Lactogens reduce endoplasmic reticulum stress-induced rodent and human β-cell death and diabetes incidence in Akita mice

• DOI: 10.2337/figshare.12168477
• Publication Date: 2020-04-24T21:29:13Z
• Authors: Ada Admin; Rosemary Li; Nagesha Guthalu K...; Joanna Filipowska; Rollie F. Hampton; Silvia Leblanc; Adolfo Garcia-Ocana; Rupangi C. Vasavada
• Keywords: Tunicamycin

Diabetes occurs due to a loss of functional β-cells, resulting from β-cell death and dysfunction. Lactogens protect rodent human β-cells <i>in vitro</i> and<i> in vivo</i> against triggers cytotoxicity relevant diabetes, many which converge onto common pathway, endoplasmic reticulum (ER) stress. However, whether lactogens modulate the ER stress pathway is unknown. This study examines if can mitigate diabetes incidence Akita mice, model stress-induced akin neonatal humans. We show that INS1 cells, primary two distinct stressors, tunicamycin thapsigargin, through activation JAK2/STAT5 pathway. expression pro-apoptotic molecules are induced by chronic cells islets. Transgenic placental lactogen mice drastically reduces severe hyperglycemia, incidence, hypoinsulinemia, death, mass observed littermates. These first studies any cell type demonstrating causing enhanced survival reduced face