The exact pathophysiology of non-alcoholic steatohepatitis (NASH) is not known. Previous studies suggest that dietary advanced glycation end products (AGEs) can cause oxidative stress in liver. We aim to study the effects of dietary AGEs on liver health and their possible role in the pathogenesis of NASH. METHODS: Two groups of mice were fed the same diet except the AGE content varied. One group was fed a high AGE diet and the second group was fed a regular AGE diet. Liver histology, alanine aminotransferase, aspartate aminotransferase, fasting glucose, fasting insulin, insulin resistance and glucose tolerance were assessed. RESULTS: Histology revealed that neutrophil infiltration occurred in the livers of the high AGE group at week 26; steatosis did not accompany liver inflammation. At week 39 livers from both groups exhibited macro- or micro-steatosis, yet no inflammation was detected. Higher insulin levels were detected in the regular AGE group at week 26 (P = 0.034), compared to the high AGE group. At week 39, the regular AGE group showed higher levels of alanine aminotransferase (P<0.01) and aspartate aminotransferase (P = 0.02) than those of the high AGE group. CONCLUSIONS: We demonstrate that a high AGE diet can cause liver inflammation in the absence of steatosis. Our results show that dietary AGEs could play a role in initiating liver inflammation contributing to the disease progression of NASH. Our observation that the inflammation caused by high AGE alone did not persist suggests interesting future directions to investigate how AGEs contribute to pro-oxidative and anti-oxidative pathways in the liver.

En caul deliveries are defined as a fetus that is delivered completely contained within an amniotic sac and are considered to be less common than 1 in 80,000 live births. Vaginal en caul births compared to abdominal or cesarean are the rarest subtype. Most en caul births are associated with prematurity and low gravida. The combination of prematurity, high gravida, vaginal en caul birth, and severe postpartum complications has not previously been described. We report a woman with gravida of 12 delivering vaginally a neonate female en caul at the extremely preterm gestational age of 23 weeks. The neonate subsequently decompensated, underwent respiratory distress, and was diagnosed with a bilateral intraventricular hemorrhage. Owing to deteriorating status, supportive care was removed and the infant was pronounced dead 5 days after delivery.

The exact pathophysiology of non‐alcoholic steatohepatitis (NASH) is not known. Previous studies suggest that dietary advanced glycation end products (AGEs) can cause oxidative stress in liver. We aim to study the effects of dietary AGEs on liver health and their possible role in the pathogenesis of NASH. Two groups of mice were fed the same diet except the AGE content varied. One group was fed a high AGE diet and the second group was fed a regular AGE diet. Liver histology, ALT, AST, fasting glucose, fasting insulin, insulin resistance and glucose tolerance were assessed. Histology revealed that neutrophil infiltration occurred in the livers of the high AGE group at week 26; steatosis was not found with the inflamed livers. At week 39 livers from both groups exhibited steatosis, yet no inflammation was detected. Higher insulin levels were detected in the regular AGE group at week 26 (P=0.034), compared to the high AGE group. At week 39, the regular AGE group showed higher levels of ALT (P<0.01) and AST (P=0.02) than those of the high AGE group. We demonstrate that a high AGE diet can cause liver inflammation in the absence of steatosis. Our results are the first to show that dietary AGE can contribute to the pathogenesis of NASH.