Melatonin 'in vitro' does not show direct effect on hepatoma (HepG2) and insulinoma (MIN6) cell lines that explain the improvement of glucose homeostasis

Author(s)

Ana Paula de Lima Barbosa

• Document type: Doctoral Thesis
• Press: Campinas, SP.
• Institution: Universidade Estadual de Campinas (UNICAMP). Faculdade de Ciências Médicas
• Defense date: 2014-12-22

Examining board members

Gabriel Forato Anhê; Emerielle Cristine Vanzela; Marcio Alberto Torsoni; Carla Roberta de Oliveira Carvalho; Luciana Chagas Caperuto

• Advisor: Gabriel Forato Anhê

Abstract

Type II Diabetes Mellitus (T2DM) is characterized by decrease of insulin sensitivity, resulting impairment glucose homeostasis. Recent studies have shown that melatonin, a hormone produced by the pineal gland, improves glucose tolerance and insulin resistance, reduce the expression of hepatic gluconeogenesis proteins (G6Pase and PEPCK) and diminish pancreatic beta cell apoptosis in vivo. However, it was unclear if melatonin could reverse the lipotoxic actions of saturated fatty acid in pancreatic beta cells and skeletal muscle, and if melatonin could decrease the expression of regulatory genes of hepatic gluconeogenesis in situ. To answer this question, we used cell cultures of insulinoma (MIN6), skeletal muscle (L6 myotubes) and hepatoma (HepG2). The results showed that melatonin reverses palmitate insulin resistance in L6 myotubes, but only at low passages, melatonin does not decrease apoptosis in MIN6 and does not alter the expression of G6pc, the encoding gene of G6Pase, in culture cell of HepG2 (AU)

• FAPESP's process: 11/02194-1 - Action of melatonin on the regulation of PEPCK in human hepatocytes (HepG2)
• Grantee: Ana Paula de Lima Barbosa
• Support Opportunities: Scholarships in Brazil - Doctorate