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Purpose The differential diagnosis of adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome remains a challenge in clinical practice. The present study was aimed at assessing the diagnostic performance of pituitary dynamic contrast-enhanced magnetic resonance imaging (dMRI), high-dose dexamethasone suppression test (HDDST), and a combination of both tests for patients with ACTH-dependent Cushing's syndrome. Methods A total of 119 consecutive patients with ACTH-dependent Cushing's syndrome confirmed surgically were enrolled: 101 with proven Cushing's disease and 18 with proven ectopic ACTH syndrome. All patients underwent pituitary dMRI and HDDST. The sensitivity and specificity of pituitary dMRI, HDDST, and a combination of both tests were determined. Results The sensitivity and specificity of pituitary dMRI for diagnosing Cushing's disease were 80.2 and 83.3%, respectively, with a positive predictive value of 96.4%. The sensitivity and specificity of HDDST were 70.3 and 77.8%, respectively, with positive predictive value of 94.7%. A combination of both tests showed that the combined criteria of more than 50% suppression of serum cortisol on HDDST and a positive pituitary dMRI finding yielded a high specificity of 94.4 and sensitivity of 59.4%. The combined criteria of more than 68% suppression on HDDST and/or a positive pituitary dMRI finding yielded a sensitivity of 86.1% and specificity of 83.3%. Conclusions Pituitary dMRI was superior to HDDST in the differential diagnosis of ACTH-dependent Cushing's syndrome. HDDST is recommended in combination with pituitary dMRI to establish a diagnosis process because of the significantly increased specificity with the combination.

With the aging world population, the prevalence of aging-related disorders is on the rise. Diseases such as Alzheimer's, type 2 diabetes mellitus (T2DM), Parkinson's, atherosclerosis, hypertension, and osteoarthritis are age-related, and most of these diseases are comorbidities or risk factors for AD; however, our understandings of molecular events that regulate the occurrence of these diseases are still not fully understood. Brain and muscle Arnt-like protein-1 (Bmal1) is an irreplaceable clock gene that governs multiple important physiological processes. Continuous research of Bmal1 in AD and associated aging-related diseases is ongoing, and this review picks relevant studies on a detailed account of its role and mechanisms in these diseases. Oxidative stress and inflammation turned out to be common mechanisms by which Bmal1 deficiency promotes AD and associated aging-related diseases, and other Bmal1-dependent mechanisms remain to be identified. Promising therapeutic strategies involved in the regulation of Bmal1 are provided, including melatonin, natural compounds, metformin, d-Ser2-oxyntomodulin, and other interventions, such as exercise, time-restricted feeding, and adiponectin. The establishment of the signaling pathway network for Bmal1 in aging-related diseases will lead to advances in the comprehension of the molecular and cellular mechanisms, shedding light on novel treatments for aging-related diseases and promoting aging-associated brain health.

Background and Objective: Type 2 Diabetes (T2D) patients are more prone to develop Alzheimer’s Disease (AD). We have previously shown that Glucagon-like peptide-1 receptor agonist exendin-4 (Ex-4) reduces tau hyperphosphorylation in T2D animals through upregulating insulin signaling, and peripheral injected Ex-4 increases insulin levels in the T2D brain. This study aims to further clarify whether the elevated insulin in the brain is produced by nerve cells under the action of Ex-4. Methods: The neuronal cell line-HT22 was treated with Ex-4 under high glucose or normal cultivation, and the number of insulin-positive cells as well as the expression levels of insulin synthesis-related genes were examined. The db/db mice were treated with the peripheral injection of Ex-4 and/or IntraCerebroVentricular (ICV) injection of siRNA to inhibit the expression of insulin synthesis- related genes and the behavior tests were carried on. Finally, plasma glucose, Cerebrospinal Fluid (CSF) glucose, CSF insulin, phosphorylation of tau, phosphorylation of AKT and GSK-3β of db/db mice were detected. Results : We found that Ex-4 promoted the expression of insulin synthesis-related genes and induced an obvious increase of insulin-positive HT-22 neuronal cells in a high glucose environment. Peripheral injection of Ex-4 improved the cognitive function of db/db mice and increased brain insulin levels which activated brain insulin signaling and subsequently alleviated tau hyperphosphorylation. However, when siRNA-neurod1 was injected to block insulin synthesis, the cognitive function of db/db mice was not improved under the action of Ex-4 anymore. Moreover, the brain insulin levels dropped to an extremely low level, and the phosphorylation level of tau increased significantly. Conclusion: This study demonstrated that Ex-4 improved cognition function by promoting brain insulin synthesis followed by the activation of brain insulin signaling and alleviation of tau hyperphosphorylation.

The circadian clock is an endogenous system designed to anticipate and adapt to daily changes in the environment. Alzheimer's disease (AD) is a progressive neurodegenerative disease, which is more prevalent in patients with type 2 diabetes mellitus (T2DM). However, the effects of circadian disruption on mental and physical health for T2DM patients are not yet fully understood, even though circadian disruption has been confirmed to promote the progression of AD in population. By housing db/db mice on a disrupted (a 6:18 light/dark cycle) circadian rhythm, we assessed the circadian gene expression, body weight, cognitive ability, and AD-related pathophysiology. Our results indicated that housing in these conditions led to disrupted diurnal circadian rhythms in the hippocampus of db/db mice and contributed to their weight gain. In the brain, the circadian-disrupted db/db mice showed a decreased cognitive ability and an increased hyperphosphorylation of tau protein, even though no difference was found in amyloid protein (Aβ) plaque deposition. We also found that the hyperphosphorylated tau protein exhibited more disruptive daily oscillations in db/db mice hippocampus under the 6:18 light/dark cycle. Circadian alterations could promote the development of AD in T2DM.

Jiaojiao Huang, Xuemin Peng, Kun Dong, Jing Tao, Yan Yang Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of ChinaCorrespondence: Yan YangDepartment of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, Hubei, 430030, People’s Republic of ChinaTel +86-27-83663331Fax +86-27-83662883Email yangyan6910@163.comAim: This study aimed to compare HOMA-IR, leptin, and resistin as the risk factors for diabetic nephropathy in the type 2 diabetes mellitus (T2DM) patients with different BMI classifications.Materials and Methods: A total of 309 patients with T2DM were enrolled in this cross-sectional study. All participants were divided into three groups according to BMI: the normal weight group (18.5 kg/m2≤BMI< 24 kg/m2), the overweight group (24kg/m2≤BMI< 28 kg/m2) and the obesity group (BMI≥ 28 kg/m2). The clinical information and laboratory examinations were recorded in detail. Leptin and resistin levels were measured using enzyme-linked immunosorbent assay (ELISA).Results: Higher HOMA-IR, leptin and resistin levels were found to be the risk factors for diabetic nephropathy when we made comparisons in the total population (P< 0.05). In the normal weight group, logistic regression analysis showed that T2DM patients with higher HOMA-IR (OR=4.210, P=0.001), leptin (OR=2.474, P=0.031) and resistin levels (OR=8.299, P< 0.001) had nearly 4-fold, 2-fold and 8-fold risk for diabetic nephropathy, respectively, after adjustments. The receiver operating characteristic (ROC) curves indicated that the area under the curves (AUCs) of HOMA-IR and resistin were 0.699 (95% CI 0.617– 0.772) and 0.790 (95% CI 0.715– 0.854), respectively, which were significantly larger than the AUC of 0.5 (all P< 0.001). However, no significant association was observed between HOMA-IR, leptin, and resistin and renal complications (all P> 0.05) in the overweight and obesity groups in both logistic regression and AUC analysis.Conclusion: Higher insulin resistance, leptin and resistin levels were observed as risk factors for diabetic nephropathy in T2DM patients with lower BMI. These were not obvious in the overweight and obese patients.Keywords: type 2 diabetes mellitus, insulin resistance, leptin, resistin, diabetic nephropathy

Rongping Fan,1,2,&ast; Lei Xie,1,2,&ast; Xuemin Peng,1,2 Bo Yu,3 Huajie Zou,1,2,4 Jiaojiao Huang,1,2 Xuefeng Yu,1,2 Daowen Wang,3 Yan Yang1,2 1Division of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People’s Republic of China; 2Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, 430030, People’s Republic of China; 3Division of Cardiology, Department of Internal Medicine and Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People’s Republic of China; 4Division of Endocrinology, Department of Internal Medicine, The Affiliated Hospital of Qinghai University, Xining, Qinghai, 810001, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Yan Yang; Daowen Wang, Division of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People’s Republic of China, Tel +86-27-83665513, Fax +86-27-83662883, Email yangyan6910@163.com; dwwang@tjh.tjmu.edu.cnAim: To explore the clinical outcomes among preadmission insulin-treated type 2 diabetes mellitus (T2DM) in intensive care units (ICU).Patients and Methods: In this retrospective observational study, 578 T2DM patients admitted to ICU were recruited from March 2011 to February 2021, which were composed of 528 patients treated with insulin after ICU admission (including 300 preadmission non-insulin-treated and 228 preadmission insulin-treated patients) and 50 patients treated without insulin before and after ICU admission. Clinical outcomes were compared between the groups. Variables of age (± 10 years), gender, blood glucose > 10 mmol/l on ICU admission, and original comorbidities were used for matching to get the 1:1 matched cohort. The Kaplan–Meier survival curves were graphed to describe the survival trend and Cox regression analysis was performed to get adjusted hazard ratio (HR).Results: Compared with the preadmission non-insulin-treated T2DM patients, preadmission insulin-treated T2DM patients had higher incidence of hypoglycemia [14.5% (33/228) vs 8.7% (26/300); p = 0.036]. In the 1:1 matched cohort, the preadmission insulin-treated T2DM patients had significantly increased mortality rate [30.0% (45/150) vs (16.0% (24/150)); adjusted HR, 1.68 (1.01– 2.80)] than preadmission non-insulin-treated T2DM patients. Compared with T2DM patients treated without insulin before and after ICU admission, preadmission insulin-treated T2DM patients had higher mortality and longer length of ICU stay (all p < 0.05).Conclusion: Preadmission insulin treatment was associated with increased mortality rate and longer length of ICU stay among T2DM patients in ICU. Preadmission insulin-treated T2DM patients might have worse clinical outcomes when they are critically ill.Keywords: insulin treatment, intensive care units, type 2 diabetes mellitus, mortality, ICU stay

Aims: This study aimed to explore the new role of telomere length (TL) in the novel classification of type 2 diabetes mellitus (T2DM) patients driven by cluster analysis. Materials and Methods: A total of 541 T2DM patients were divided into 4 subgroups by k-means analysis: mild obesity-related diabetes (MOD), severe insulin-deficient diabetes (SIDD), severe insulin-resistant diabetes (SIRD), and mild age-related diabetes (MARD). After patients with insufficient data were excluded, further analysis was conducted on 246 T2DM patients. The TL was detected using telomere restriction fragment, and the related diabetic indexes were also measured by clinical standard procedures. Results: The MARD group had significantly shorter TLs than the MOD and SIDD groups. Then, we subdivided all T2DM patients into the MARD and NONMARD groups, which included the MOD, SIDD, and SIRD groups. The TLs of the MARD group, associated with age, were discovered to be significantly shorter than those of the NONMARD group (p = 0.0012), and this difference in TL disappeared after metformin (p = 0.880) and acarbose treatment (p = 0.058). The linear analysis showed that metformin can more obviously reduce telomere shortening in the MARD group (r = 0.030, 95% CI 0.010–0.051, p = 0.004), and acarbose can more apparently promote telomere attrition in the SIRD group (r = –0.069, 95% CI –0.100 to –0.039, p< 0.001) compared with other T2DM patients after adjusting for age and gender. Conclusions: The MARD group was found to have shorter TLs and benefit more from the antiaging effect of metformin than other T2DM. Shorter TLs were observed in the SIRD group after acarbose use.

Type 2 diabetes mellitus (T2DM) patients are at a higher risk of developing Alzheimer’s disease (AD). Mounting evidence suggests the emerging important role of circadian rhythms in many diseases. Circadian rhythm disruption is considered to contribute to both T2DM and AD. Here, we review the relationship among circadian rhythm disruption, T2DM and AD, and suggest that the occurrence and progression of T2DM and AD may in part be associated with circadian disruption. Then, we summarize the promising therapeutic strategies targeting circadian dysfunction for T2DM and AD, including pharmacological treatment such as melatonin, orexin, and circadian molecules, as well as non-pharmacological treatments like light therapy, feeding behavior, and exercise.

Circadian rhythms, type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) are closely related and interacted with each other. We have previously showed circadian disruption aggravated progression of AD in T2DM mice. Time-restricted feeding (TRF) is shown to be a potential synchronizer. This study aims to determine whether TRF has a protective effect against the circadian disruption-aggravated progression of AD in T2DM. 6-week-old male diabetic (db/db) mice and wildtype (wt/wt) mice were kept under normal 12:12 light/dark cycles or altered 6:18 light/dark cycles (dark extended to 18 h) with or without TRF (food restricted to 8 h during the active (dark) period). After 8 weeks, three behavioral tests (open field test, novel object recognition test, barnes maze test) were performed and the circadian gene expression, body weight, lipid levels and AD-associated tau phosphorylation were evaluated. We found altered light/dark cycles contributed to disruptive circadian rhythms in the hippocampus of db/db mice, while TRF prevented this effect. TRF also ameliorated circadian disruption-aggravated increased body weight and lipid accumulation in db/db mice. Importantly, the db/db mice under circadian disruption showed impaired cognition accompanied by increased tau phosphorylation, whereas TRF reversed these changes. The altered light/dark cycles only affected circadian rhythms but not other indicators like plasma/liver lipids, cognition and tau phosphorylation in the wt/wt mice. Collectively, TRF has a protective effect against altered light/dark cycles-aggravated AD progression in diabetic mice.

Aims: Although insulin treatment is widely used in critically ill patients with type 2 diabetes mellitus in the intensive care unit (ICU), the clinical outcomes of insulin treatment remain unclear. This retrospective study aimed to explore the impact of insulin treatment on mortality and ICU stay among patients with type 2 diabetes. Methods: We consecutively recruited 578 ICU patients with type 2 diabetes, from 2011 to 2021. According to their medication history regarding insulin use before and after ICU admission, these patients were categorized into three groups: N-N (treated without insulin before and after ICU admission), N-I (treated without insulin before and with insulin after ICU admission) and I-I (treated with insulin before and after ICU admission). Clinical characteristics were analyzed, and clinical outcomes including mortality and the length of ICU stay were compared between the groups. Propensity score matching was performed to obtain comparable subpopulation and the Kaplan-Meier survival curves were graphed to describe the survival trend of different groups. Results: Compared with the N-N group, the N-I and I-I groups had significantly higher ICU mortality rates [20.0% (N-I) and 24.6% (I-I) vs. 0.0% (N-N); p < 0.001; respectively] and longer lengths of ICU stay [ 8.5 (N-I), 9 (I-I) vs. 6 (N-N), p < 0.05, respectively]. After propensity score matching, the N-I group had a significantly higher ICU mortality (15.4% vs. 0.0%, p = 0.025) and poorer survival rates (log-rank p = 0.040) than the N-N group. The length of ICU stay was significantly longer in the I-I group than in the N-N group (10 vs. 7, p = 0.026). Conclusions: Insulin treatment was associated with increased ICU mortality rate and longer length of ICU stay among critically ill patients with type 2 diabetes. Caution is warranted for the regular application of insulin in critical patients with type 2 diabetes.

Background: Leukocyte telomere length (LTL) has been revealed to be associated with aging-related diseases such as metabolic syndrome (MetS) and Type 2 diabetes mellitus (T2DM). We aimed to investigate the correlation of LTL with MetS and its components in T2DM patients in this cross-sectional study. Materials and Methods: A total of 344 T2DM patients were enrolled into this study. LTL was measured by Southern blot-based terminal restriction fragment length analysis. MetS was clinically defined by 2007 Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults. Results: Of 344 T2DM patients, 53% had MetS. T2DM patients with MetS had significantly longer LTL than those without MetS (6451.95 ± 51.10 base pairs vs. 6076.13 ± 55.13 base pairs, P < 0.001), especially when T2DM patients had poor glycemic control (hemoglobin A1c ≥7%). Meanwhile, the trend of longer LTL was associated with the increased components of MetS in T2DM patient. Finally, LTL had a significant association with MetS (odds ratio [OR]: 2.096, 95% confidence interval [CI] 1.337–3.285, P = 0.001), low levels of high-density lipoprotein-cholesterol (HDL-C) (OR: 2.412, 95% CI 1.350–4.308, P = 0.003) in T2DM patients. Conclusion: T2DM patients with MetS had a significantly longer LTL than those without MetS. The longer LTL was especially evident in T2DM patients with poor glycemic control. Longer LTL was positively associated with MetS, particularly low levels of HDL-C in T2DM patients.

Introduction: Type 2 diabetes mellitus (T2DM) has a significantly increased risk of developing Alzheimer’s disease (AD). Amyloid-β (Aβ) as one of the main pathological features in AD increases in the brain of T2DM. A recent study identified a protective novel subset of microglial­ in AD—disease-associated microglia (DAM), the activation of which depends on TREM2(a myeloid cell membrane receptor) to phagocytose Aβ plaques. However, as to how T2DM increases Aβ deposition and the relationship between T2DM with DAM remain elusive. Objective: This study aims to explore the relationship between progression of T2DM with DAM and Aβ. Methods: In vivo experiment, the deposition of Aβ, inflammation as well as the phenotype of DAM were evaluated by RT-PCR and immunofluorescence in the cortex and hippocampus of 10-,15-,20-week old db/db mice and the age-matched WT control. Additionally, the effects of high insulin-induced insulin resistance (100nM) on the DAM signature markers and the production of inflammatory cytokines in BV-2 microglial cells were investigated in vitro. Results: We found the soluble and insoluble Aβ40, Aβ42, Aβ plaques as well as inflammation in the cortex and hippocampus increased in the progression of T2DM. Correspondingly, the DAM phenotype was reduced in the cortex and hippocampus at relatively early stage of T2DM (10 weeks and 15 weeks), while it increased reactively at the late stage (20 weeks). Likewise, high insulin-stimulated BV-2 microglial cells showed reduced Trem2 level and DAM signature markers and increase inflammation as well as Erk1/2 level. However, after the treatment of Erk1/2 inhibitor, the BV-2 cells under high insulin showed restored Trem2 level and DAM phenotype. Conclusion: T2DM brain has decreased DAM phenotype at a relatively early stage, which may explain the increased Aβ deposition. This may involve Erk1/2 -Trem2 signaling pathway, which could be a potential candidate especially at early stages for preventing T2DM-induced AD. Disclosure X. Peng: None. Funding National Natural Science Foundation of China (81974114)

The circadian clock is an endogenous system designed to anticipate and adapt to daily changes in the environment. Alzheimer’s disease (AD) is a progressive neurodegenerative disease, which is more popular in patients with type 2 diabetes mellitus (T2DM). However, the effect of circadian disorder on mental and physical health for T2DM patients are not yet fully understood, even though circadian disruption has been confirmed to promote the progression of AD in population. By housing db/db mice on a disrupted (6:18 light/dark cycle) circadian rhythm, we assessed the circadian gene expression, body weight, cognitive ability and AD-related pathophysiology. Our results indicated housing in these conditions had disrupted diurnal circadian rhythms in hippocampus and contributed to weight gain. In the brain, circadian-disrupted db/db mice showed a decreased cognitive ability and an increased hyperphosphorylation of tau protein, even though no difference was found in Aβ deposition. We also found that the hyperphosphorylated tau protein exhibited more disruptive daily oscillations in db/db mice hippocampus under 6:18 light/dark cycle. circadian alterations could promote the development of AD in T2DM.

Purpose The differential diagnosis of ACTH-dependent Cushing’s syndrome remains a challenge in clinical practice. The aim of the present study was to assess the diagnostic performance of pituitary dynamic enhanced MRI(dMRI), high-dose dexamethasone suppression test༈HDDST༉and combination of both tests in patients with ACTH-dependent Cushing’s syndrome. Methods 119 consecutive cases with surgery confirmed ACTH-dependent Cushing’s syndrome were enrolled: 101 patients with proven Cushing’s disease and 18 patients with proven ectopic ACTH syndrome. All patients underwent pituitary dMRI and HDDST. The sensitivity and the specificity of pituitary dMRI, HDDST, and combination of both tests were calculated. Results The sensitivity and specificity of the pituitary dMRI for the diagnosis of Cushing’s disease was 80.2% and 83.3% respectively, and the positive predictive value was 96.4%. The sensitivity and specificity of HDDST was 70.3% and 77.8%, and the positive predictive value was 94.7%. Regarding the combination of both tests, the combined criteria of a more than 50% suppression of serum cortisol in HDDST and a positive finding in pituitary dMRI had given a high specificity of 94.4% and a sensitivity of 59.4%. The combined criteria of a greater than 68% suppression in HDDST and/or a positive finding in pituitary dMRI, provide a sensitivity of 86.1% and a specificity of 83.3%. Conclusions Pituitary dMRI was superior to HDDST in the differential diagnosis of ACTH-dependent Cushing’s syndrome. HDDST was recommended to combined with pituitary dMRI in the diagnosis process because of the significantly increased specificity of the combination.

The circadian clock is an endogenous system designed to anticipate and adapt to daily changes in the environment. Alzheimer's disease (AD) is a progressive neurodegenerative disease, which is more prevalent in patients with type 2 diabetes mellitus (T2DM). However, the effects of circadian disruption on mental and physical health for T2DM patients are not yet fully understood, even though circadian disruption has been confirmed to promote the progression of AD in population. By housing db/db mice on a disrupted (a 6:18 light/dark cycle) circadian rhythm, we assessed the circadian gene expression, body weight, cognitive ability, and AD-related pathophysiology. Our results indicated that housing in these conditions led to disrupted diurnal circadian rhythms in the hippocampus of db/db mice and contributed to their weight gain. In the brain, the circadian-disrupted db/db mice showed a decreased cognitive ability and an increased hyperphosphorylation of tau protein, even though no difference was found in amyloid protein (Aβ) plaque deposition. We also found that the hyperphosphorylated tau protein exhibited more disruptive daily oscillations in db/db mice hippocampus under the 6:18 light/dark cycle. Circadian alterations could promote the development of AD in T2DM.

Highlights • Glycemic control may be affected during the epidemic of COVID-19. • The factors affecting glycemic control in patients with type 2 diabetes included age, education level, glucose monitoring equipment availability, medication adherence and the frequency of self-monitoring of blood glucose. • The factor affecting glycemic control in patients with type 1 diabetes was education level. • During the pandemic, diabetes self-management education should focus on medication adherence and glucose monitoring., Aims This study assessed factors contributing to glycemic control among diabetes mellitus patients complying with home quarantine during the epidemic of coronavirus disease 2019 (COVID-19). Methods We conducted an analytical cross-sectional study by telephone with 1159 patients with type 2 diabetes mellitus(T2DM)and 96 patients with type 1 diabetes mellitus (T1DM)who were discharged from the endocrinology department of a hospital from January 1, 2019, to January 24, 2020. According to their fasting blood glucose (FBG) and 2-h postprandial BG (2hPBG) values, the patients were divided into the well-controlled BG group and the poorly controlled BG group. The main evaluation indicators included sociodemographic variables, health risk variables and adherence to self-management behaviors. Results In total, 74.46% of the T2DM patients and 64.89% of the T1DM patients had poor glycemic control. T2DM patients with poor glycemic control were more likely to be older (odds ratio (OR): 1.017 [95% confidence interval (CI) 1.003-1.030]; P=0.013), have fewer than 12 years of education (OR: 1.646 [95% CI 1.202-2.255]; P=0.002), lack a BG meter at home (OR: 2.728 [95% CI 1.205-6.179]; P=0.016), have a lower degree of medication compliance (OR: 1.627 [95% CI 1.076-2.460]; P=0.021), and engage in less self-monitoring of BG (SMBG) per week (OR: 10.884 [95% CI 5.883-20.139]; P

Aeolian deposits (including aeolian sands and loess deposits) are widely distributed in the Poyang Lake region located in the middle reaches of the Yangtze River. The chronology and provenance, and their environmental implications, of these aeolian sediments have been debated for decades. Based on the OSL chronology, sedimentology, grain size analysis, and elementary data, we conclude that: (1) The source materials for the aeolian sediments in the Poyang Lake region originated from the local flood plains of the Yangtze River and its tributary Ganjiang River, whose fine materials were transported by the strong northwestern winter monsoon wind. (2) Aeolian deposits occurred throughout Late Pleistocene. Loess has a timing interval of 160–25 ka, concentrating in 115–50 ka. Sand accumulated as early as 115 ka, actively occurred during 85–80 ka. (3) Compared with the channel of the Yangtze River of today, the channel was further to the north before 80–85 ka in the Last Interglaciation, and shifted southward afterward.