Effect of Human Myotubes-Derived Media on Glucose-Stimulated Insulin Secretion. (14th February 2017)
- Record Type:
- Journal Article
- Title:
- Effect of Human Myotubes-Derived Media on Glucose-Stimulated Insulin Secretion. (14th February 2017)
- Main Title:
- Effect of Human Myotubes-Derived Media on Glucose-Stimulated Insulin Secretion
- Authors:
- Mizgier, Maria L.
Cataldo, Luis R.
Gutierrez, Juan
Santos, José L.
Casas, Mariana
Llanos, Paola
Contreras-Ferrat, Ariel E.
Moro, Cedric
Bouzakri, Karim
Galgani, Jose E. - Other Names:
- Camastra Stefania Academic Editor.
- Abstract:
- Abstract : 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 after meals is pivotal for adapting to increased glycemia and might drive insulin secretion through muscle-released factors (e.g., myokines). We hypothesized that insulin influences 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 ( p < 0.05 ) . Meanwhile, conditioned media from insulin-treated myotubes did not influence GSIS. In beta cells, GSIS was similar across conditions. In conclusion, factors being present inAbstract : 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 after meals is pivotal for adapting to increased glycemia and might drive insulin secretion through muscle-released factors (e.g., myokines). We hypothesized that insulin influences 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 ( p < 0.05 ) . Meanwhile, conditioned media from insulin-treated myotubes did not influence GSIS. In beta cells, GSIS was similar across conditions. In conclusion, factors being present in noninsulin-stimulated muscle cell-derived media appear to influence GSIS in mice islets. … (more)
- Is Part Of:
- Journal of diabetes research. Volume 2017(2017)
- Journal:
- Journal of diabetes research
- Issue:
- Volume 2017(2017)
- Issue Display:
- Volume 2017, Issue 2017 (2017)
- Year:
- 2017
- Volume:
- 2017
- Issue:
- 2017
- Issue Sort Value:
- 2017-2017-2017-0000
- Page Start:
- Page End:
- Publication Date:
- 2017-02-14
- Subjects:
- Diabetes -- Periodicals
Diabetes -- Pathophysiology -- Periodicals
Diabetes -- Prevention -- Periodicals
Diabetes -- Etiology -- Periodicals
Diabetes -- Epidemiology -- Periodicals
Diabetes -- Pathogenesis -- Periodicals
616.462005 - Journal URLs:
- https://www.hindawi.com/journals/jdr/ ↗
- DOI:
- 10.1155/2017/1328573 ↗
- Languages:
- English
- ISSNs:
- 2314-6745
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 23058.xml