Research Article Effect of Human Myotubes-Derived Media on Glucose-Stimulated Insulin Secretion Maria L. Mizgier, 1 Luis R. Cataldo, 1 Juan Gutierrez, 1 José L. Santos, 1 Mariana Casas, 2 Paola Llanos, 2,3 Ariel E. Contreras-Ferrat, 4 Cedric Moro, 5 Karim Bouzakri, 6,7 and Jose E. Galgani 1,8 1 Departamento de Nutrici´ on, Diabetes y Metabolismo, Escuela de Medicina, Pontifcia Universidad Cat´ olica de Chile, Santiago, Chile 2 Centro de Estudios Moleculares de la C´ elula, Instituto de Ciencias Biom´ edicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile 3 Institute for Research in Dental Sciences, Facultad de Odontolog´ ıa, Universidad de Chile, Santiago, Chile 4 Exercise Science Laboratory, School of Kinesiology, Faculty of Medicine, Universidad Finis Terrae, Santiago, Chile 5 INSERM UMR1048, Institut des Maladies M´ etaboliques et Cardiovasculaires, Universit´ e Paul Sabatier, Toulouse, France 6 Departement de G´ en´ etique et D´ eveloppement, CMU, Universit´ e de Gen` eve, Gen` eve, Switzerland 7 UMR DIATHEC, EA 7294, Centre Europ´ een d’Etude du Diab` ete, Universit´ e de Strasbourg, Strasbourg, France 8 UDA-Ciencias de la Salud, Carrera de Nutrici´ on y Diet´ etica, Escuela de Medicina, Pontifcia Universidad Cat´ olica de Chile, Santiago, Chile Correspondence should be addressed to Jose E. Galgani; jgalgani@uc.cl Received 29 October 2016; Revised 1 January 2017; Accepted 17 January 2017; Published 14 February 2017 Academic Editor: Stefania Camastra Copyright © 2017 Maria L. Mizgier et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fasting to postprandial transition requires a tight adjustment of insulin secretion to its demand, so tissue (e.g., skeletal muscle) glucose supply is assured while hypo-/hyperglycemia are prevented. High muscle glucose disposal afer meals is pivotal for adapting to increased glycemia and might drive insulin secretion through muscle-released factors (e.g., myokines). We hypothesized that insulin infuences myokine secretion and then increases glucose-stimulated insulin secretion (GSIS). In conditioned media from human myotubes incubated with/without insulin (100 nmol/L) for 24 h, myokines were qualitatively and quantitatively characterized using an antibody-based array and ELISA-based technology, respectively. C57BL6/J mice islets and Wistar rat beta cells were incubated for 24 h with control and conditioned media from noninsulin- and insulin-treated myotubes prior to GSIS determination. Conditioned media from insulin-treated versus nontreated myotubes had higher RANTES but lower IL6, IL8, and MCP1 concentration. Qualitative analyses revealed that conditioned media from noninsulin- and insulin-treated myotubes expressed 32 and 23 out of 80 myokines, respectively. Islets incubated with conditioned media from noninsulin-treated myotubes had higher GSIS versus control islets ( < 0.05). Meanwhile, conditioned media from insulin-treated myotubes did not infuence GSIS. In beta cells, GSIS was similar across conditions. In conclusion, factors being present in noninsulin-stimulated muscle cell- derived media appear to infuence GSIS in mice islets. 1. Introduction Regulation of insulin secretion is critical for understanding glucose homeostasis under (patho)physiological conditions. Such regulation is particularly complex in the transition from fasting to postprandial state on which its secretion must be tightly adjusted to insulin needs, so tissue glucose supply is assured while hypo- and hyperglycaemia are prevented. Skeletal muscle plays an active role controlling circulating glucose concentration. On the one hand, this tissue is a major site of insulin-stimulated glucose disposal [1], which is crucial in the adaptation to the rapid increase in glucose fux into Hindawi Journal of Diabetes Research Volume 2017, Article ID 1328573, 9 pages https://doi.org/10.1155/2017/1328573