Pancreatic β-cells respond to fuel pressure with an early metabolic switch.

ABSTRACT: Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogenous toxicity from metabolites produced in excess amounts upon increased glucose availability. In order to handle excess fuel, the β-cells possess specific metabolic pathways, but little is known about these pathways. We present a study of β-cell metabolism under increased fuel pressure using a stable isotope resolved NMR approach to investigate early metabolic events leading up to β-cell dysfunction. The approach is based on a recently described combination of ¹³C metabolomics combined

SUBMITTER: Malinowski RM 

PROVIDER: S-EPMC7508987 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature