Introduction: The effect of comorbid cardiometabolic diseases (CMDs), including diabetes, heart diseases, and stroke, on dementia remains unclear.Methods: A cohort of 2648 dementia‐free adults aged ≥60 years was followed up for 12 years. An active lifestyle was defined in accordance with the engagement in leisure activities and/or a social network. Cox models were used in data analysis.Results: The multiadjusted hazard ratio (HR, 95% confidence interval) of dementia was 1.41 (1.07–1.86) for one, 2.38 (1.58–3.59) for two, and 4.76 (2.04–11.13) for three CMDs. In joint exposure analysis, the HR of dementia was 3.36 (2.14–5.30) for participants with CMDs plus an inactive lifestyle and 1.32 (0.95–1.84) for those with CMDs plus an active lifestyle (reference: no CMDs plus active lifestyle). An active lifestyle delayed dementia onset by 3.50 years in people with CMDs.Discussion: CMDs, especially when comorbid, are associated with increased dementia risk; however, leisure activities and social integration mitigate this risk.

Currently, cerebral infarction (CI) is the leading cause of disability and the second leading cause of mortality in China, seriously affecting patient quality of life. Ischemia (IS) is considered to be the early stage of CI. The present study aims to investigate the variation of intestinal microbial communities in patients with CI and IS using high throughput sequencing technology, and then analyze the results to identify a novel potential pathogenic mechanism of CI and IS. In total, 8 patients with CI, 2 patients with IS and 10 healthy volunteers as a control were selected. Throughput sequencing technology was used to analyze the character and microbial population of the gut. The abundance of Escherichia, Bacteroides, Megamonas, Parabacteroides, Akkermansia, Prevotella, Faecalibacterium, Dialister, Bifidobacterium and Ruminococcus was the significant difference in the intestinal microbial communities of the CI and IS patients compared with the healthy group. It was also observed that CI and IS were closely associated with internal glucose metabolism. The intestinal gut disturbance of CI patients may be one of the causes inducing CI by glucose metabolism and maybe considered as a potential method to predict the disease.

Statins may decrease chronic kidney diseases (CKDs) risk, but their underlying molecular mechanisms are not completely understood. Recent studies indicate Endothelial-to-mesenchymal transition (EndMT) plays an important role contributing to renal interstitial fibrosis. In the present study, we first investigated whether lovastatin could ameliorate renal fibrosis via suppression of EndMT and its possible mechanism. In vitro experiments, lovastatin significantly ameliorated microalbuminuria and pathologic changes in diabetic rats. Double labeling immunofluorescence showed lovastatin could inhibit EndMT in glomeruli. Furthermore, lovastatin could inhibit oxidative stress and down-regulate TGF-β1-Smad signaling. Consistent alterations were observed in vivo that lovastatin substantially suppressed EndMT and TGF-β1 signaling induced by high glucose in glomerular endothelial cells (GEnCs). These data indicated that lovastatin could ameliorate EndMT in glomeruli in diabetic nephropathy, the mechanism of which might be at least partly through suppression of oxidative stress and TGF-β1/Smad signaling pathway.

Olfactory dysfunction could be an early indicator of cognitive decline in type 2 diabetes (T2D). However, whether obesity affects olfaction in people with T2D is unclear. This question needs to be addressed, because most people with T2D are obese. Importantly, whether different contributing factors leading to obesity (e.g., different components of diet or gain in weight) affect specific olfactory functions and underlying mechanisms is unknown. We examined whether two T2D-inducing obesogenic diets, one containing a high proportion of fat (HFD) and one with moderate fat and high sugar (Western diet, WD), affect odor detection/discrimination, odor-related learning, and olfactory memory in the mouse. We also investigated whether the diets impair adult neurogenesis, GABAergic interneurons, and neuroblasts in the olfactory system. Here, we further assessed olfactory cortex volume and cFos expression-based neuronal activity. The WD-fed mice showed declined odor-related learning and olfactory memory already after 3 months of diet intake (p = 0.046), although both diets induced similar hyperglycemia and weight gain compared to those of standard diet-fed mice (p = 0.0001 and p < 0.0001, respectively) at this time point. Eight months of HFD and WD diminished odor detection (p = 0.016 and p = 0.045, respectively), odor-related learning (p = 0.015 and p = 0.049, respectively), and olfactory memory. We observed no changes in the investigated cellular mechanisms. We show that the early deterioration of olfactory parameters related to learning and memory is associated with a high content of sugar in the diet rather than with hyperglycemia or weight gain. This finding could be exploited for understanding, and potentially preventing, cognitive decline/dementia in people with T2D. The mechanisms behind this finding remain to be elucidated.

This meta-analysis was performed to evaluate the effect of cognitive behavioural therapy (CBT) in improving the depression symptoms of patients with diabetes. Literature search was conducted in PubMed and Embase up to October 2016 without the initial date. The pooled SMD (standard mean difference) and its 95% confidence interval (CI) were calculated by Revman 5.3. Subgroup analyses were performed by type of diabetes and evaluation criteria of depression. A total of five randomized control trials involving 834 patients with diabetes mellitus (including 417 patients in CBT group and 417 patients in control group) were included in this meta-analysis. The pooled estimates indicated significant improvement of depression by CBT compared with routine approaches in overall outcomes (SMD =–0.33, 95% CI =–0.46 to –0.21, P<0.00001), post-intervention outcomes (SMD =–0.43, 95% CI =–0.73 to –0.12, P=0.006) and outcomes after 12 months intervention (SMD =–0.38, 95% CI = –0.54 to –0.23, P<0.0001). Subgroup analyses showed that the results were not influenced by the type of diabetes. However, the effect of CBT on improving the depression symptoms disappeared when only using CES-D (Centre for Epidemiological Studies scale for Depression) to evaluate depression.