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Background: Dyslipidemia may contribute to low bone turnover in patients with type 2 diabetes (T2D) through mediating oxidative stress and atherosclerosis. The low-density lipoprotein cholesterol/apoprotein B (LDL-C/Apo B) ratio is a surrogate marker of small and density low-density lipoprotein cholesterol (sd-LDL-C), a most harmful group of LDL-Cs. The present study aimed to investigate the association between the LDL-C/Apo B ratio and bone turnover in patients with T2D. Methods: This study was a cross-sectional study enrolled patients with T2D from January 2021 to December 2021. Each participant was assessed for lipid profiles, bone turnover markers (BTMs), lumbar spine (L1-L4) and hip dual-energy X-ray absorptiometry (DXA) scans. Osteoporosis was diagnosed as a T-score lower than or equal to -2.5 at the spine or hip. Results: A total of 335 patients with T2D were enrolled in the study, and the LDL-C/Apo B ratio ranged from 0.78 to 4.00. Along with the LDL-C/Apo B ratio tertile ascending, osteocalcin (OC), C-terminal telopeptide (CTx) and N-terminal propeptide of type-I procollagen (PINP) levels gradually increased (all p < 0.05). There were no differences in lumbar spine and hip T-score, proportion of osteoporosis (all p > 0.05) among the three subgroups. The LDL-C/Apo B ratio was positively correlated with lnOC (r = 0.244, p < 0.001), lnCTx (r = 0.226, p < 0.01) and lnPINP (r = 0.211, p < 0.001). These significant positive correlations persisted even when divided into male and female subgroups. Furthermore, three multiple linear regression analyses were constructed to investigate the independent association of the LDL-C/Apo B ratio with the BTMs levels. After adjusting for other clinical parameters, the LDL-C/Apo B ratio was still significantly associated with OC level (β = 0.199, t = 3.348, p < 0.01), CTx level (β = 0.238, t = 4.084, p < 0.001) and PINP level (β = 0.162, t = 2.741, p < 0.01). Conclusion: The LDL-C/Apo B ratio was significantly and positively associated with BTMs in patients with T2D. In clinical practice, more attention should be paid to the patients with T2D whose LDL-C/Apo B ratio is relatively low for the purpose of maintaining bone health. [ABSTRACT FROM AUTHOR]

Background and Aims: We explored the associations among fruit consumption, physical activity, and their dose-response relationship with all-cause and cardiovascular disease (CVD) mortality in type 2 diabetic patients.Methods and Results: We prospectively followed 20,340 community-dwelling type 2 diabetic patients aged 21-94 years. Information on diets and physical activity was collected using standardized questionnaires. All-cause and CVD mortality were assessed. Hazard ratios (HRs) for all-cause mortality were estimated with Cox regression models, and HRs for CVD mortality were derived from a competing risk model. Restricted cubic spline regression was used to analyze dose-response relationships. We identified 1362 deaths during 79,844 person-years. Compared to non-consumption, fruit consumption >42.9 g/d was inversely associated with all-cause mortality (HR 0.76; 95% CI 0.64-0.88), CVD mortality (HR 0.69, 0.51-0.94) and stroke mortality (HR 0.57, 0.36-0.89), but not with heart disease mortality (HR 0.93, 0.56-1.52). The HRs comparing the top vs bottom physical activity quartiles were 0.44 (0.37-0.53) for all-cause mortality, 0.46 (0.33-0.64) for CVD mortality, 0.46 (0.29-0.74) for stroke mortality and 0.51 (0.29-0.88) for heart disease mortality. Lower fruit consumption combined with a lower physical activity level was associated with a greater mortality risk. A nonlinear threshold of 80 g fruit/day was identified; all-cause mortality risk was reduced by approximately 24% at this value. A physical activity threshold of eight metabolic equivalents (MET) h/day was also identified, after which the risk of mortality did not decrease.Conclusions: Fruit consumption and physical activity may reduce all-cause, CVD, and stroke mortality in type 2 diabetic patients. [ABSTRACT FROM AUTHOR]

Background: Body composition alterations may participate in the pathophysiological processes of type 2 diabetes (T2D). A sedentary lifestyle may be responsible for alterations of body composition and adverse consequences, but on which body composition of patients with T2D and to what extent the sedentary lifestyle has an effect have been poorly investigated. Methods: We recruited 402 patients with T2D for this cross-sectional study. All patients received questionnaires to evaluate sedentary time and were further divided into three subgroups: low sedentary time (LST, < 4 h, n = 109), middle sedentary time (MST, 4–8 h, n = 129) and high sedentary time (HST, > 8 h, n = 164). Each patient underwent a dual energy X-ray absorptiometry (DXA) scan to detect body composition, which included body fat percentage (B-FAT), trunk fat percentage (T-FAT), appendicular skeletal muscle index (ASMI), lumbar spine bone mineral density (BMD) (LS-BMD), femoral neck BMD (FN-BMD), hip BMD (H-BMD) and total BMD (T-BMD). Other relevant clinical data were also collected. Results: With increasing sedentary time (from the LST to HST group), B-FAT and T-FAT were notably increased, while ASMI, LS-BMD, FN-BMD, H-BMD and T-BMD were decreased (p for trend < 0.01). After adjustment for other relevant clinical factors and with the LST group as the reference, the adjusted mean changes [B (95% CI)] in B-FAT, T-FAT, ASMI, LS-BMD, FN-BMD, H-BMD and T-BMD in the HST group were 2.011(1.014 to 3.008)%, 1.951(0.705 to 3.197)%, − 0.377(− 0.531 to − 0.223) kg/m2, − 0.083(− 0.124 to − 0.042) g/cm2, − 0.051(− 0.079 to − 0.024) g/cm2, − 0.059(− 0.087 to − 0.031) g/cm2 and − 0.060(− 0.088 to − 0.033) g/cm2, p < 0.01, respectively. Conclusions: A sedentary lifestyle may independently account for increases in trunk and body fat percentage and decreases in appendicular skeletal muscle mass and BMD of the lumbar spine, femoral neck, hip and total body in patients with T2D. [ABSTRACT FROM AUTHOR]

Beta-actin (ACTB) loss-of-function mutations result in a pleiotropic developmental disorder of kidney. The present study aims to explore whether the common variants at the ACTB gene contribute to diabetic kidney disease (DKD) susceptibility in patients with type 2 diabetes mellitus (T2DM). From the baseline population of 20,340 diabetic patients, 1,510 DKD cases and 1,510 age-matched T2DM controls were selected. All subjects were Han Chinese. Three tagging single nucleotide polymorphisms (SNPs), rs852423, rs852426, and rs2966449, at the ACTB gene were genotyped. Logistic regression was performed to estimate the association with DKD. SNPs, rs852426 and rs2966449, were significantly associated with DKD [additive model; odds ratio (OR), 1.217 and 1.151; P = 0.001 and 0.018, respectively]. The association of rs852426 with DKD still remained statistically significant after Bonferroni correction and particularly significant in the population older than 70 years rather than the 70 years or younger (P = 0.047 for heterogeneity test). Furthermore, the association of rs852426 with DKD was observed in populations of male and females without smoking, drinking, and with duration for T2DM 10–20 years. The association of rs2966449 with DKD was also found in the populations older than 70 years, male, not smoking, not drinking, and with duration for T2DM over 20 years. The estimated glomerular filtration rate (eGFR) levels of the individuals with TT or CC genotypes of rs2966449 were significantly lower than that of TC genotype in DKD cases (P = 0.021). The present study provides evidence that the ACTB variants, i.e., rs852426 and rs2966449, may confer the genetic susceptibility to DKD in a Han Chinese population. [ABSTRACT FROM AUTHOR]

Objectives: Prolonged heart rate-corrected QT(QTc) interval is related to ventricular arrhythmia and cardiovascular mortality, with considerably high prevalence of type 2 diabetes. Additionally, long-term glycaemic variability could be a significant risk factor for diabetic complications in addition to chronic hyperglycaemia. We compared the associations of long-term glycaemic variability versus sustained chronic hyperglycaemia with the QTc interval among type 2 diabetes patients. Methods: In this cross-sectional study, 2904 type 2 diabetes patients were recruited who had undergone at least four fasting plasma glucose (FPG) and 2-hour postprandial plasma glucose (PPG) measurements (at least once for every 3 months, respectively) during the preceding year. Long-term glycaemic variabilities of FPG and 2-hour PPG were assessed by their standard deviations (SD-FPG and SD-PPG, respectively), and chronic fasting and postprandial hyperglycaemia were assessed by their means (M-FPG and M-PPG, respectively). HbA1c was also determined upon enrolment to assess current overall glycaemic control. QTc interval was estimated from resting 12-lead electrocardiograms, and more than 440 ms was considered abnormally prolonged. Results: Patients with prolonged QTc interval (≥440 ms) had greater M-FPG, M-PPG, SD-PPG and HbA1c than those with normal QTc interval but comparable SD-FPG. QTc interval was correlated with M-FPG, M-PPG, SD-PPG and HbA1c (r = 0.133, 0.153, 0.245 and 0.207, respectively, p = 0.000) but not with SD-FPG (r = 0.024, p = 0.189). After adjusting for metabolic risk factors via multiple linear regression analysis, SD-PPG, M-PPG and HbA1c (t = 12.16, 2.69 and 10.16, respectively, p = 0.000) were the major independent contributors to the increased QTc interval. The proportion of prolonged QTc interval increased significantly from 10.9% to 14.2% to 26.6% for the first (T1) to second (T2) to third (T3) tertiles of SD-PPG. After adjusting via multiple logistic regression analysis, the odd ratios of prolonged QTc interval of the T2 and T3 versus the T1 of SD-PPG were 1.15 (95% CI, 0.82–1.60) and 2.62 (1.92–3.57), respectively. Conclusions: Increased long-term variability of PPG is a strong independent risk factor for prolonged QTc interval in type 2 diabetes patients, in addition to long-term postprandial hyperglycaemia and current HbA1c. [ABSTRACT FROM AUTHOR]

Objective: The insulin-pancreatic acinar axis may play a major role in pancreatic function. Amylase is an exocrine enzyme that is produced by pancreatic acinar cells, and low serum amylase levels may be associated with endocrine diseases, such as metabolic syndrome and diabetes. We hypothesized that low serum amylase levels may be associated with impaired islet β cell function in type 2 diabetes. Therefore, we investigated the relationship between the serum amylase levels and islet β cell function in patients with early type 2 diabetes. Methods: The cross-sectional study recruited 2327 patients with a mean of 1.71±1.62 years since their diagnosis of type 2 diabetes, and all participants were treated with lifestyle intervention alone. Serum amylase levels, the 75-g oral glucose tolerance test (OGTT) and metabolic risk factors were examined in all participants. The insulin sensitivity index (Matsuda index, ISIMatsuda) and insulin secretion index (ratio of total area-under-the-insulin-curve to glucose-curve, AUCins/glu) were derived from the OGTT. Integrated islet β cell function was assessed by the Insulin Secretion-Sensitivity Index-2 (ISSI-2) (ISIMatsuda multiplied by AUCins/glu). Results: Serum amylase levels in the normal range were significantly correlated with ISIMatsuda, AUCins/glu and ISSI-2 (r = 0.203, 0.246 and 0.413, respectively, p<0.001). The association of the serum amylase levels with ISSI-2 (adjusted r = 0.363, p<0.001) was closer than the association with ISIMatsuda (adjusted r = 0.191, p<0.001) and AUCins/glu (adjusted r = 0.174, p<0.001) after adjusting for the anthropometric indices, time since the diagnosis of diabetes, lipid profiles, uric acid levels, estimated glomerular filtration rate, HbA1c levels, smoking and drinking using the partial correlation test. After adjusting for these metabolic risk factors in the multivariate regression analysis with the amylase levels as the dependent variable, ISSI-2 was the major independent contributor to the serum amylase levels (β = 0.416, t = 21.72, p<0.001). Meanwhile, in a comparison of the groups with the highest and lowest quartiles of serum amylase levels, the mean difference in logISSI-2 was 0.902 (95% CI 0.823 to 0.982), and after adjusting for metabolic risk factors, the mean difference in logISSI-2 was 0.610 (0.537 to 0.683). Conclusions: Serum amylase levels in the normal range are positively associated with integrated islet β cell function in patients with early type 2 diabetes, as assessed by ISSI-2. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: The reduction of podocyte number and density per glomerulus has been linked to the development of proteinuria and the progression of disease in patients with diabetic nephropathy (DN). However, it has been recognized that measurement of podocyte number by light microscope is quite difficult because of the complexity of both podocyte and glomerular structure, which is not suitable for clinical research. In our research institute, we used WT1 as podocyte marker to evaluate the podocyte lesion. Methods: In our experiment, we selected the C-terminal antibody of WT1 to stain the nuclei and the N-terminal antibody of WT1 to stain the cytoplasma of podocytes. Forty patients were enrolled with type 2 diabetes and proven to have DN by renal biopsy analysis. DN patients were classified into three groups based on the degree of proteinuria: microalbuminuria (n =10, 30–300mg/24h), overt proteinuria (n =15, 0.5–3.5g/24h), and heavy proteinuria (n =15, >3.5g/24h). Results: The results demonstrated that the podocyte number was markedly decreased in patients with DN (30–51% reduction). There was a significant negative correlation between the proteinuria and both podocyte density and number. The cover area density of podocyte cytoplasma in glomerulus was also significantly decreased in all DN patients (39–80% reduction). A significant inverse correlation was observed between the cover area density and the degree of proteinuria. The correlation coefficient (r =−0.85) was much higher than that between proteinuria and podocyte density (r =−0.56) or podocyte number (r =−0.36). Conclusion: In conclusion, podocyte damage occurred in patients with DN, even in the early stage and became more dramatic during the course of proteinuria progression. WT1 staining, using the polyclonal antibody to stain the nuclei and monoclonal antibody to stain the cytoplasma of podocytes together, is a valuable alternative technique in the study of podocyte injury. [Copyright &y& Elsevier]

Objective: To investigate the influence of age at menarche (AM) and age at natural menopause (ANM) on glycemic control in patients with type 2 diabetes mellitus (T2DM).Methods: A cross-sectional study was undertaken in Jiangsu, China. Logistic regression was used to evaluate the association between AM/ANM and glycemic control.Results: 1195 (14.3%) premenopausal and 7149 (85.7%) postmenopausal women were included in this study. With the increase of AM per 1 year, patients had a low risk of uncontrolled FPG (≥7 mmol/L) and uncontrolled HbA1c (≥7%), as well as poor glycemic control (FPG ≥7 mmol/L and HbA1c ≥7%) after adjusting for age and BMI (model I, P < 0.05) with odds ratio (OR) 0.965, 0.978 and 0.962 respectively. Whereas after adjusting for age, BMI, education, duration of diabetes, smoking, drinking and antidiabetic treatment (model II) as well as further plus diabetic familial history and physical activity (model III), the association between AM and glycemic control was not significant (P > 0.05). Compared with premenopausal women, postmenopausal women had a low risk of uncontrolled FPG and uncontrolled HbA1c after adjusting for confounders in model II (P < 0.05). Furthermore, both patients with early ANM (<45 years) and late ANM (>55 years) had a high risk of uncontrolled HbA1c as well as poor glycemic control even adjusted for full confounders in model III (P < 0.05 for all).Conclusion: Early AM, early and late ANM were significantly associated with worse glycemic control. Ascertaining the AM and ANM in women with T2DM may help to identify the risk predisposed to worse glycemic control. [ABSTRACT FROM AUTHOR]

Aim: We aim to study association serum creatinine(cr) variability and albuminuria progression.Methods: We conducted a retrospective cohort study on patients with Type 2 Diabetes Mellitus at a Diabetes Centre in Singapore ("discovery cohort"). Outcome is worsening of urinary albumin-to-creatinine(ACR) across stages. Cr variability was expressed as adjusted cr-intrapersonal standard deviation(SD) and coefficient-of-variation(cr-CV). A separate cohort was used for validating association between cr variability and albuminuria progression ("validation cohort").Results: Over median follow-up of 4.2 years, 38.4% of 636 patients had albuminuria progression in the discovery cohort. Increasing log-transformed adjusted cr-intrapersonal SD and cr-CV were significantly associated with albuminuria progression: HRs 1.43 (95%CI 1.11-1.85) and 1.44 (1.11-1.87) respectively in the discovery cohort, and HRs 1.94 (1.09-3.45) and 1.91 (1.05-3.45) respectively in the validation cohort. When stratified by baseline urinary ACR, higher cr variability was significantly associated with albuminuria progression in patients with normoalbuminuria but not microalbuminuria.Conclusions: Cr variability independently predicts albuminuria onset. This is evident in patients with normoalbuminuria, suggesting that higher cr variability could herald albuminuria onset. [ABSTRACT FROM AUTHOR]