Glycogen metabolism in the glucose-sensing and supply-driven β-cell
(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)
- author
- Andersson, Lotta E.
LU
; Nicholas, Lisa M.
LU
; Filipsson, Karin
LU
; Sun, Jiangming
LU
; Benavente, Anya Medina LU ; Al-Majdoub, Mahmoud LU ; Fex, Malin LU ; Mulder, Hindrik LU
and Spégel, Peter LU
- organization
- publishing date
- 2016-12-01
- 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
-
- pmid:27943300
- wos:000390390600010
- scopus:84996572984
- 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
- 2025-01-12 18:37:16
@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}}, }