a modest increase in apoptotic cell death in both the HFD-OB and HFD-NOB rat atria was detected. Taken together, our findings demonstrated that the impact of chronic HFD on atria displayed in the diet-induced obese rats was observed in HFD-fed rats in the absence of obesity as well.
Congenital long QT syndromes (LQTS) are inherited heart diseases that can present as palpitations, syncope (fainting), seizures, cardiac arrest, and sudden death. Acquired LQTS mostly occurs as a result of exposure to an environmental stressor that is responsible for the excessive prolongation of the QT interval. The most common environmental stressor is adverse drug reactions, which can lead to drug-induced LQTS (di-LQTS). Female gender has been increasingly recognized as an independent risk factor for di-LQTS, which in females is influenced by other factors, including age, menstrual cycle, and hormone replacement therapy. The estrogen-mediated reduced repolarization reserve in women is believed to be responsible for their higher susceptibility to di-LQTS. More studies, especially randomized trials, should be carried out to confirm these findings, and elucidate the clinical impact of gender disparity in modifying the risk of di-LQTS in women, with the ultimate goal of promoting the clinical safety of medication. In this article, we review current knowledge about di-LQTS, specifically in women, and discuss methods for the prevention of di-LQTS in females.
Mutations in the human ether-à-go-go-related gene (hERG) are responsible for long-QT syndrome (LQTS) type 2 (LQT2). In the present study, a heterozygous missense mutation (A561V) linked to LQT2, syncope and epilepsy was identified in the S5/pore region of the hERG protein. The mutation, A561V, was prepared and subcloned into hERG-pcDNA3.0. Mutant plasmids were co-transfected into HEK-293 cells, which stably express wild-type (WT) hERG, in order to mimic a heterozygous genotype, and the whole-cell current was recorded using a patch-clamp technique. Confocal microscopy was performed to evaluate the membrane distribution of the hERG channel protein using a green fluorescent protein tagged to the N-terminus of hERG. A561V-hERG decreased the amplitude of the WT-hERG currents in a concentration-dependent manner. In addition, A561V-hERG resulted in alterations to activation, inactivation and recovery from inactivation in the hERG protein channels. Further evaluation of hERG membrane localization indicated that the A561V-hERG mutant protein was unable to travel to the plasma membrane, which resulted in a trafficking-deficient WT-hERG protein. In conclusion, A561V-hERG exerts a potent dominant-negative effect on WT-hERG channels, resulting in decreased hERG currents and impairment of hERG membrane localization. This may partially elucidate the clinical manifestations of LQTS patients who carry the A561V mutation.
Vaspin, a novel adipocyte factor secreted from visceral adipose tissues, is associated with obesity and insulin resistance and can regulate glucose and lipid metabolism, increase insulin sensitivity, and suppress inflammation; however, the underlying mechanisms remain unknown. Proliferation and maladaptive differentiation are important pathological mechanisms underlying obesity. This study aimed to evaluate the effects of vaspin on the proliferation and differentiation of preadipocyte 3T3-L1 cells and to explore the likely mechanisms responsible for 3T3-L1 differentiation. Vaspin was added to cultured 3T3-L1 cells, and the differentiation of adipocytes was evaluated using Oil Red O staining. The AKT signaling pathway and specific differentiation factors related to the differentiation of preadipocyte 3T3-L1 cells, peroxisome proliferator-activated γ and the CCAAT/enhancer-binding protein (C/EBP) family, were evaluated using reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses during the early phase of differentiation. Additionally, adiponectin mRNA, interleukin-6 mRNA (IL-6 mRNA), and glucose transporter-4 (GLUT4) protein levels were measured in the differentiated adipocytes. The results indicated that vaspin promotes the intracellular accumulation of lipids and increases differentiation-related factors, including peroxisome proliferator-activated receptor γ, C/EBPα, and free fatty acid-binding protein 4 (FABP4), in a dose-dependent manner. Additionally, vaspin (200 ng/mL) increased the mRNA and protein levels of C/EBPβ, peroxisome proliferator-activated γ, C/EBPα, and FABP4. Moreover, compared with the control, significantly smaller eight-day differentiated adipocytes were observed, and these cells exhibited decreased IL-6 mRNA and increased GLUT4 mRNA levels; these results also indicated the potential of vaspin to promote the insulin-mediated AKT signaling pathway during the early phase of differentiation. In conclusion, vaspin is able to promote the differentiation of 3T3-L1 preadipocytes and may increase their sensitivity to insulin and suppress obesity.
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