Glycogen metabolism in the glucose-sensing and supply-driven β-cell

FEBS Lett. 2016 Dec;590(23):4242-4251. doi: 10.1002/1873-3468.12460. Epub 2016 Nov 5.

Abstract

Glycogen metabolism in β-cells may affect downstream metabolic pathways controlling insulin release. We examined glycogen metabolism in human islets and in the rodent-derived INS-1 832/13 β-cells and found them to express the same isoforms of key enzymes required for glycogen metabolism. Our findings indicate that glycogenesis is insulin-independent but influenced by extracellular glucose concentrations. Levels of glycogen synthase decrease with increasing glucose concentrations, paralleling accumulation of glycogen. We did not find cAMP-elicited glycogenolysis and insulin secretion to be causally related. In conclusion, our results reveal regulated glycogen metabolism in human islets and insulin-secreting cells. Whether glycogen metabolism affects insulin secretion under physiological conditions remains to be determined.

Keywords: INS-1 832/13; human islets; insulin secretion.

Publication types

  • Letter

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Cell Line
  • Colforsin / pharmacology
  • Extracellular Space / drug effects
  • Extracellular Space / metabolism
  • Glucose / pharmacology*
  • Glycogen / metabolism*
  • Glycogen Synthase / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells / drug effects*
  • Insulin-Secreting Cells / metabolism*

Substances

  • Insulin
  • Colforsin
  • Glycogen
  • Glycogen Synthase
  • Glucose
  • 1-Methyl-3-isobutylxanthine