Acarbose, a clinically approved α-glucosidase inhibitor for type 2 diabetes, has limited efficacy due to gastrointestinal side effects, highlighting the need for delivery systems that modulate release and improve tolerability. This study aimed to develop and characterize acarbose-guar gum solid dispersions (AGSDs) and evaluate their physicochemical, in vitro, and in vivo properties. Solid-state characterization confirmed amorphous molecular dispersion with spherical particles and drug-polymer interactions. Among the developed solid dispersions, AGSD-3 showed the highest drug entrapment efficiency (84.24 ± 0.48%) and controlled dissolution (86.19 ± 1.66% over 24 h), compared to free acarbose. It exhibited strong enzyme inhibition with IC50 values of 6.97 ± 0.21 μg/mL (α-glucosidase) and 12.86 ± 0.18 μg/mL (α-amylase), along with favourable cytocompatibility and hemocompatibility. In high-fat diet (HFD)-fed, streptozotocin (STZ)-induced diabetic rat model, AGSD-3 at 50 mg/kg significantly reduced body weight and blood glucose (p < 0.001), while gastrointestinal side effects, such as diarrhoea, were limited to a single day (score 1), indicating improved tolerability compared to acarbose alone. Treatment also restored pancreatic weight (p < 0.001) and histology, and attenuated oxidative stress, and inflammation (p < 0.001), indicating protective effects against diabetes-induced tissue damage. Overall, these findings suggest that guar gum-based solid dispersion represents a promising strategy to enhance the therapeutic efficacy and tolerability of acarbose for diabetes management.

Exocrine pancreatic insufficiency (EPI) is the inability of the pancreas to produce essential digestive enzymes for fat metabolism, leading to systemic and nutritional repercussions. Although its manifestations are typically digestive, systemic complications such as enteric hyperoxaluria can occur. We present a 68-year-old man with insulin-dependent diabetes mellitus, who developed steatorrheic diarrhea and significant weight loss. Computed tomography revealed an atrophic pancreas with diffuse calcifications. Based on a diagnosis of chronic pancreatitis, pancreatic enzyme replacement therapy (PERT) was initiated empirically with clinical improvement. Three years later, while asymptomatic from a gastrointestinal perspective, he developed bilateral calcium oxalate nephrolithiasis progressing to end-stage renal disease, requiring hemodialysis. This was interpreted as oxalate nephropathy secondary to enteric hyperoxaluria, favored by suboptimal PERT dosing and poor follow-up adherence. PERT was optimized to 40,000 units per meal with good nutritional and digestive outcomes. The etiological study for EPI showed no obstructive or systemic causes. This case highlights the importance of suspecting EPI when systemic complications like secondary hyperoxaluria appear. Early diagnosis remains challenging and requires close monitoring, as specific guidelines to prevent irreversible renal damage are lacking; early recognition can significantly improve prognosis and quality of life.

Pancreatic exocrine insufficiency (PEI) is a common but frequently under-recognised condition that often presents with non-specific gastrointestinal symptoms, which may be subtle in early stages. Evidence from studies published between 2000 and 2026 indicates that, although the leading causes of PEI are pancreatic diseases such as chronic or autoimmune pancreatitis, pancreatic cancer, and pancreatic surgery, it is also increasingly recognised in common conditions including diabetes mellitus and ageing. Clinically, PEI should be suspected in patients presenting with diarrhoea, steatorrhoea, bloating, weight loss, or abdominal discomfort, particularly when malnutrition or micronutrient deficiencies are present. These deficiencies are associated with clinically relevant complications, including osteoporosis and cardiovascular disease, highlighting the importance of timely diagnosis and appropriate management. Pancreatic enzyme replacement therapy remains the cornerstone of treatment, with currently available porcine-derived formulations demonstrating high efficacy, although future research should explore alternative enzyme sources and novel therapeutic approaches.

Euglycemic ketoacidosis is metabolic acidosis with elevated ketone bodies despite normal or mildly elevated glucose levels and has rarely been reported in nonobese individuals without diabetes using tirzepatide. A 23-year-old Japanese woman without obesity presented with a 4-day history of nausea, vomiting, and diarrhea after the second self-administered dose of tirzepatide (2.5 mg) obtained through an aesthetic clinic without ongoing medical supervision. She had no history of diabetes, alcohol consumption, or carbohydrate restriction. Laboratory results showed high anion gap metabolic acidosis (anion gap: 25.9 mmol/L) [normal reference range (ref): 8-16 mmol/L], elevated serum β-hydroxybutyrate (5.5 mmol/L) (ref: <0.07 mmol/L) and acetoacetate (1.4 mmol/L) (ref: <0.01-0.07 mmol/L), with concomitant metabolic alkalosis compatible with vomiting and mild hyperglycemia (196 mg/dL [SI:10.9 mmol/L]) (ref: 70-100 mg/dL [SI: 3.9-5.6 mmol/L]). No definitive infectious source was identified on evaluation, and euglycemic ketoacidosis was diagnosed. She received intravenous fluids containing glucose, electrolytes, and continuous insulin infusion, which rapidly corrected the acidosis. Her symptoms resolved within several days, and follow-up evaluation confirmed normal glucose tolerance. This case adds to the limited clinical evidence of tirzepatide-associated euglycemic ketoacidosis in a non-obese individual without diabetes. Caution is warranted regarding the off-label use of tirzepatide for aesthetic weight reduction.