ECE2019 Guided Posters Adrenal and Neuroendocrine - Clinical (1) (10 abstracts)
Melatonin prevented beta cell senescence against glucolipotoxicity
Mi-kyung Kim 1, , Hye Sook Jung 2 , Jeong Eun Jang 1 , Tae Nyun Kim 1 , Min Jeong Kwon 1 , Soon Hee Lee 1 , Byung Doo Rhee 1 & Jeong Hyun Park 1,
1Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Inje University, Busan, Republic of Korea; 2Paik Institute for Clinical Research, Molecular Therapy Lab, Inje University, Busan, Republic of Korea.
Beta cell senescence is being regarded as the one of the mechanisms of beta cell dysfunction. Melatonin secreted primarily from the pineal glandregulates a variety of physiological functions, such as sleep, circadian rhythms, and neuroendocrine actions. Melatonin has also very strong anti-oxidant effects. The effects of melatonin on the pancreatic beta cell senescence induced by glucolipotoxicity have not been studied. INS-1 cells were exposed to 33mM glucose with palmitate 200uM (glucolipotoxicity: HG+palmitate (HGP)) with or without melatonin. Cell viability and apoptosis were assessed by MTT assay and Annexin V staining. We compared senescence β-Galactosidase (SA-β-Gal) staining and p16INK4aimmunostaining depending on melatonin treatment against HGP. We assessed phospho-p38 MAPK, Sirt1 and p16 protein expression with and without melatonin. CDK4 protein and anti-oxidant enzyme were assessed in both conditions. Melatonin increased INS-1 cell viability and decreased apoptosis against HGP. SA-β-Gal and p16INK4a immunostaining were increased in HGP, and melatonin significantly reversed them. Melatonin decreased phospho-p38 MAPK and p16INK4a protein expression in 24 hours. Melatonin increased Sirt1, Mn-SOD and catalase expression against HGP. In conclusion, we found that melatonin prevent beta cell senescence induced by metabolic stresses like glucolipotoxicity. The effects of melatonin on beta cell aging may be related with phospho-p38 MAPK and p16INK4a pathway, and anti-oxidant system.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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