Abnormal acinar-β-cell crosstalk in type 2 diabetes

Shirin Geravandi; Amin Ardestani

doi:10.1016/j.tem.2023.08.006

Abnormal acinar-β-cell crosstalk in type 2 diabetes

Trends Endocrinol Metab. 2023 Nov;34(11):685-687. doi: 10.1016/j.tem.2023.08.006. Epub 2023 Aug 19.

Authors

Shirin Geravandi¹, Amin Ardestani²

Affiliations

¹ Centre for Biomolecular Interactions Bremen, University of Bremen, Bremen, Germany.
² Centre for Biomolecular Interactions Bremen, University of Bremen, Bremen, Germany. Electronic address: ardestani.amin@gmail.com.

PMID: 37599202
DOI: 10.1016/j.tem.2023.08.006

Abstract

Cellular crosstalk plays a vital role in maintaining pancreas homeostasis. Recently, in Cell Metabolism, Basile et al. demonstrated that aberrant upregulation of acinar-cell-specific pancreatic elastase CELA3B within endocrine islets reduces β-cell viability in type 2 diabetes (T2D). This identifies detrimental acinar-β-cell crosstalk as a novel pathogenic mechanism in diabetes.

Keywords: acinar cell; beta cell; cell crosstalk; exocrine pancreas; type 2 diabetes.