Effects of phlorizin on metabolism and function of pancreatic β-cell
Hellman, Bo ; Lernmark, Ake LU
; Sehlin, Janove
and Täljedal, Inge Bert
(1972)
In Metabolism
21(1).
p.60-66
- Abstract
The effects of phlorizin on several parameters of β-cell function were studied with microdissected islets of obese-hyperglycemic mice. At a concentration of 10 mM, phlorizin significantly depressed insulin release, glucose transport, glucose oxidation, and the level of fructose 1,6-diphosphate, when tested in the presence of 10 mM glucose. Whereas 1 mM phlorizin inhibited glucose transport by about 50%, the glucose-stimulated insulin release remained unaffected by 1-5 mM phlorizin. In the absence of glucose, 10 mM phlorizin significantly stimulated insulin release but had no effect on the islet levels of glucose 6-phosphate or fructose 1,6-diphosphate. The results corroborate our previous hypothesis of a mediated glucose transport into... (More)
The effects of phlorizin on several parameters of β-cell function were studied with microdissected islets of obese-hyperglycemic mice. At a concentration of 10 mM, phlorizin significantly depressed insulin release, glucose transport, glucose oxidation, and the level of fructose 1,6-diphosphate, when tested in the presence of 10 mM glucose. Whereas 1 mM phlorizin inhibited glucose transport by about 50%, the glucose-stimulated insulin release remained unaffected by 1-5 mM phlorizin. In the absence of glucose, 10 mM phlorizin significantly stimulated insulin release but had no effect on the islet levels of glucose 6-phosphate or fructose 1,6-diphosphate. The results corroborate our previous hypothesis of a mediated glucose transport into the pancreatic β-cell. Insulin release does not seem to be governed by the glucose transport in toto. Stimulation of insulin release might rather be elicited by the binding of glucose to a distinct membrane receptor, which accounts for but a minor fraction of the total glucose uptake.
(Less)
- author
- Hellman, Bo
; Lernmark, Ake
LU
; Sehlin, Janove
and Täljedal, Inge Bert
- publishing date
- 1972-01-01
- type
- Contribution to journal
- publication status
- published
- in
- Metabolism
- volume
- 21
- issue
- 1
- pages
- 60 - 66
- publisher
- Elsevier
- external identifiers
-
- scopus:0015252281
- pmid:4550294
- ISSN
- 0026-0495
- DOI
- 10.1016/0026-0495(72)90020-0
- language
- English
- LU publication?
- no
- id
- 26fcc6a2-85e3-45b2-828e-95665e2a2c62
- date added to LUP
- 2019-09-18 12:24:47
- date last changed
- 2024-03-13 07:59:02
@article{26fcc6a2-85e3-45b2-828e-95665e2a2c62,
abstract = {{<p>The effects of phlorizin on several parameters of β-cell function were studied with microdissected islets of obese-hyperglycemic mice. At a concentration of 10 mM, phlorizin significantly depressed insulin release, glucose transport, glucose oxidation, and the level of fructose 1,6-diphosphate, when tested in the presence of 10 mM glucose. Whereas 1 mM phlorizin inhibited glucose transport by about 50%, the glucose-stimulated insulin release remained unaffected by 1-5 mM phlorizin. In the absence of glucose, 10 mM phlorizin significantly stimulated insulin release but had no effect on the islet levels of glucose 6-phosphate or fructose 1,6-diphosphate. The results corroborate our previous hypothesis of a mediated glucose transport into the pancreatic β-cell. Insulin release does not seem to be governed by the glucose transport in toto. Stimulation of insulin release might rather be elicited by the binding of glucose to a distinct membrane receptor, which accounts for but a minor fraction of the total glucose uptake.</p>}},
author = {{Hellman, Bo and Lernmark, Ake and Sehlin, Janove and Täljedal, Inge Bert}},
issn = {{0026-0495}},
language = {{eng}},
month = {{01}},
number = {{1}},
pages = {{60--66}},
publisher = {{Elsevier}},
series = {{Metabolism}},
title = {{Effects of phlorizin on metabolism and function of pancreatic β-cell}},
url = {{http://dx.doi.org/10.1016/0026-0495(72)90020-0}},
doi = {{10.1016/0026-0495(72)90020-0}},
volume = {{21}},
year = {{1972}},
}