Type 2 diabetes mellitus (T2DM) is closely associated with obesity and metabolic disturbances. Although diet quality has been linked to metabolic outcomes, its role relative to adiposity remains unclear. This study aimed to evaluate differences in biochemical parameters across body mass index (BMI) categories and examine relationships between diet quality and biochemical markers.

This cross-sectional study included 150 individuals with T2DM aged 46-60 years attending an endocrinology outpatient clinic between September 2023 and May 2024. Participants were classified as being of normal weight, overweight, or obese based on BMI. Diet quality was assessed using three-day food consumption records and calculated using the Healthy Eating Index-2015 (HEI-2015). Biochemical parameters were obtained from medical records. Between-group comparisons were performed using one-way ANOVA with Bonferroni post hoc tests and Pearson correlation analysis was used to assess associations. Benjamini-Hochberg false discovery rate (BH-FDR) correction was applied for multiple testing.

Several biochemical parameters differed significantly across BMI categories (p <0.05). Obese individuals had higher triglyceride, uric acid, C-reactive protein, liver function, and fasting insulin levels, whereas normal-weight individuals had higher high-density lipoprotein cholesterol and estimated glomerular filtration rate. No significant differences were observed in HEI-2015 scores across BMI groups (p >0.05). Weak correlations between diet quality and biochemical markers were not significant after BH-FDR correction.

Biochemical parameters differed across BMI categories, highlighting the role of adiposity in metabolic risk. Associations between diet quality and biochemical markers were limited, suggesting that BMI-based stratification may be more informative than diet quality alone.

Diabetic retinopathy (DR) is a leading cause of visual impairment and blindness in industrialized countries, resulting from diabetes mellitus. Prostaglandin E₂ (PGE₂), synthesized by cyclooxygenases, contributes to inflammation and apoptosis via the E-prostanoid receptor 2 (EP₂R). Our previous studies demonstrated that EP₂R antagonists mitigate inflammation and microvascular dysfunction in streptozotocin (STZ)-induced DR. Given the paracrine role of extracellular vesicles (EVs) in DR, we hypothesized that EVs derived from human endothelial cells (ECs) may regulate the PGE₂/EP₂R pathway in DR. Using an STZ-induced diabetic mouse model, we administered intravitreal injections of AAV2-shEP₂R and evaluated retinal histology, optical coherence tomography, and biochemical markers. EV morphology, size, and concentration from high glucose (HG)-treated ECs were analyzed. Small RNA expression in plasma EVs from DR patients was assessed via deep sequencing. EP₂R inhibition via AAV2-mediated knockdown significantly reduced retinal vascular leakage, leukostasis, and retinal Müller cell (rMC) activation. MiRNA profiling revealed elevated levels of miR-423-5p and miR-21-5p in EVs from HG-treated ECs, which were suppressed in EVs from EP₂R antagonist-treated cells. Notably, deep sequencing of plasma EVs from DR patients confirmed significant upregulation of these miRNAs compared to healthy controls. MiR-423-5p and miR-21-5p function as key paracrine mediators promoting Müller cell activation and retinal microvascular dysfunction in DR. These findings highlight the potential of circulating EVs as vehicles for miRNA-based therapeutic interventions in DR.

Clostridium innocuum is an anaerobic gram-positive spore-forming bacteria, a commensal member of the human gut microbiome. We encountered a case of bacteremia with this organism as a complication of a foot ulcer in a middle-aged patient with diabetes, end-stage renal disease, and malnutrition. A systematic review of the limited number of previously reported cases of C. innocuum bacteremia is presented, along with a brief narrative review the organism's association with other diseases, ranging from diarrhea and local infections to modulating inflammatory bowel disease and kidney disease.

Sleep disturbances affect up to half of older adults with type 2 diabetes mellitus (T2DM) and represent a clinically meaningful but under addressed dimension of diabetes care. Metformin, the universally recommended first-line agent for T2DM, exerts multiple pleiotropic effects, including modulation of AMPK signaling, circadian clock gene expression, neuroinflammation, and neuropathic pain, that are each mechanistically relevant to sleep regulation. Although metformin may influence pathways relevant to sleep, the evidence linking metformin use to sleep outcomes in older adults with T2DM has not been systematically reviewed. This narrative review was conducted in accordance with the SANRA framework, drawing on a systematic search of PubMed, Scopus, and Web of Science covering literature published between 2008 and 2025. Studies were included if they reported sleep outcomes in T2DM patients aged 60 years or older involving metformin, or if they provided mechanistic evidence relevant to the metformin-sleep interface. Both subjective and objective sleep measures were considered alongside mechanistic, pharmacological, and safety evidence. Metformin's pleiotropic pharmacology converges on four biologically plausible pathways through which sleep may be improved in elderly T2DM patients: glycemic stabilization reducing nocturia, AMPK-dependent attenuation of neuroinflammation, modulation of circadian clock gene expression, and neuroprotective effects preserving sleep-regulating neural circuits. Available clinical evidence suggests modest improvements in sleep-related outcomes, particularly among patients with Pittsburgh Sleep Quality Index scores above 5, although observational study designs and the absence of dedicated randomized trials limit causal inference. Rare adverse sleep effects, including vivid dreams and nightmares, appear uncommon and generally resolve with dose adjustment. Further randomized controlled trials are warranted to determine the effects of metformin on sleep outcomes in elderly patients with T2DM.

Pancreatic resection is associated with a high frequency of postoperative new-onset diabetes mellitus (NODM). The present study aimed to quantify the rate and investigate potential risk factors for NODM after distal pancreatectomy.

Data on patients undergoing distal pancreatectomy between 2010 and 2020 were obtained from the Swedish National Pancreatic and Periampullary Cancer Registry and cross-referenced with the Swedish National Diabetes Register. Uni- and multivariable competing risk regression analyses were conducted to model sub-distribution hazards (SHR) of NODM between groups.

A total of 1,034 patients were included, with 290 (28%) developing NODM postoperatively. The risk of NODM was reduced for female patients (SHR 0.73, p = 0.014) and those in the minimally invasive surgery group (SHR 0.54, p = 0.002). Conversely, the risk was increased for obese patients (SHR 2.23, p < 0.001), older patients (SHR 1.01, p = 0.006), patients with American Society of Anesthesiologists classifications 2 and 3 (SHR 2.03, p < 0.001 and SHR 1.61, p = 0.037, respectively), and those with benign pancreatic tumors (SHR 1.43, p = 0.020).

NODM was common among patients after distal pancreatectomy, with several patient and surgical factors influencing risk. A minimally-invasive approach was associated with a lower risk of NODM after surgery. This association warrants further study, but should be interpreted cautiously due to potential selection bias and residual confounding, but it warrants further study.

This perspective outlines a clinical roadmap for integrating adjunctive metabolic therapies into the care of people with type 1 diabetes. Despite major advances in insulin delivery and technology, cardiometabolic risk, weight gain, and glycemic variability remain significant challenges. We propose an evidence-based approach, which expands beyond insulin alone and highlights a metabolic therapy tree: low-hanging fruit such as incretin-based therapies and amylin analogs; slightly higher fruit including sodium-glucose linked transporter inhibitors unlocked through safety engineering and continuous ketone monitoring; and emerging targets such as glucagon modulation and fibroblast growth factor 21 analogs.

Even with the most advanced insulin preparations and delivery systems currently available, it is challenging for many people with type 1 diabetes (T1D) to achieve target levels of glycemic management. Adjunct therapy in T1D consists of adding glucose-lowering agents besides insulin with the aim of lowering hemoglobin A1c (HbA1c) and improving other health outcomes, including weight. It is an attractive potential strategy for achieving glycemic targets and other benefits in this T1D subpopulation. While not yet Food and Drug Adminstration (FDA)-approved for this use, incretin-based therapies (glucagon-like peptide-1 receptor agonist-based therapy) and sodium-glucose cotransporter-1/2 (SGLT-1/2) inhibitors are being prescribed off-label for T1D.

Diabetes-related kidney disease (DKD) is a major complication of type 1 diabetes (T1D) and remains a leading cause of kidney failure and cardiovascular risk. In this article, we summarize the biologic rationale and emerging clinical evidence for adjunctive kidney-protective therapies in T1D. We frame DKD pathophysiology in T1D around 3 interrelated domains: hyperglycemia-driven kidney stress, maladaptive tubular-glomerular hemodynamics and hyperfiltration, and inflammatory and fibrotic injury amplified by mineralocorticoid receptor signaling. The rapid growth in mechanistic understanding, clinical trial evidence, and early translation to T1D supports the incorporation of adjunctive kidney-protective therapies into the future management of DKD in T1D.

Sodium-glucose cotransporter inhibitors, glucagon-like peptide 1 receptor agonists and mineralocorticoid receptor blockers have revolutionized type 2 diabetes and by providing substantial cardiovascular and renal protection in this. This article summarizes the data for these newer agents in type 1 diabetes (T1D). Here we also emphasize the need for more long-term studies of these agents in T1D to assess their impact on cardiovascular risk.

This article highlights the increased risk of cardiovascular and renal disease in individuals with type 1 diabetes (T1D). In recent years, the treatment landscape of type 2 diabetes has been revolutionized beyond strictly glycemic and metabolic effects by drugs, which have been shown to have additional benefits, including substantial cardiovascular and renal protection. However, until very recently, individuals with T1D were excluded from most trials that evaluated cardiovascular disease (CVD) and chronic kidney disease (CKD) risk with these agents. Here we discuss the data highlighting the high CVD, heart failure (HF), and CKD risk in T1D.