Huili Wei

Associations between Longer Habitual Day Napping and Non-Alcoholic Fatty Liver Disease in an Elderly Chinese Population

Context Both longer habitual day napping and Non-Alcoholic Fatty Liver Disease (NAFLD) are associated with diabetes and inflammation, but the association between day napping and NAFLD remains unexplored. Objective To investigate the association between the duration of habitual day napping and NAFLD in an elderly Chinese population and to gain insight into the role of inflammatory cytokines in this association. Design and Setting We conducted a series of cross-sectional studies of the community population in Chongqing, China, from 2011 to 2012. Participants Among 6998 participants aged 40 to 75 years, 6438 eligible participants were included in the first study and analyzed to observe the association between day napping duration and NAFLD. In a separate study, 80 non-nappers and 90 nappers were selected to identify the role of inflammatory cytokines in this association. Logistic regression models were used to examine the odds ratios (ORs) of day nap duration with NAFLD. Results Day nappers had a significantly higher prevalence of NAFLD (P<0.001). Longer day napping duration was associated in a dose-dependent manner with NAFLD (P trend <0.001). After adjustment for potential confounders, the ORs were 1.67 (95% CI 1.13–2.46) for those reporting 0.5–1 h and 1.49 (95% CI 1.01–2.19) for those reporting >1 h of day napping compared with individuals who did not take day naps (all P<0.05). Longer-duration day nappers had higher levels of IL-6 and progranulin (PGRN) but lower levels of Secreted frizzled-related protein-5 (SFRP5, all P trend <0.001). After adjusting for IL-6, PGRN, and SFRP5, the association between day napping duration and NAFLD disappeared (all P>0.05). Conclusion Longer day napping duration is associated with a higher prevalence of NAFLD, and inflammatory cytokines may be an essential link between day napping and NAFLD.

In vitro and in vivo inhibition of mTOR by 1,25-dihydroxyvitamin D3 to improve early diabetic nephropathy via the DDIT4/TSC2/mTOR pathway

We investigated whether 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3) could improve early diabetic nephropathy through the DNA-damage-inducible transcript 4/tuberous sclerosis 2/mammalian target of rapamycin pathway. Rat mesangial cells were cultured in media containing normal glucose or high glucose and were treated with or without 1,25(OH)2D3. Mesangial cells proliferation was measured. Streptozotocin-induced diabetic rats were injected intravenously with a recombinant lentivirus against the rat vitamin D receptor gene. Urinary and serum albumin, fasting plasma glucose, serum triglyceride, total cholesterol, calcium, parathyroid hormone and serum 25-dihydroxy-vitamin D (25(OH)D) levels, mean glomerular volume, glomerular basement membrane thickness and total kidney volume were determined. The expressions of vitamin D receptor, DNA-damage-inducible transcript 4, and mammalian target of rapamycin were measured. 1,25(OH)2D3 inhibited the proliferation of mesangial cells induced by hyperglycemia. 1,25(OH)2D3 also significantly reduced albumin excretion, mean glomerular volume, glomerular basement membrane, and total kidney volume in rats with diabetic nephropathy. The expression of DNA-damage-inducible transcript 4 was elevated by 1,25(OH)2D3 treatment. The phosphorylation of mammalian target of rapamycin was reduced by 1,25(OH)2D3 treatment. Vitamin D receptor gene silencing blocked all of the above results. The current study demonstrates that 1,25(OH)2D3 can effectively inhibit mesangial cells proliferation induced by hyperglycemia, thus suppressing the development of diabetic nephropathy. This study also shows that the nephron-protective effect of 1,25(OH)2D3 occurs partly through the DDIT4/TSC2/mTOR pathway.

1,25-Dihydroxyvitamin-D3 prevents the development of diabetic cardiomyopathy in type 1 diabetic rats by enhancing autophagy via inhibiting the β-catenin/TCF4/GSK-3β/mTOR pathway

Diabetic cardiomyopathy (DCM) can increase the risk of heart failure and death in diabetic patients. However, no effective approaches are available to prevent its progression and development. Studies have shown that vitamin D is greatly implicated in cardiac hypertrophy and fibrosis, and there is a high prevalence of vitamin D deficiency in diabetic patients. In this study, we investigated whether 1,25-Dihydroxyvitamin-D3 (1,25D3) can improve DCM through a vitamin D receptor (VDR)-dependent mechanism associated with autophagy and the β-catenin/T-cell factor/lymphoid enhancer factor (TCF4)/glycogen synthase kinase-3β (GSK-3β)/mammalian target of rapamycin (mTOR) pathway. In this study, streptozotocin (STZ)-induced type 1 diabetic rats were established and were treated with 1,25D3 and/or chloroquine and/or VDR gene silencing for 8 weeks before being sacrificed. Compared with untreated diabetic rats, 1,25D3 partly attenuated the myocardial hypertrophy and interstitial fibrosis, improved cardiac function and restored the impaired cardiac autophagy in diabetic rats, all of which were reversed by silencing the VDR gene in diabetic rats. In high-glucose cultured H9C2 cells, 1,25D3 increased autophagy in a dose-dependent manner. Besides, the β-catenin/TCF4/GSK-3β and mTOR signaling were activated both in diabetic rats and in high-glucose cultured H9C2 cells. Treatment with 1,25D3 inhibited the β-catenin/TCF4/GSK-3β and mTOR signaling in H9C2 cells, whereas co-treatment with lithium chloride (LiCl) reversed this situation and abolished the beneficial effect of 1,25D3 on autophagy. These data suggest that 1,25D3 may improve DCM in type 1 diabetic rats by modulating autophagy through the β-catenin/TCF4/GSK-3β and mTOR pathway. Vitamin D may exist as a new therapeutic target for the treatment of DCM.

Plasma Periostin Levels Are Increased in Chinese Subjects with Obesity and Type 2 Diabetes and Are Positively Correlated with Glucose and Lipid Parameters

The purpose of this study is to examine the relations among plasma periostin, glucose and lipid metabolism, insulin resistance and inflammation in Chinese patients with obesity (OB), and type 2 diabetes mellitus (T2DM). Plasma periostin levels in the T2DM group were significantly higher than the NGT group (P < 0.01). Patients with both OB and T2DM had the highest periostin levels. Correlation analysis showed that plasma periostin levels were positively correlated with weight, waist circumference (WC), body mass index (BMI), waist-hip ratio (WHR), fasting plasma glucose (FPG), 2 h postchallenge plasma glucose (2 h PG), glycated hemoglobin (HbA1c), triglyceride (TG), total cholesterol (TC), fasting insulin (FINS), homeostasis model assessment of insulin resistance (HOMA-IR), TNF-α, and IL-6 (P < 0.05 or 0.001) and negatively correlated with high-density lipoprotein cholesterol (HDL-C) (P < 0.001). Multiple linear regression analysis showed that TG, TNF-α, and HOMA-IR were independent related factors in influencing the levels of plasma periostin (P < 0.001). These results suggested that Chinese patients with obesity and T2DM had significantly higher plasma periostin levels. Plasma periostin levels were strongly associated with plasma TG, chronic inflammation, and insulin resistance.

Associations between sitting time and non-alcoholic fatty liver diseases in Chinese male workers: a cross-sectional study

Objectives Various studies have revealed a close association between sedentary behaviour and metabolic diseases, yet the association between sedentary time and non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, we investigated the association between sitting time and NAFLD in a Chinese male population and explored its underlying mechanism. Study design A cross-sectional study. Setting Chongqing, China. Participants Our study included 2054 male participants; all of the participants were of Han nationality. Primary outcome measures Sitting time was assessed using a self-reported questionnaire concerning the time devoted to sitting behaviour. Various clinical and demographic biomarkers were measured. Logistic regression analyses were used to investigate the ORs and the 95% CIs between sitting time and NAFLD. Results We found a higher proportion of NAFLD across the tertiles of sitting time (p trend=0.003). Multivariate linear regression analyses showed sitting time independently correlated with homoeostasis model assessment for insulin resistance (HOMA-IR), alanine aminotransferase, γ-glutamyl transpeptidase, body mass index, triglyceride and the high-sensitive C reactive protein (hsCRP) (all p<0.05). Further logistic regression analyses showed that longer sitting time (>7.1 hours/day) was associated with a higher prevalence of NAFLD (OR 1.09; 95% CI (1.04 to 1.67)) after adjusting for confounders. However, this association was insignificant after further adjusting for hsCRP (OR 1.03; 95% CI (0.92 to 1.84)). Conclusions Sitting time was positively associated with the prevalence of NAFLD, and this association might be affected by inflammation.

Association Between the Visceral Adiposity Index and Homeostatic Model Assessment of Insulin Resistance in Participants With Normal Waist Circumference

We assessed the correlation between the visceral adiposity index (VAI; a useful indicator of adipose distribution and function) and homeostatic model assessment of insulin resistance (HOMA-IR) in participants with normal waist circumference. A cross-sectional study was conducted, which included 1834 Chinese adults. The blood pressure, anthropometric measurements, fasting and postprandial blood glucose, fasting insulin, and lipid profiles were measured. The VAI and HOMA-IR were calculated. Participants were divided into 4 groups according to the HOMA-IR level, and the correlation between the VAI and HOMA-IR was analyzed. The VAI gradually increased across the HOMA-IR quartiles (P < .05), and a Pearson correlation analysis showed that VAI was positively related to the HOMA-IR (P < .001) in males and females. After adjusting for the other covariates, VAI was independently correlated with the HOMA-IR. A logistic regression analysis indicated that VAI elevation was the main risk factor for the increased HOMA-IR in both genders. Overall, the VAI was closely correlated with the HOMA-IR in a population without central obesity.

1,25(OH)2D3 improves cardiac dysfunction, hypertrophy, and fibrosis through PARP1/SIRT1/mTOR-related mechanisms in type 1 diabetes

Scope: Diabetic cardiomyopathy is one of the most important cardiac complications associated with diabetes. However, the mechanisms underlying diabetic cardiomyopathy remain unclear. The PARP1, SIRT1, and mTOR pathways have been implicated in cardiac diseases, and they are also associated with diabetes. 1,25(OH)2D3 was recently recognized as a potential PARP1inhibitor in a macrophage cell line. The aim of our study was to investigate whether 1,25(OH)2D3 can improve diabetic cardiomyopathy through a vitamin D receptor (VDR)‐dependent mechanism associated with the PARP1/SIRT1/mTOR pathway. Methods and results: 1,25(OH)2D3‐treated diabetic rats displayed improved left ventricular wall thickness and end‐diastolic/systolic diameter, end‐diastolic/systolic volume, left ventricular ejection fraction, fractional shortening, atrial natriuretic peptide, and brain natriuretic peptide gene expression, and interstitial fibrosis compared with untreated diabetic rats, while silencing the VDR gene in DM rats blocked the above results. 1,25(OH)2D3 treatment also decreased PARP1 and increased SIRT1 expression levels and repressed the phosphorylation of mTOR. Treating neonatal cardiomyocytes with 1,25(OH)2D3 and a PARP1 inhibitor decreased PARP1 and increased SIRT1 protein expression. Conclusion: The present study demonstrates that 1,25(OH)2D3 treatment has the potential to improve diabetic cardiomyopathy in rats and suggests that VD‐VDR signaling induces this protective effect against diabetic cardiomyopathy might partly through the PARP1/SIRT1/mTOR pathway.

Serum brain-derived neurotrophic factor levels and sleep disorders in Chinese healthy and newly diagnosed type 2 diabetic subjects

The aims of the present study were to detect serum brain‐derived neurotrophic factor (BDNF) protein concentrations in healthy and diabetic subjects with sleep disorders and to explore correlations among serum BDNF concentrations, metabolic parameters and inflammation.

Plasma C1q/TNF-Related Protein-3 (CTRP-3) and High-Mobility Group Box-1 (HMGB-1) Concentrations in Subjects with Prediabetes and Type 2 Diabetes

Aims. To detect the association of C1q/TNF-related protein-3 (CTRP-3) and high-mobility group box-1 (HMGB-1) in subjects with prediabetes (pre-DM) and newly diagnosed type 2 diabetes (nT2DM). Methods. 224 eligible participants were included. The 75 g oral glucose tolerance test (OGTT) and several clinical parameters of metabolic disorders and cytokines were measured. All participants were divided into three groups: normal glucose tolerance (NGT, n = 62), pre-DM (n = 111), and nT2DM group (n = 56). Results. Plasma CTRP-3 concentrations were significantly lower in subjects with pre-DM and nT2DM than that of the NGT group, while plasma HMGB-1 levels were higher in pre-DM and nT2DM group compared with the NGT group (P < 0.05). A multiple linear regression analysis showed both plasma CTRP-3 and HMGB-1 concentrations were independently associated with homeostasis model assessment for insulin resistance (HOMA-IR) and interleukin-6 (IL-6) (P < 0.05 for all). Further multiple logistical regression analyses revealed that both plasma CTRP-3 and HMGB-1 levels were significantly associated with pre-DM and nT2DM after adjusting for several confounders (P < 0.001 for all). Conclusions. Circulating CTRP-3 and HMGB-1 concentrations might be promising biomarkers to predict prediabetes and type 2 diabetes.

Relationship between serum adipsin and the first phase of glucose-stimulated insulin secretion in individuals with different glucose tolerance

To detect serum adipsin levels in individuals with different glucose tolerance, and investigate the relationship between adipsisn and the first phase of insulin secretion.