Air pollution exposure has been linked with glucose dysregulation in pregnant women; however, evidence on these associations with fetal glucose homeostasis is unclear yet. We therefore aimed to evaluate the association of prenatal exposure to particulate matter (PM) and traffic indicators with fetal glucose homeostasis in cord blood samples. A total of 169 mother-infant pairs recruited from Mobini hospital of Sabzevar, Iran, were included in this cross-sectional study. Maternal exposure to PMs was estimated using land use regression models. Moreover, traffic indicators (i.e., total street length in 100, 300 and 500 m buffers and distance from residential home to the nearest major roads) were calculated based on the street map of Sabzevar. Cord blood glucose and insulin concentrations, HOMA-ꞵ, HOMA-S and HOMA-IR were used as glucose homeostasis markers. Higher maternal exposure to PM and PM were associated with higher cord blood glucose and insulin concentrations and HOMA-IR. Moreover, total streets length in 300 m buffer was positively associated with cord blood glucose and insulin concentrations and HOMA-IR. An increase in distance to major roads was associated with higher HOMA-ꞵ and HOMA-S and lower cord blood glucose and insulin concentrations as well as HOMA-IR. Overall, we found prenatal exposure to PMs and traffic indicators was associated with a higher risk of glucose homeostasis dysregulation in the fetus.
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http://dx.doi.org/10.1016/j.envres.2021.111504 | DOI Listing |
J Biol Chem
January 2025
Laboratory of Immunogenetics, Pennington Biomedical Research Center, Baton Rouge, LA, 70808, USA; Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. Electronic address:
Pancreatic islet β-cells express the Cpt1a gene, which encodes the enzyme carnitine palmitoyltransferase 1A (CPT1A), an enzyme that facilitates entry of long chain fatty acids into the mitochondria. Because fatty acids are required for glucose-stimulated insulin secretion, we tested the hypothesis that CPT1A is essential to support islet β-cell function and mass. In this study, we describe genetic deletion of Cpt1a in pancreatic tissue (Cpt1a) using C57BL/6J mice.
View Article and Find Full Text PDFNat Metab
January 2025
CECAD Excellence Center, University of Cologne, Cologne, Germany.
Dysfunctions in autophagy, a cellular mechanism for breaking down components within lysosomes, often lead to neurodegeneration. The specific mechanisms underlying neuronal vulnerability due to autophagy dysfunction remain elusive. Here we show that autophagy contributes to cerebellar Purkinje cell (PC) survival by safeguarding their glycolytic activity.
View Article and Find Full Text PDFNoncoding RNA Res
April 2025
Kresge Eye Institute, Wayne State University, Detroit, MI, USA.
Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc), is also downregulated.
View Article and Find Full Text PDFBrain Behav Immun Health
February 2025
Laboratory of Immuno-Endocrinology, Diabetes and Metabolism, Instituto de Investigaciones en Medicina Traslacional (IIMT), CONICET-Universidad Austral, Pilar, Argentina.
Pancreatic β-cells are specialized in secreting insulin in response to circulating nutrients, mainly glucose. Diabetes is one of the most prevalent endocrine-metabolic diseases characterized by an imbalance in glucose homeostasis, which result mainly from lack of insulin production (type 1 diabetes) or insufficient insulin and peripheral insulin resistance (type 2 diabetes), both influenced by genetic and environmental components. Pancreatic β-cell dysfunction and islet inflammation are common characteristics of both types of the disease.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
January 2025
Department of Microbiology, Immunology, & Cell Biology, West Virginia University School of Medicine, 64 Medical Center Drive, Morgantown, WV, 26506, USA.
Human neonates are predisposed to an increased risk of mortality from infection due to fundamental differences in the framework of innate and adaptive immune responses relative to those in the adult population. As one key difference in neonates, an increase in the immunosuppressive cytokine, IL-27, is responsible for poor outcomes in a murine neonatal model of bacterial sepsis. In our model, the absence of IL-27 signaling during infection is associated with improved maintenance of body mass, increased bacterial clearance with reduced systemic inflammation, and decreased mortality rates that correlate to preservation of glucose homeostasis and insulin production.
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