Pancreatic β Cells Inhibit Glucagon Secretion from α Cells: An In Vitro Demonstration of α-β Cell Interaction.
MIN-6
co-culture
glucagon secretion
insulin secretion
α-TC6-1
α–β cell interaction
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
30 Jun 2021
30 Jun 2021
Historique:
received:
10
06
2021
revised:
25
06
2021
accepted:
27
06
2021
entrez:
2
7
2021
pubmed:
3
7
2021
medline:
28
7
2021
Statut:
epublish
Résumé
Interactions between endocrine α and β cells are critical to their secretory function in vivo. The interactions are highly regulated, although yet to be fully understood. In this study, we aim to assess the impact of α and β cell co-culture on hormone secretion. Mouse clonal cell lines α-TC6-1 (α cell line) and MIN-6 (β cell line) were cultured independently or in combination in a medium containing 5.5, 11.1, or 25 mM glucose, respectively. After 72 h, hormone release was measured using insulin and glucagon secretion assays, the cell distribution was visualized by inverted microscopy and an immunocytochemistry assay, and changes in gene expressions were assessed using the RT-PCR technique. The co-culture of the two cell lines caused a decrease in glucagon secretion from α-TC1-6 cells, while no effect on insulin secretion from MIN-6 cells was revealed. Both types of cells were randomly scattered throughout the culture flask, unlike in mice islets in vivo where β cells cluster in the core and α cells are localized at the periphery. During the α-β cell co-culture, the gene expression of glucagon (Gcg) decreased significantly. We conclude that islet β cells suppress glucagon secretion from α cells, apparently via direct cell-to-cell contact, of which the molecular mechanism needs further verification.
Identifiants
pubmed: 34209449
pii: nu13072281
doi: 10.3390/nu13072281
pmc: PMC8308288
pii:
doi:
Substances chimiques
Glucagon
9007-92-5
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Aarhus Universitet
ID : no number
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