Background::Pancreatic β-cells elevate insulin production and secretion through a compensatory mechanism to override insulin resistance under metabolic stress conditions. Deficits in β-cell compensatory capacity result in hyperglycemia and type 2 diabetes (T2D). However, the mechanism in the regulation of β-cell compensative capacity remains elusive. Nuclear factor-Y (NF-Y) is critical for pancreatic islets’ homeostasis under physiological conditions, but its role in β-cell compensatory response to insulin resistance in obesity is unclear.Methods::In this study, using obese ( ob/ob) mice with an absence of NF-Y subunit A (NF-YA) in β-cells ( ob, Nf-ya βKO) as well as rat insulinoma cell line (INS1)-based models, we determined whether NF-Y-mediated apoptosis makes an essential contribution to β-cell compensation upon metabolic stress. Results::Obese animals had markedly augmented NF-Y expression in pancreatic islets. Deletion of β-cell Nf-ya in obese mice worsened gluco

作者：He Siyuan；Yu Xiaoqian；Cui Daxin；Liu Yin；Yang Shanshan；Zhang Hongmei；Hu Wanxin；Su Zhiguang

来源：中华医学杂志英文版 2023 年 136卷 8期