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Purpose: The Chinese Healthy Eating Index (CHEI) is a valid instrument to assess the diet quality of the Chinese population, but evidence regarding the relationship between CHEI and the risk of diabetes remains limited. We aimed to investigate the prospective association of CHEI with diabetes among Chinese adults., Methods: 1563 adults free of diabetes at baseline and with at least two survey data from 1997 to 2018 were included. Dietary information was collected by three consecutive 24-h recalls combined with household food inventory, and long-term diet quality was evaluated by the CHEI. Diabetes was defined as self-reported physician-diagnosed diabetes and/or fasting blood glucose ≥ 7.0 mmol/L, and/or HbA1c ≥ 6.5%. Cox proportional hazard models and restricted cubic spline analysis were used to estimate the associations between CHEI and diabetes., Results: During a median follow-up of 12.0 years, 192 (10.3%) participants developed new-onset diabetes. Generally, a five-point higher CHEI score was significantly associated with a 17% lower risk of diabetes (HR, 0.83; 95%CI 0.71-0.97). In stratified analysis, inverse associations between CHEI and diabetes were more vigorous in females (HR, 0.68; 95%CI 0.54-0.85) than in males (P for interaction = 0.01). In addition, there was an L-shaped association between CHEI and diabetes risk in the whole population (P for non-linearity = 0.026), while no significant non-linear association was observed in females or males, respectively., Conclusion: Our results suggested that a long-term higher-quality diet evaluated by CHEI was significantly associated with lower risks of diabetes, and the favorable associations were more pronounced among females., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Cellular senescence and iron accumulation were separately observed in diabetic nephropathy (DN). Limited evidence supports that iron was significantly accumulated in senescent cells. We aimed to explore whether iron is involved in the pathogenesis role of senescence in DN. Renal cells were treated with high glucose (HG, 35 mM) for 10 or 15 days, and DN mice were induced by high-fat diet and streptozotocin. Gene ontology enrichment, gene set enrichment analysis analysis, β-galactosidase staining, 5-ethynyl-2-deoxyuridine staining, and western blot depicted the upregulated senescence pathway in vitro and in vivo of DN. Lactate dehydrogenase (LDH) release was increased by HG and reversed by p16/p21 knockdown, and the supernatant of HG-treated cells caused increased LDH release from normal cells. Iron metabolism-related protein expression was disordered after HG exposure concomitant with senescence. Ferric ammonium citrate (50 μM) upregulated gamma-H2A.X variant histone and increased the senescence markers in HG-treated cells. The treatment of deferoxamine (0.5 μM) had the opposite effect. Compared to the non-DN individual, increased ferritin and senescence markers were verified in DN mice and patients, and the co-localization of ferritin and senescence markers was observed by immunofluorescence. These results suggested that accumulated iron was correlated with aggravated DNA damage and accelerated senescence, and revealed the role of iron in the cellular senescence of diseases., (© 2024 Wiley Periodicals LLC.)

Metabolic dysfunction-associated fatty liver disease (MAFLD) is the crucial pathogenesis for intra-hepatic and extra-hepatic diseases, especially in elderly adults. Lifestyle management may be a modifiable cost-effective measure for MAFLD prevention, but the evidence is limited. A total of 23,408 middle-aged and elderly individuals were included in a longitudinal study from 2008 to 2018. Combined lifestyle scores (range 0-6) were evaluated by BMI, smoking, drinking, diet, physical activity, and sleep. Logistic regression models were used to calculate ORs for the risks of MAFLD and specific subtypes. The mean age of participants was 61.7 years, and 44.5% were men. Compared with poor lifestyle (scores 0-2), ORs (95% CIs) of the ideal lifestyle (scores 5-6) were 0.62 (0.57-0.68) for MAFLD, 0.31 (0.28-0.34) for MAFLD with excess weight and obesity, 0.97 (0.75-1.26) for MAFLD with diabetes, and 0.56 (0.51-0.62) for MAFLD with metabolic dysregulation. Additionally, lifestyle improvement was associated with lower risks of MAFLD (OR, 0.76; 95% CI, 0.68-0.86), MAFLD with excess weight and obesity (OR, 0.72; 95% CI, 0.63-0.81), MAFLD with diabetes (OR, 0.74; 95% CI, 0.54-1.02) and MAFLD with metabolic dysregulation (OR, 0.49; 95% CI, 0.43-0.55), respectively. Our findings suggest that adherence to a combined healthy lifestyle was associated with lower risks of MAFLD, particularly in excess weight/obese individuals or those with metabolic dysregulation.

Background: The aetiology of diabetes is complex with limited treatment strategies. Growing animal studies have shown that targeted antiageing can improve the outcomes of diabetes. However, population evidence is limited. This study aims to evaluate the associations of biological ageing with all-cause and cause-specific mortality among people with diabetes., Methods: A total of 5278 people with diabetes from the National Health and Nutrition Examination Survey 1999-2014 were included. Biological ageing was measured from different perspectives, including phenotypic age, biological age, telomere length and klotho concentration. Phenotypic/biological age acceleration was the residual resulting from a linear model when regressing phenotypic/biological age on chronological age. Cox proportional hazards models were used to examine the relationships between ageing and all-cause, cardiovascular disease (CVD), and cancer mortality., Results: Over median follow-up for 7.3 years, 1355 diabetics died. There was a positive and linear association of mortality with phenotypic age acceleration (HR all-cause 1.04; HR CVD 1.04; HR cancer 1.04, p<0.001) and biological age acceleration (HR all-cause 1.03; HR CVD 1.04; HR cancer 1.03, p<0.001). Telomere length was inversely associated with all-cause mortality (tertile (T)3 vs T1: HR 0.67, p<0.05). The concentration of klotho had a U-shaped relationship with mortality (T2 vs T1: HR all-cause 0.62; HR CVD 0.48; HR cancer 0.47, p<0.05). Further, stratified analysis by age and sex found that the associations of ageing-related markers with mortality were more significant in the aged and female subgroup., Conclusions: Biological ageing was positively associated with mortality among people with diabetes, indicating therapies targeting antiageing could be encouraged to halt the progression of diabetes., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Aims/introduction: Elevated serum cancer antigen 19-9 (CA19-9) levels have been found in diabetes patients in most observational studies; however, whether there is a causal association between CA19-9 and diabetes mellitus is unclear., Materials and Methods: Our study was carried out based on the Dongfeng-Tongji cohort comprising 27,009 individuals. We first investigated the associations between serum CA19-9 levels and incident diabetes mellitus risk in a prospective cohort study (12,700 individuals). Then, we explored the potential causal relationship between CA19-9 and diabetes mellitus risk in a cross-sectional study (3,349 diabetes mellitus patients and 8,341 controls) using Mendelian randomization analysis. A weighted genetic risk score was calculated by adding the CA19-9 increasing alleles in five single-nucleotide polymorphisms (rs17271883, rs3760776 and rs3760775 in FUT6, rs11880333 in CA11, rs265548 in B3GNT3, and rs1047781 in FUT2), which were identified in a previous genome-wide association study on serum CA19-9 levels., Results: In the prospective study, a total of 1,004 incident diabetes mellitus patients were diagnosed during a mean 4.54-year follow-up period. Elevated serum CA19-9 level was associated with a higher incident diabetes risk after adjustment for confounders, with a hazard ratio of 1.20 (95% confidence interval 1.11-1.30) per standard deviation (12.17 U/mL) CA19-9 increase. Using the genetic score to estimate the unconfounded effect, we did not find a causal association of CA19-9 with diabetes risk (odds ratio per weighted CA19-9-increasing allele: 0.99, 95% confidence interval 0.94-1.04; P = 0.61)., Conclusions: The present study did not support a causal association of serum CA19-9 with diabetes risk. CA19-9 might be a potential biomarker of incident diabetes mellitus risk., (© 2019 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)

Background: We examined the association between metabolically healthy obese (MHO) and diabetes incidence in a middle-aged and elderly population and whether the association differed by the presence of nonalcoholic fatty liver disease (NAFLD)., Methods: We examined 17 801 participants without diabetes at study entry (7980 males and 9821 females with a mean age of 63.2 years) derived from the Dongfeng-Tongji cohort study (median follow-up: 4.6 years). Participants were divided into six groups based on BMI (normal weight, overweight, or obese) and metabolic health (healthy/unhealthy) defined by the Adult Treatment Panel III criteria. The MHO was defined as BMI greater than 28.0 kg/m 2 with 0 or 1 of four metabolic abnormalities (elevated blood pressure, triglyceridaemia, hyperglycaemia, low HDL cholesterol). The hazard ratio (HR) and 95% confidence interval (CI) for incident diabetes were derived from the Cox proportional hazard regression model., Results: During 79 843 person-years of follow-up, 1453 individuals developed diabetes. Compared with metabolically healthy normal weight (MH-NW) individuals, the multivariable-adjusted HRs (95% CI) were 1.74 (1.16-2.59) for MHO and 2.15 (1.65-2.81) for metabolically unhealthy obese subjects after adjusting for age, sex, smoking, alcohol drinking, physical activity, fruit and vegetable consumption, family history of diabetes, fasting glucose, waist circumference, and NAFLD. Among those without NAFLD, MHO individuals showed higher incidence of diabetes (multivariate-adjusted HR = 2.71, 95% CI: 1.47-5.00) than MH-NW individuals., Conclusions: The MHO phenotype was associated with increased incidence of diabetes in a middle-aged and elderly population, and the association did not differ by the presence or absence of NAFLD., (© 2019 John Wiley & Sons, Ltd.)

Aims: Observational studies indicated that resting heart rate (RHR) was associated with diabetes mellitus (DM) risk; however, it remains unclear whether the association between RHR and DM is causal. We aimed to examine whether there was causal association of RHR with DM risk., Methods: A prospective study including 16,201 middle-aged and older Chinese (7031 males and 9170 females) derived from the Dongfeng-Tongji cohort was performed. Cox proportional hazard regression models were conducted to estimate the associations between RHR and incident DM risk. In 7481 participants, 65 single nucleotide polymorphisms related to RHR were genotyped. A genetic risk score (GRS) of RHR was calculated based on the RHR-associated variants. The causal associations of RHR with DM risk were investigated by Mendelian randomization analysis., Results: During a mean (SD) follow-up of 4.5 (0.5) years, 1110 diabetes were identified. Compared with the referential RHR group (≤ 60 beats per minute [bpm]), individuals with RHR > 80 bpm have a higher incident diabetes risk, with a hazard ratio of 1.40 (95% confidence interval [CI], 1.05-1.88). With per SD increase in the weighted genetic risk score, the resting heart rate increased by 0.71 bpm (95% CI 0.49-0.93). By using the GRS to estimate the unconfounded effect, we found that higher resting heart rate did not have a causal effect on diabetes risk (OR 1.00 [95% CI 0.95-1.05])., Conclusions: The present study supported a positive but not a causal association of RHR with incident diabetes risk. More studies are needed to verify our findings.

Background: Whether cigarette smoking and moderate drinking are associated with non-alcoholic fatty liver disease (NAFLD)has not been fully described. This study investigated the separate and joint effects of smoking and moderate drinking on Chinese men with NAFLD. Methods: Across-sectional assay from DFTJ Cohort study was performed with a size of 9432 elderly Chinese men excluding excessive alcohol consumption (<210g/week). Fatty liver was diagnosed by standardized ultrasonographic inspection. The odds ratio (OR) of alcohol consumption and smoking for the prevalence of NAFLD were analyzed using multiple logistic regression with multiple adjustments. Results: The prevalence of NAFLD in current smokers (pack-year≥40) and drinkers (80~210g/week or drinking duration≥35years) was significantly higher than that in non-smokers and non-drinkers, respectively. The combination of current smoking (pack-year≥40) and drinking (80~210g/week) was associated with the highest risk of NAFLD (OR 1.85; 95% confidence interval [CI] 1.28–2.68;P<0.01). The similar combined effect was found in participants with pack-year≥40 and drinking duration≥35 years (OR 1.72; 95% CI 1.26–2.34;P<0.01). Moreover, an interaction was observed between current smoking and moderate drinking in NAFLD. Conclusions: In elderly Chinese men, cigarette smoking and moderate alcohol consumption exerts an evident joint effect and interaction on the prevalence of NAFLD, although both are significantly and independently associated with NAFLD prevalence. Such findings highlight particular significance of avoidance of cigarette and alcohol on NAFLD prevention. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study is to examine the bidirectional association between nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). Methods: The data was derived from the Dongfeng-Tongji cohort study, which was established in 2008 and followed until October 2013. NAFLD was classified as none, mild, moderate/severe based on ultrasound examination. The analysis to examine the association between NAFLD and incident T2DM risk included 18,111 participants free of diabetes at baseline and the duration of follow-up was 4.60 ± 0.60 years. Cox proportional regression model was used to calculate the hazard ratio (HR) for the association. The analysis to investigate the association between T2DM and incident NAFLD risk included 12,435 participants free of NAFLD at baseline. Logistic regression model was used to calculate the odd ratio (OR) of NAFLD. Results: Compared with those without NAFLD, individuals with mild or moderate/severe NAFLD had a monotonic elevated risk of developing T2DM (HR: 1.88 [95% CI: 1.63–2.18] and 2.34 [1.85–2.96], respectively) after adjustment for potential confounders. In a parallel analysis, compared to participants with fasting plasma glucose < 6.1 mmol/L, the ORs of developing NAFLD in subjects with impaired fasting glucose and T2DM were 1.35 (95% CI: 1.16–1.57) and 1.40 (95% CI: 1.22–1.62), respectively. Conclusions: Our results provide compelling evidence that the NAFLD-T2DM association is bidirectional in Chinese population. [ABSTRACT FROM AUTHOR]