β Cell Dysfunction in Type 2 Diabetes: Drained of Energy?

Jakob G Knudsen; Patrik Rorsman

doi:10.1016/j.cmet.2018.12.015

β Cell Dysfunction in Type 2 Diabetes: Drained of Energy?

Cell Metab. 2019 Jan 8;29(1):1-2. doi: 10.1016/j.cmet.2018.12.015.

Authors

Jakob G Knudsen¹, Patrik Rorsman²

Affiliations

¹ Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK.
² Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK; Metabolic Physiology, Department of Physiology, University of Göteborg, Box 430, SE-405 30 Göteborg, Sweden. Electronic address: patrik.rorsman@hmc.ox.ac.uk.

PMID: 30625305
DOI: 10.1016/j.cmet.2018.12.015

Abstract

Type 2 diabetes is a progressive disorder, but exactly how the progression occurs remains unknown. In this issue of Cell Metabolism, Zhang et al. (2019) present evidence that diabetes, via hyperglycemia, leads to aberrant insertion of a mitochondrial ion channel in the plasma membrane, rendering it leaky to key intracellular signaling molecules with resultant suppression of insulin secretion.

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MeSH terms

Diabetes Mellitus, Type 2*
Humans
Hyperglycemia*
Insulin Secretion
Insulin-Secreting Cells*
Mitochondria
Voltage-Dependent Anion Channel 1

Substances

VDAC1 protein, human
Voltage-Dependent Anion Channel 1