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We aimed to assess whether the safety outcomes exerted by sodium-glucose cotransporter 2 (SGLT2) inhibitors were associated with different renal function at baseline.

We searched randomized controlled trials comparing SGLT2 inhibitors with placebo in participants simultaneously involving the entire range of estimated glomerular filtration rate (eGFR) levels at baseline in one study. According to eGFR, we divided the population into two subgroups with eGFR <60ml/min/1.73m
and eGFR≥60ml/min/1.73m
. Data from the CANVAS program, CREDENCE, EMPA-REG OUTCOME, DECLARE-TIMI 58, DAPA-HF, and EMPA-REG RENAL were included. SGLT2 inhibitors significantly reduced the risk of all serious adverse events (HR 0.91 [95% CI 0.87 to 0.95], p<0.001) and acute kidney injury (HR 0.74 [95% CI 0.64 to 0.85], p<0.001). Except for high risk of genital infection, SGLT2 inhibitors did not increase the risk of amputation, fracture, hyperkalemia, hypoglycemia, volume depletion, or urinary tract infection. Further analyses showed that these safety outcomes were similar between subgroups (p-interaction>0.05). For osmotic diuresis, SGLT2 inhibitors significantly increased the risk by 75% (p=0.036), and subgroup analyses showed that this effect was completely attributed to the increase in patients with eGFR ≥60ml/min/1.73m
(p-interaction<0.001).

The indication of no risk of osmotic diuresis in patients with eGFR<60ml/min/1.73m
and the consistency of other safety outcomes across different baseline renal function may allow additional individuals to safely use SGLT2 inhibitors.
The indication of no risk of osmotic diuresis in patients with eGFR less then 60 ml/min/1.73 m2 and the consistency of other safety outcomes across different baseline renal function may allow additional individuals to safely use SGLT2 inhibitors.Bone fragility is one of the possible complications of diabetes, either type 1 (T1D) or type 2 (T2D). Bone fragility can affect patients of different age and with different disease severity depending on type of diabetes, disease duration and the presence of other complications. Fracture risk assessment should be started at different stages in the natural history of the disease depending on the type of diabetes and other risk factors. The risk of fracture in T1D is higher than in T2D, imposing a much earlier screening and therapeutic intervention that should also take into account a patient's life expectancy, diabetes complications etc. The therapeutic armamentarium for T2D has been enriched with drugs that may influence bone metabolism, and clinicians should be aware of these effects. Considering the complexity of diabetes and osteoporosis and the range of variables that influence treatment choices in a given individual, the Working Group on bone fragility in patients with diabetes mellitus has identified and issued recommendations based on the variables that should guide screening of bone fragility and management of diabetes and bone fragility (A)ge, (B)MD, (C)omplications, (D)uration of disease, & (F)ractures (ABCD&F). Consideration of these parameters may help clinicians identify the best time for screening, the appropriate glycaemic target and anti-osteoporosis drug for patients with diabetes at risk of or with bone fragility.
Obesity has been linked to the development of hypertension, but the comparison of relationships between different obesity parameters with hypertension are scarcely studied with nationally representative Chinese adults samples. We sought to compare the predictive strengths of different obesity indicators to hypertension.

Data in this study were obtained from the Chinese National Stroke Prevention Project with a nationally representative sample of Chinese aged 40 years and older. A total of 162,880 individuals were included. Xevinapant Multi-level analyses and Receiver Operating Characteristic (ROC) curves were used to examine the risk of hypertension in relation to different obesity parameters, including body mass index (BMI), waist circumference (WC), lipid accumulation product index (LAP), visceral adiposity index (VAI), and body adiposity index (BAI). As results, the BMI, WC, LAP, VAI, and BAI were positively associated with the risk of hypertension (P<0.001). In total, BMI had the strongest association with hypertension when compared with other obesity indicators, and one SD up of BMI would increase the risk of hypertension by 53.9% (95% CI 1.514-1.566). For men, WC was most associated with hypertension, and one SD up of WC would increase the risk of hypertension by 73.3% (95% CI 1.685-1.782). For women, BMI showed the strongest predictive power, one SD up of BMI would increase the risk of hypertension by 51.0% (95% CI 1.479-1.543).

BMI, WC, LAP, VAI, and BAI are all positively corrected to hypertension, but gender disparities should be considered in predicting hypertension by obesity indicators.
BMI, WC, LAP, VAI, and BAI are all positively corrected to hypertension, but gender disparities should be considered in predicting hypertension by obesity indicators.
Coronary artery bypass graft (CABG) using autologous saphenous vein continues to be a gold standard procedure to restore the supply of oxygen-rich blood to the heart muscles in coronary artery disease (CAD) patients with or without type 2 diabetes mellitus (T2DM). However, CAD patients with T2DM are at higher risk of graft failure. While failure rates have been reduced through improvements in procedure-related factors, much less is known about the molecular and cellular mechanisms by which T2DM initiates vein graft failure. This review gives novel insights into these cellular and molecular mechanisms and identifies potential therapeutic targets for development of new medicines to improve vein graft patency.

One important cellular process that has been implicated in the pathogenesis of T2DM is protein O-GlcNAcylation, a dynamic, reversible post-translational modification of serine and threonine residues on target proteins that is controlled by two enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Protein O-GlcNAcylation impacts a range of cellular processes, including trafficking, metabolism, inflammation and cytoskeletal organisation. Altered O-GlcNAcylation homeostasis have, therefore, been linked to a range of human pathologies with a metabolic component, including T2DM.

We propose that protein O-GlcNAcylation alters vascular smooth muscle and endothelial cell function through modification of specific protein targets which contribute to the vascular re-modelling responsible for saphenous vein graft failure in T2DM.
We propose that protein O-GlcNAcylation alters vascular smooth muscle and endothelial cell function through modification of specific protein targets which contribute to the vascular re-modelling responsible for saphenous vein graft failure in T2DM.
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