The role of glucose restriction in host antiviral defense remains elusive. Here, we investigate the impact of pre-existing hypoglycemia on host susceptibility to influenza infections. We find that mouse models with intermittent hypoglycemia exhibit heightened vulnerability to influenza A virus (IAV) infections at low to moderate exposure levels. This vulnerability is attributed to reduced expression of TRIM5 in the lung subsequent to hypoglycemic stress. Hypoglycemic stress activates AMPK protein to down-regulate ERK1/2 signaling and inhibit the transactivation activity of AP-1, thereby suppressing Trim5 transcription. Diminished expression of TRIM5 renders the animals more susceptible to influenza infections as it compromises pulmonary antiviral immunity by attenuating type I interferon (IFN-I) production and signaling. These findings provide mechanistic insights into how pre-existing hypoglycemia detrimentally impacts host antiviral defense, and establish TRIM5 as a molecular link connecting metabolic stress to innate antiviral immunity.

The glucose-dependent glucagonotropic effects of glucose-dependent insulinotropic polypeptide (GIP) variants in type 1 diabetes (T1D) are incompletely understood. We investigated whether native full-length GIP[1-42] and its truncated variant GIP[1-30]NH2 increase glucagon concentrations during insulin-induced hypoglycemia in individuals with T1D. During euglycemia, both GIP variants increased glucagon [statistically significantly for GIP(1-30)NH2 only] and norepinephrine, but insulin suppressed glucagon levels similarly across interventions. High-dose GIP[1-42] was associated with slightly reduced glucose requirements during recovery from hypoglycemia, suggestive of increased hepatic glucose production through either glucagon or norepinephrine action.

Solitary fibrous tumors are mesenchymal neoplasms that make up 2% of soft tissue tumors. Doege-Potter syndrome (DPS) occurs between 5-10% of patients with solitary fibrous tumor of the pleura (SFTP). Little is mentioned about DPS in the relapse setting, where malignant transformation should always be ruled out (until 12% of cases) according to tumor size, histopathologic aspects (including mitotic index) and immunohistochemical markers. This is the first case of Doege-Potter syndrome in the setting of a fibrous tumor relapse of the pleura without malignant transformation described in Colombia.

Background: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual GLP-1/glucose-dependent insulinotropic polypeptide receptor agonists (GLP-1/GIP RAs) effectively manage type 2 diabetes mellitus (T2DM). Recent medication shortages have impacted patient access to treatment. The objectives of this study were to evaluate the effect of incretin therapy shortages on glycemic control and adverse patient outcomes. This retrospective cohort study evaluated the impact of interruptions in therapy on patients receiving maintenance doses of incretin therapy for at least three months. Patients were excluded if they were not on adequate maintenance doses, had missing hemoglobin A1c (HbA1c) levels, discontinued therapy due to side effects or cost, or had a history of chronic glucocorticoid use or organ transplant. The primary outcome was HbA1c levels before and after therapy interruption. Secondary outcomes were the incidence of gastrointestinal issues, hyperglycemia, and hypoglycemia-related hospital/clinic visits. A total of 71 patients were included. The median therapy duration was 9 months. Patients had a baseline HbA1c of 6.9%. Following interruption, 25.4% of patients had glucose-lowering therapy additions to their regimen, 35.2% dosage adjustments, and 39.4% no changes. HbA1c increased significantly to 7.2% at 12 months (P < 0.001). No significant differences were observed in adverse events or clinic/hospital visits (P = 0.571 and P = 1.00). Shortages of incretin therapy significantly increased patients' HbA1c levels up to 12 months post interruption. Long-term shortages or restrictions of these agents are likely to lead to adverse clinical outcomes. Further studies are needed to assess the outcomes of prolonged shortages or restrictions of these therapies.

Diabetes mellitus (DM) and cancer are major global health challenges that increasingly coexist due to shared risk factors including aging, obesity, sedentary behavior, and chronic low-grade inflammation. Beyond being a common comorbidity, DM-particularly type 2 diabetes-has emerged as an important modifier of cancer risk, progression, treatment tolerance, and survival. Epidemiological studies consistently associate DM with a higher incidence of several malignancies, including pancreatic, liver, colorectal, breast, and endometrial cancers, as well as increased cancer-specific and overall mortality. The biological link between dysglycemia and cancer is complex and multifactorial. Chronic hyperglycemia, hyperinsulinemia, and insulin resistance promote tumor development and progression through altered cellular metabolism (Warburg effect), activation of insulin and insulin-like growth factor pathways, systemic inflammation, oxidative stress, immune dysfunction, and changes in the tumor microenvironment and gut microbiota. This review summarizes current evidence on the interplay between dysglycemia and cancer and explores how integrating continuous glucose monitoring (CGM)-based strategies into multidisciplinary oncology care may improve both metabolic and oncologic outcomes. A comprehensive search of online databases, including PubMed, ISI Web of Science, and Scopus, was conducted to identify studies assessing the impact of glycemic disturbances and glycemic control on cancer outcomes. Poor glycemic control and increased glucose variability are associated with worse oncologic outcomes, higher rates of treatment-related complications, reduced adherence to therapy, and diminished efficacy of chemotherapy, targeted agents, and immune checkpoint inhibitors. Severe hypoglycemia has also emerged as an independent predictor of poor prognosis. Although HbA1c has long been the cornerstone of glycemic assessment, it incompletely captures the dynamic glucose fluctuations commonly observed during cancer therapy. CGM provides a more comprehensive and clinically meaningful assessment of glycemic control, with the potential to reduce hypoglycemia, improve glycemic stability, and enhance tolerance and adherence to anticancer treatments. Current evidence indicates that diabetes and dysglycemia are key modifiers of cancer risk, progression, treatment tolerance, and survival. Optimizing glycemic control may therefore contribute to improved cancer outcomes. CGM represents a promising tool for personalizing diabetes management in oncology settings.

GLP-1 receptor agonists (GLP-1 RAs) are increasingly used for weight management in patients with obesity, yet their safety in those with comorbid type 1 diabetes (T1D) remains uncertain due to concerns about diabetic ketoacidosis (DKA). This targets trial emulation using OneFlorida+ EHR data (2014-2024). After 1:1 time-conditional propensity score matching, the cohort included 651 GLP-1 RA initiators and 651 matched non-initiators with T1D meeting anti-obesity medication criteria. DKA incidence rates were 13.5 vs. 21.8 per 1,000 person-years. GLP-1 RA initiation was not significantly associated with DKA (hazard ratio [HR], 0.62; 95% confidence interval [CI]: 0.33-1.17) or severe hypoglycemia (HR, 0.52; 95% CI: 0.17-1.55) but was associated with fewer hospitalizations (HR, 0.74; 95% CI: 0.62-0.90) and emergency department visits (HR, 0.73; 95% CI: 0.57-0.92). These findings suggest that GLP-1 RAs may be safely prescribed in adults with T1D and obesity without increasing acute diabetes complications, while potentially reducing healthcare utilization.

Continuous glucose monitoring (CGM) has markedly advanced diabetes care by enabling real-time visualization of glycaemic variability, prevention of hypoglycaemia, and direct integration into therapeutic decision-making. As CGM use expands in routine practice and automated insulin delivery systems, however, accuracy has become a critical determinant of treatment safety. This mini-review summarizes recent advances in CGM accuracy management across three major driving forces: (1) accelerating technological innovation, including multi-analyte sensors, non-invasive devices, and artificial intelligence (AI)-based signal processing; (2) systematization and international harmonization of regulatory accuracy frameworks, exemplified by U.S. Food and Drug Administration (FDA) integrated CGM (iCGM) and the proposed CGM in Europe (eCGM) concept; and (3) growing societal demands for transparency, including public disclosure of performance data and strengthened lot-to-lot evaluation. We outline the four key dimensions of CGM accuracy-analytical accuracy, clinical accuracy, trend accuracy, and precision. We then review the evolution of regional accuracy standards, focusing on highly influential frameworks in the United States and Europe. Key considerations in accuracy-study design are discussed, along with clinical risks associated with reduced accuracy optimization, and progress toward global standardization. Finally, we examine future directions in the era of next-generation technologies, such as multi-analyte and non-invasive sensors, AI-driven accuracy optimization, and progress toward international standardization. This review provides an overview of the current landscape and future directions of CGM accuracy management in an era where fluctuations in accuracy directly affect treatment safety. We aim to clarify the perspectives required in both clinical practice and research to ensure safe and effective use of CGM.