Background and aims: Obesity, especially abdominal obesity, has been considered a risk factor for diabetic complications. Many abdominal obesity indices have been established, including neck circumference (NC), waist-to-hip ratio (WHR), lipid accumulation product (LAP), visceral adiposity index (VAI) and the Chinese visceral adiposity index (CVAI). However, studies investigating the associations between these indices and diabetic complications are limited. The objective of this study was to investigate the associations of the abdominal obesity indices with cardiovascular and cerebrovascular disease (CVD), diabetic kidney disease (DKD) and diabetic retinopathy (DR). Methods: A total of 4658 diabetic participants were enrolled from seven communities in Shanghai, China, in 2018. Participants completed questionnaires and underwent blood pressure, glucose, lipid profile, and urine albumin/creatinine ratio measurements; fundus photographs; and anthropometric parameters, including height, weight, waist circumference (WC), NC and hip circumference (HC). Results: In men, a one standard deviation (SD) increase in CVAI level was significantly associated with a greater prevalence of CVD (OR 1.35; 95% CI 1.13, 1.62) and DKD (OR 1.38; 95% CI 1.12, 1.70) (both P < 0.05). In women, a one SD increase in CVAI level was significantly associated with a greater prevalence of CVD (OR 1.32; 95% CI 1.04, 1.69) and DKD (OR 2.50; 95% CI 1.81, 3.47) (both P < 0.05). A one SD increase in NC was significantly associated with a greater prevalence of CCA plaque in both men (OR 1.26; 95% CI 1.10, 1.44) and women (OR 1.20; 95% CI 1.07, 1.35). These associations were all adjusted for potential confounding factors. Conclusions: CVAI was most strongly associated with the prevalence of CVD and DKD among the abdominal obesity indices, and NC was unique associated with the prevalence of CCA plaque in Chinese adults with diabetes. Trial registration ChiCTR1800017573, www.chictr.org.cn. Registered 04 August 2018.

Observational studies have suggested strong associations between sleep duration and many cardiovascular diseases (CVDs), but causal inferences have not been confirmed. We aimed to determine the causal associations between genetically predicted sleep duration and 12 CVDs using both linear and nonlinear Mendelian randomization (MR) designs. Genetic variants associated with continuous, short (≤6 h) and long (≥9 h) sleep durations were used to examine the causal associations with 12 CVDs among 404 044 UK Biobank participants of White British ancestry. Linear MR analyses showed that genetically predicted sleep duration was negatively associated with arterial hypertension, atrial fibrillation, pulmonary embolism, and chronic ischaemic heart disease after correcting for multiple tests (P < 0.001). Nonlinear MR analyses demonstrated nonlinearity (L-shaped associations) between genetically predicted sleep duration and four CVDs, including arterial hypertension, chronic ischaemic heart disease, coronary artery disease, and myocardial infarction. Complementary analyses provided confirmative evidence of the adverse effects of genetically predicted short sleep duration on the risks of 5 out of the 12 CVDs, including arterial hypertension, pulmonary embolism, coronary artery disease, myocardial infarction, and chronic ischaemic heart disease (P < 0.001), and suggestive evidence for atrial fibrillation (P < 0.05). However, genetically predicted long sleep duration was not associated with any CVD. This study suggests that genetically predicted short sleep duration is a potential causal risk factor of several CVDs, while genetically predicted long sleep duration is unlikely to be a causal risk factor for most CVDs. Causal associations of short and long sleep durations with 12 cardiovascular diseases: linear and nonlinear Mendelian randomization analyses in UK Biobank. All associations are significant at a Bonferroni threshold of P < 4.2E-03 (corrected for 12 outcomes). CVD, cardiovascular disease; SNP, single nucleotide polymorphism.

The aim of this study was to test whether current and past night shift work was associated with incident atrial fibrillation (AF) and whether this association was modified by genetic vulnerability. Its associations with coronary heart disease (CHD), stroke, and heart failure (HF) were measured as a secondary aim. This cohort study included 283 657 participants in paid employment or self-employed without AF and 276 009 participants free of CHD, stroke, and HF at baseline in the UK Biobank. Current and lifetime night shift work information was obtained. Cox proportional hazard models were used. Weighted genetic risk score for AF was calculated. During a median follow-up of 10.4 years, 5777 incident AF cases were documented. From ‘day workers’, ‘shift but never/rarely night shifts’, and ‘some night shifts’ to ‘usual/permanent night shifts’, there was a significant increasing trend in the risk of incident AF (P for trend 0.013). Usual or permanent night shifts were associated with the highest risk [hazard ratio (HR) 1.16, 95% confidence interval (CI) 1.02–1.32]. Considering a person’s lifetime work schedule and compared with shift workers never working nights, participants with a duration over 10 years and an average 3–8 nights/month frequency of night shift work exposure possessed higher AF risk (HR 1.18, 95% CI 0.99–1.40 and HR 1.22, 95% CI 1.02–1.45, respectively). These associations between current and lifetime night shifts and AF were not modified by genetic predisposition to AF. Usual/permanent current night shifts, ≥10 years and 3–8 nights/month of lifetime night shifts were significantly associated with a higher risk of incident CHD (HR 1.22, 95% CI 1.11–1.35, HR 1.37, 95% CI 1.20–1.58 and HR 1.35, 95% CI 1.18–1.55, respectively). These associations in stroke and HF were not significant. Both current and lifetime night shift exposures were associated with increased AF risk, regardless of genetic AF risk. Night shift exposure also increased the risk of CHD but not stroke or HF. Whether decreasing night shift work frequency and duration might represent another avenue to improve heart health during working life and beyond warrants further study. This study demonstrates that both current and lifetime night shift exposures were associated with increased risk of atrial fibrillation and coronary heart disease.

In addition to improving glucose metabolism, liraglutide, a glucagon-like peptide-1 receptor agonist, has weight-loss effects. The underlying mechanisms are not completely understood. This study was performed to explore whether liraglutide could lower weight by modulating the composition of the gut microbiota in simple obese and diabetic obese rats. In our study, Wistar and Goto-Kakizaki (GK) rats were randomly treated with liraglutide or normal saline for 12 weeks. The biochemical parameters and metabolic hormones were measured. Hepatic glucose production and lipid metabolism were also assessed with isotope tracers. Changes in gut microbiota were analyzed by 16S rRNA gene sequencing. Both glucose and lipid metabolism were significantly improved by liraglutide. Liraglutide lowered body weight independent of glycemia status. The abundance and diversity of gut microbiota were considerably decreased by liraglutide. Liraglutide also decreased obesity-related microbial phenotypes and increased lean-related phenotypes. In conclusion, liraglutide can prevent weight gain by modulating the gut microbiota composition in both simple obese and diabetic obese subjects.

Epidemiologic studies have revealed that early-life conditions influence later risk of chronic diseases. We aimed to explore whether exposure to Chinese famine between 1959 and 1962 during fetal and childhood period was related with metabolic syndrome (MS) in adulthood. 6445 subjects from SPECT-China study were divided into fetal-exposed (1959-1962), childhood-exposed (1949-1958), adolescence/young adult-exposed (1921-1948), non-exposed (1963-1974) and non-exposed (after 1975). MS was defined by the International Diabetes Federation criteria. The prevalences of MS in the non-exposed (1963-1974), fetal and childhood-exposed were 16.4%, 20.1% and 19.1% in men and 13.5%, 23.7% and 33.5% in women, respectively. After adjustment for age, compared with non-exposed (1963-1974), fetal and childhood-exposed women had significantly higher prevalences of MS (P < 0.05), but not in men. Famine exposure during the fetal period (OR 1.47, 95% CI 1.05, 2.07) and childhood (OR 1.80, 95% CI 1.22, 2.67) was associated with higher risk of MS in women after adjusting for age (both P < 0.05). Further adjustments for age, smoking, rural/urban residence and economic status did not significantly attenuate this association. Exposure to famine in early life had sex-specific association with MS. It also suggests the adverse effects of malnutrition might extend beyond the 'first 1000 days' and last 9 years.

Objective. The neutrophil-to-lymphocyte ratio (NLR) is an inexpensive and easily measurable laboratory index indicating systemic inflammation, while the application of many other inflammatory markers has been limited in daily clinical practice. However, large population studies about investigating the associations of the NLR level with diabetic complications including cardiovascular and cerebrovascular diseases (CVD), diabetic kidney disease (DKD), and diabetic retinopathy (DR) in the same population were limited. The aim of our study is to evaluate the associations between the NLR level and the prevalence of CVD, DKD, and DR in adults with diabetes simultaneously. Methods. A cross-sectional survey of 4,813 diabetic adults was conducted in seven communities in China. Persons underwent several medical examinations, including the measurement of anthropometric factors, blood pressure, routinely analyzed leukocyte characteristics, glucose, lipid profiles, urine albumin/creatinine ratio, and fundus photographs. Results. Compared with the first quartile of the NLR level, the odds of having CVD was significantly increased by 21% for participants in the highest quartile (OR 1.21; 95% CI 1.00, 1.47) (P for trend<0.05). Similarly, the prevalence of DKD among participants in the highest quartile of the NLR level was significantly increased by 150% (OR 2.50; 95% CI 1.95, 3.19) (P for trend<0.05). However, no association was found between the NLR level and the prevalence of DR (P for trend>0.05). These associations were all fully adjusted. Conclusions. A higher NLR level was associated with an increased prevalence of CVD and DKD, other than DR, in diabetic adults.