JAMES L. ROSENBERG¹, WILLIAM WOOLLEY¹, IHSAN ELNUNU¹, JULIA KAMML², DAVID S. KAMMER², CLAIRE ACEVEDO^1,3,*

BIOCELL, Vol.47, No.7, pp. 1651-1659, 2023, DOI:10.32604/biocell.2023.028014

Abstract Age and diabetes have long been known to induce an oxidative reaction between glucose and collagen, leading to the accumulation of advanced glycation end-products (AGEs) cross-links in collagenous tissues. More recently, AGEs content has been related to loss of bone quality, independent of bone mass, and increased fracture risk with aging and diabetes. Loss of bone quality is mostly attributed to changes in material properties, structural organization, or cellular remodeling. Though all these factors play a role in bone fragility disease, some common recurring patterns can be found between diabetic and age-related bone fragility. The main pattern we will discuss… More >

YUEHUA SHI^1,#, QIUYING YAN^2,#, QIN LI³, WEI QIAN¹, DONGYAN QIAO¹, DONGDONG SUN², HONG YU^1,*

BIOCELL, Vol.47, No.1, pp. 165-173, 2023, DOI:10.32604/biocell.2022.023043

Abstract The placenta plays an important role in nutrient transport to maintain the growth and development of the embryo. Gestational diabetes mellitus (GDM), the most common complication during pregnancy, highly affects placental function in late gestation. Advanced glycation end-products (AGEs), a complex and heterogeneous group of compounds engaged by the receptor for AGEs (RAGE), are closely associated with diabetes-related complications. In this study, AGEs induced a decrease in the expression of tight junction (TJ) proteins in BeWo cells and increased the paracellular permeability of trophoblast cells by regulating RAGE/NF-κB. Sprague-Dawley (SD) rats injected with 100 mg/kg AGEs-rat serum albumin (RSA) via… More >