Islet alpha-cells do not influence insulin secretion from beta-cells through cell-cell contact

Endocrine. 2007 Feb;31(1):61-5. doi: 10.1007/s12020-007-0004-0.

Abstract

Interactions between the endocrine cells in islets of Langerhans influence their secretory function, and disruption of islet structure results in impaired insulin secretory responses to both nutrient and non-nutrient stimuli. We have previously demonstrated that insulin-secreting MIN6 cells show enhanced secretory responses when grown as islet-like structures (pseudoislets) suggesting that homotypic cell-cell interactions between beta-cells are important for normal function. We have now extended this experimental model to study the role of heterotypic interactions between insulin-expressing and glucagon-expressing cells by measuring the organization and secretory function of pseudoislets formed from MIN6 and alphaTC1 cells. The direct alpha-cell to beta-cell contact in the heterogenous MIN6/alphaTC1 pseudoislets was sufficient to enable the formation of anatomically correct islet-like structures, with a central core of MIN6 cells surrounded by a periphery of alphaTC1 cells. However, the presence of alphaTC1 cells had no detectable effect on insulin secretory responses to nutrient or non-nutrient stimuli. In contrast, exogenous glucagon enhanced insulin secretion, in accordance with a paracrine role for alpha-cell-derived glucagon in the regulation of insulin secretion rather than direct, contact-mediated effects of alpha-cells on neighbouring beta-cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Culture Techniques
  • Cell Line
  • Glucagon / metabolism
  • Glucagon-Secreting Cells / metabolism
  • Glucagon-Secreting Cells / physiology*
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / physiology*
  • Mice

Substances

  • Insulin
  • Glucagon