Dyslipidemia is prevalent among Nigerians with diabetes mellitus (DM), but its treatment has not been well-studied. The objective of this study was to determine the prevalence, treatment rates and control of dyslipidemia among DM patients in northern Nigeria.

We conducted a multicenter, cross-sectional study of dyslipidemia in DM patients, and noted cardiovascular disease (CVD) risk factors, lipid-lowering treatments, body mass index, blood pressure, HbA1c, lipid profile, glomerular filtration rate and proteinuria. Outcome measures were the rate and treatment of dyslipidemia and attainment of low density lipoprotein cholesterol target for primary prevention of CVD. Binomial logistic regression was used to analyze associations between participant characteristics and dyslipidemia. Hosmer-Lemeshow goodness-of-fit test was used to evaluate the model fit. Statistical analysis was performed with the SPSS version 25 program.

The study enrolled 403 participants (58.8% females), of whom 59.6% had dyslipidemia. Besides DM and dyslipidemia, other risk factors for CVD were hypertension (56.8%), obesity (52.6%), chronic kidney disease (36.5%), atrial fibrillation (7.9%), heart failure (5.0%), cigarette smoking (4.7%), excess alcohol use (2.0%), and previous CVD (14.4%). Logistic regression analysis showed dyslipidemia was significantly associated with female gender (odds ratio = 1.68, P = 0.029) and proteinuria (odds ratio = 2.26, P = 0.004). Among those with dyslipidemia, 51.3% took lipid-lowering treatments comprising statins (50.8%) and clofibrate (2.9%). None took other lipid-lowering treatments, and only 17.1% attained the target for primary prevention of CVD.

Three-fifths of patients had dyslipidemia, but only a sixth attained the treatment target. Treatment for dyslipidemia included statins and fibrates, but not niacin, ezetimibe, bempedoic acid, icosapent ethyl, inclisiran or PCSK9 inhibitors recommended for those who failed intensive statin therapy. There is the need for better access to non-statin treatment and physician adherence to clinical practice guidelines.

As the global incidence of diabetes and its associated treatment costs rise, continuous glucose monitors (CGMs) constitute a valuable tool for patient self-monitoring. However, market dominance of a few well-known brands, predominantly in populations with type 1 diabetes, limits the adoption of more cost-effective alternatives that might offer improved clinical outcomes. To address this, an expert roundtable evaluated barriers to efficient CGM use, identifying challenges such as regional care board variations, lack of patient-centred prescribing and insufficient training for both patients and healthcare professionals (HCPs). The panel suggested implementing more individualised prescribing, such as accessible readers for elderly patients, and expanding HCP education. Moreover, more streamlined integration of CGM data into electronic health records would reduce admin burden, while helping to facilitate remote monitoring to encourage patient self-management. Individualised CGM prescription, alongside improved workflows for HCPs around prescribing and addressing patient queries, could significantly lower healthcare costs while improving diabetes care in the UK.

Amylin is a pancreatic beta-cell hormone that sits at a systems hub connecting key aspects of energy metabolism. Amylin physiologically controls satiation, slows gastric emptying and limits postprandial glucagon release, while its actions also link homeostatic eating controls with reward driven behaviours via defined central nervous system pathways. Further, at least under certain conditions, aggregating amylin exerts a strong pathophysiological impact on the destruction of pancreatic beta-cells in Type 2 diabetes mellitus (T2D), providing a plausible explanation for why a T2D-like disease entity is only observed in a few mammalian species. This review will provide a brief summary of selected aspects of our current understanding of the biology of amylin and outlines how this knowledge has recently been translated into effective pharmacotherapy for obesity and diabetes, including long-acting analogs combination approaches with other peptide hormones.

This article begins by providing historical insight into the discovery, development, and use of glucagon-like peptide-1 receptor (GLP-1R) agonist medications in the treatment of type 2 diabetes and obesity. Next, the mechanism of action and impacts of GLP-1R agonists are discussed, along with an overview of the Food and Drug Administration-approved GLP-1R agonists currently on the market. Comparison in effects on weight loss of the available GLP-1R agonists is briefly discussed, along with its use in the context of bariatric surgery. Finally, perioperative considerations for surgical patients using GLP-1R agonists are reviewed along with suggested recommendations.

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease. ELAVL1, an RNA-binding protein, is involved in the regulation of genes closely associated with DN pathogenesis, whereas suPAR acts as a circulating mediator that promotes podocyte damage and contributes to proteinuric kidney disorders. However, whether ELAVL1 regulates suPAR release in DN remains unexplored.

Clinical samples from patients with DN were collected and analyzed. In vitro, podocytes were treated with high glucose, and ELAVL1 or PLAUR (encoding uPAR) was knocked down or overexpressed using lentiviral transduction. In db/db mice, podocyte-specific manipulation of Elavl1 or Plaur was performed via adeno-associated virus-mediated delivery. Renal function was assessed by measuring the urinary albumin-to-creatinine ratio (UACR) and serum creatinine. Glomerular pathology and inflammatory markers were evaluated histologically and biochemically.

ELAVL1 was upregulated in DN and positively correlated with podocyte injury. Knockdown of ELAVL1 mitigated hyperglycemia-induced podocyte damage and inflammatory responses. Mechanistically, ELAVL1 directly bound to and stabilized PLAUR mRNA, leading to increased uPAR protein expression and elevated suPAR secretion. The protective effects of ELAVL1 knockdown were reversed by PLAUR overexpression in podocytes. In diabetic mice, podocyte-specific knockdown of Elavl1 or Plaur markedly lowered circulating suPAR levels and alleviated renal dysfunction and histopathological injury. Moreover, restoration of the PLAUR-suPAR axis abolished the renoprotective benefits conferred by Elavl1 knockdown.

Hyperglycemia-induced ELAVL1 upregulates PLAUR and suPAR release from podocytes, promoting renal inflammation and injury. Targeting the ELAVL1-PLAUR-suPAR axis may offer a therapeutic strategy for DN.

Sodium-glucose cotransporter 2 inhibitors (SGLT2) were initially developed as antihyperglycemic agents for the management of type 2 diabetes mellitus (T2DM). This study sought to evaluate the impact of sodium-glucose cotransporter 2 inhibitors on blood glucose levels in patients with HFrEF without diabetes.

This randomized controlled trial included 130 patients without diabetes diagnosed with HF classified as NYHA class II to IV, with an ejection fraction (EF) below 40% as determined by echocardiography within the preceding three months. Baseline assessments included serum creatinine, random and fasting blood glucose, 2-hour postprandial glucose, HbA1c, urine acetone, BMI, blood pressure, and serum electrolytes (sodium, potassium, magnesium, ionized calcium, and phosphorus). After three months of treatment, all these clinical and laboratory parameters were reassessed in both groups.

Treatment led to significant improvements in cardiac function, including reductions in left ventricular diameters and volumes, and increases in ejection fraction, tricuspid annular plane systolic excursion, and right ventricular fractional area change (P<0.05). Glycemic control also improved, with significant decreases in fasting, postprandial, HbA1c, and random blood glucose (P<0.001). Serum creatinine, magnesium, and phosphorus levels increased significantly (P<0.001). Adverse events were minimal, with only one patient showing urine acetone positivity (1.5%, P=0.99), and no symptomatic hypoglycemia, ketoacidosis, or significant hypotension occurred.

SGLT2 inhibitors safely reduce blood glucose in patients with HFrEF without diabetes without causing hypoglycemia, highlighting their potential cardiovascular and metabolic benefits and supporting their use in this population.

Pluripotent stem cell (PSC)-based therapies hold the potential to unlock cures for numerous diseases, including, but not limited to, Parkinson's disease, macular degeneration, heart failure, type 1 diabetes, and cancer. Yet as protocols to differentiate PSCs into therapeutically useful cell types have progressed rapidly, immunological rejection remains a major barrier that may limit the widespread use of such PSC-based therapies. In recent years, strategies to genetically modify PSCs to prevent immunological rejection of the downstream cell product have become a point of emphasis. Here, we provide an immunological perspective on these strategies, discussing the breadth of rejection mechanisms that have been uncovered through decades of research and the relative simplicity of designing PSC immune evasion strategies to circumvent these mechanisms. We focus in particular on how these strategies apply to the treatment of type 1 diabetes.

Type 2 diabetes mellitus (T2DM) is associated with increased cardiovascular risk, enhanced platelet activation, and substantial interindividual variability in response to aspirin. However, the term 'aspirin resistance' has been used inconsistently and is strongly influenced by the assay applied. In many cases, apparent non-response may reflect exposure-related pseudoresistance rather than true pharmacodynamic failure, particularly in the setting of enteric-coated formulations, impaired absorption, poor adherence or pharmacological interactions. This systematic review with narrative synthesis, conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISRMA) 2020, evaluated the prevalence, determinants, and clinical relevance of aspirin hyporesponsiveness in T2DM. Searches of PubMed, Embase, the Cochrane Library, and Latin American and Caribbean Health Sciences Literature identified 21 eligible studies. The reported prevalence varied widely (0-57%), mainly owing to differences in study populations, aspirin formulations, platelet function assays, and cut-off definitions. Small pharmacodynamic studies suggested that twice-daily aspirin regimens may provide greater suppression of platelet reactivity than once-daily dosing, whereas pharmacokinetic/pharmacodynamic evidence consistently indicated reduced thromboxane B2 suppression with enteric-coated aspirin. However, evidence linking laboratory-defined hyporesponsiveness with clinical outcomes was limited and inconsistent, and the largest available randomised outcome trial did not show a reduction in major cardiovascular events with twice-daily aspirin. Overall, aspirin hyporesponsiveness in T2DM appears to be multifactorial and insufficiently standardised. Current evidence does not support routine platelet function testing or empirical dose escalation. Clinical management should prioritise confirming the indication for aspirin, assessing adherence, selecting the appropriate formulation, avoiding clinically relevant drug interactions, and optimising overall cardiometabolic risk.