Embryonic and Neonatal Exposure to High-Fat Diet Disrupted Pancreatic Oxidative and Endoplasmic Reticulum Homeostasis Alongside Islet Insulin Output in Pubertal Rats

High-fat diet (HFD), adversely affects redox and/or endoplasmicreticulum (ER) stress status in pancreatic islets and disrupts glucosehomeostasis. Additionally, maternal HFD can cause metabolic disordersin offspring at an older age. Hence, we studied the impact of HFDduring pregnancy and lactation on oxidative stress and ER stressindices along with the quantity of insulin produced and releasedby the pancreatic islets in pubertal rat offspring. For this, pregnantrats were allocated into two groups fed either with the standard(S) or high-fat (HF) diet during pregnancy and lactation. After weaning,male pups from each group consumed standard diet until puberty.At puberty, the offspring plasma levels of glucose, insulin, leptinand corticosterone were assessed along with their ability to handlea glucose load. Finally, offspring pancreases were evaluated foroxidative and ER stress biomarkers as well as for isolated islets’glucose-induced insulin release (GIR) and content. The data obtainedshowed that the offspring from the HF group had elevated intra-abdominalfat mass and plasma corticosterone and leptin levels, but reducedbody weight. HFD also increased pancreatic MDA level, whereas itdecreased catalase activity. In the HF group, protein levels ofpancreatic immunoglobulin heavy-chain binding protein (BIP), CCAAT/enhancer-bindingprotein homologous protein (CHOP), and wolframin ER transmembraneglycoprotein (WFS1) were increased. However, glucose tolerance andhomeostatic model assessment for insulin resistance (HOMA-IR) indexin the HF offspring did not change. The isolated pancreatic isletsof the HF group showed disturbed glucose-induced insulin release (GIR)with unchanged insulin content. It can be concluded that maternalconsumption of HFD leads to a rise in pancreatic markers of oxidativeand ER stress in pubertal offspring and the increased pancreatic Wolframsyndrome 1 (WFS1) level could be a crucial factor in preservingglucose homeostasis.