Infants born to diabetic mothers are at increased risk for symptomatic hypoglycemia and death after birth. A 36-year-old G4P3 mother with a history of gestational diabetes and newly diagnosed type II insulin-dependent diabetes gave birth at home, in the care of a midwife, to a macrosomic infant girl (10 lbs.). Several hours after birth, the infant became lethargic and was found to be hypoglycemic (blood sugar: 28 mg/dL). Glucose and sugar water were administered by the midwife; however, the infant continued to decompensate. Emergency medical services were called, and the infant was transported to the hospital where, despite resuscitative efforts, she died. An autopsy and review of the literature was performed. At autopsy, characteristic features of maternal-fetal glucose dysregulation were identified, including fetal macrosomia, cardiomegaly, hepatomegaly, and severe pancreatic islet cell hypertrophy/hyperplasia. Developmental abnormalities and other potential causes of death were not identified. Although deaths due to hypoglycemia cannot be reliably diagnosed postmortem using vitreous glucose levels, a clinical history of maternal glucose dysregulation in combination with certain gross and histologic findings should prompt a pathologist to consider maternal-fetal glucose dysregulation as a diagnosis of exclusion and cause of death.
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http://dx.doi.org/10.1111/1556-4029.14247 | DOI Listing |
Brain Res
January 2025
Department of Geriatric Medicine, Xuanwu Hospital, Capital Medical University, China National Clinical Research Center for Geriatric Medicine, Beijing 100053, China.
Objective: Effective methods for establishing an aged animal model of diabetes and glycemic fluctuation have rarely been investigated. The aim of the study was to explore the feasibility of inducing glycemic fluctuation in aged Sprague-Dawley rats and to evaluate the corresponding changes in cognitive function.
Methods: Male rats aged 48 weeks were fed a high-fat and high-glucose diet and given streptozotocin intraperitoneally to establish a rat model of type 2 diabetes mellitus (T2DM).
Curr Pharm Des
January 2025
Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, University of Palermo, Palermo, Italy.
Background: In recent years, sodium-glucose co-transporter 2 inhibitors (SGLT2i) have emerged as a valuable treatment for type 2 diabetes (T2D) and heart failure. Despite these medications seeming to be safe in older people, the literature about SGLT2i and frailty is still limited. This study aims to evaluate whether SGLT2i use is associated with increased survival in older adults and if frailty can affect the findings.
View Article and Find Full Text PDFFunction (Oxf)
January 2025
Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan.
The ATP-sensitive potassium (KATP) channels, composed of Kir6.2 and SUR1 subunits, are essential for glucose homeostasis. While the role of pancreatic KATP channels in regulating insulin secretion is well-documented, the specific contributions of neuronal KATP channels remain unclear due to challenges in precisely targeting neuronal subpopulations.
View Article and Find Full Text PDFDiabetes
January 2025
Department of Biology & Institute of Biochemistry, Carleton University, Ottawa, ON, Canada.
Cancer survivors have an increased risk of developing Type 2 diabetes compared to the general population. Patients treated with cisplatin, a common chemotherapeutic agent, are more likely to develop metabolic syndrome and Type 2 diabetes than age- and sex-matched controls. Surprisingly, the impact of cisplatin on pancreatic islets has not been reported.
View Article and Find Full Text PDFDiabetic kidney disease (DKD) progression is often marked by early glomerular endothelial cell (GEC) dysfunction, including alterations in the fenestration size and number linked to impaired glomerular filtration. However, the cellular mechanisms regulating GEC fenestrations remain poorly understood due to limitations in existing models, challenges in imaging small fenestrations , and inconsistencies between and findings. This study used a logic-based protein-protein interaction network model with normalized Hill functions for dynamics to explore how glucose-mediated signaling dysregulation impacts fenestration dynamics in GECs.
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