Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

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

Andersson, Lotta E. LU ; Nicholas, Lisa M. LU ; Filipsson, Karin LU ; Sun, Jiangming LU orcid ; Benavente, Anya Medina LU ; Al-Majdoub, Mahmoud LU ; Fex, Malin LU ; Mulder, Hindrik LU orcid and Spégel, Peter LU (2016) In FEBS Letters 590(23). p.4242-4251
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... (More)

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.

(Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
human islets, INS-1 832/13, insulin secretion
in
FEBS Letters
volume
590
issue
23
pages
10 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:84996572984
  • pmid:27943300
  • wos:000390390600010
ISSN
0014-5793
DOI
10.1002/1873-3468.12460
language
English
LU publication?
yes
id
19d73080-95b5-4e87-88c2-f7dffa49bc5a
date added to LUP
2016-12-29 10:26:40
date last changed
2025-10-14 10:52:11
@article{19d73080-95b5-4e87-88c2-f7dffa49bc5a,
  abstract     = {{<p>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.</p>}},
  author       = {{Andersson, Lotta E. and Nicholas, Lisa M. and Filipsson, Karin and Sun, Jiangming and Benavente, Anya Medina and Al-Majdoub, Mahmoud and Fex, Malin and Mulder, Hindrik and Spégel, Peter}},
  issn         = {{0014-5793}},
  keywords     = {{human islets; INS-1 832/13; insulin secretion}},
  language     = {{eng}},
  month        = {{12}},
  number       = {{23}},
  pages        = {{4242--4251}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{FEBS Letters}},
  title        = {{Glycogen metabolism in the glucose-sensing and supply-driven β-cell}},
  url          = {{http://dx.doi.org/10.1002/1873-3468.12460}},
  doi          = {{10.1002/1873-3468.12460}},
  volume       = {{590}},
  year         = {{2016}},
}