Asprosin impairs insulin secretion in response to glucose and viability through TLR4/JNK-mediated inflammation

• Published in: Molecular and cellular endocrinology Vol. 486; pp. 96 - 104
• Main Authors: Lee, Taeseung, Yun, Subin, Jeong, Ji Hoon, Jung, Tae Woo
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 15.04.2019
• Subjects: adipokines; Animals; Apoptosis; Apoptosis - drug effects; Asprosin; blood serum; Cell Survival - drug effects; cell viability; Cyclic AMP - biosynthesis; dose response; free fatty acids; glucose; Glucose - toxicity; Humans; Inflammation; Inflammation - metabolism; Inflammation - pathology; Insulin Secretion; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - pathology; islets of Langerhans; JNK; MAP Kinase Signaling System - drug effects; Mice; Microfilament Proteins - metabolism; MIN6; mitogen-activated protein kinase; noninsulin-dependent diabetes mellitus; Oxidative Stress - drug effects; p38 Mitogen-Activated Protein Kinases - metabolism; palmitates; Palmitates - toxicity; patients; Peptide Fragments - metabolism; Peptide Hormones - metabolism; phosphorylation; Phosphorylation - drug effects; Recombinant Proteins - pharmacology; small interfering RNA; therapeutics; TLR4; Toll-like receptor 4; Toll-Like Receptor 4 - metabolism; transcription factor NF-kappa B; tumor necrosis factors; β-Cell; MIN6; JNK; Inflammation; siRNA; TLR4; Asprosin; Apoptosis; β-Cell

Severe inflammation in the islets is observed in obese patients with type 2 diabetes. Inflammation in the islets is caused by obesity-induced serum free fatty acids. Asprosin is a fasting-induced adipokine, which contributes to hepatic glucose production. However, the effects of asprosin on inflamma...