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The higher organization of beta-cells into spheroid structures termed islets of Langerhans is critical for the proper regulation of insulin secretion. Thus, rodent beta-cells form a functional syncytium that integrates and propagates information encoded by secretagogues, producing a "gain-of-function" in hormone release through the generation of coordinated cell-cell activity. By contrast, human islets possess divergent topology, and this may have repercussions for the cell-cell communication pathways that mediate the population dynamics underlying the intraislet regulation of insulin secretion. This is pertinent for type 2 diabetes mellitus pathogenesis, and its study in rodent models, because environmental and genetic factors may converge on these processes in a species-specific manner to precipitate the defective insulin secretion associated with glucose intolerance. The aim of the present minireview is therefore to discuss the structural and functional underpinnings that influence insulin secretion from human islets, and the possibility that dyscoordination between individual beta-cells may play an important role in some forms of type 2 diabetes mellitus.

Original publication

DOI

10.1210/me.2013-1278

Type

Journal article

Journal

Mol Endocrinol

Publication Date

2013

Volume

27

Pages

1984 - 1995

Keywords

Electrophysiological Phenomena/drug effects Genome-Wide Association Study Glucose/pharmacology Humans Insulin/chemistry/*metabolism Insulin Secretion Insulin-Secreting Cells/metabolism Islets of Langerhans/cytology/drug effects/*metabolism/*physiology