The acquisition of increased insulin-responsive hexose transport in 3T3-L1 adipocytes correlates with expression of a novel transporter gene
The expression of two genes encoding facilitated glucose transporter proteins was studied during the differentiation of the 3T3-L1 fibroblastic cell line into adipocytes. The mRNA encoding the widely expressed HepG2/brain glucose transporter (GTI) is detectable in fibroblasts and its abundance remai...
Gespeichert in:
Veröffentlicht in: | The Journal of biological chemistry 1989-11, Vol.264 (33), p.19994-19999 |
---|---|
Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | The expression of two genes encoding facilitated glucose transporter proteins was studied during the differentiation of the
3T3-L1 fibroblastic cell line into adipocytes. The mRNA encoding the widely expressed HepG2/brain glucose transporter (GTI)
is detectable in fibroblasts and its abundance remains unchanged during differentiation. On the other hand, the mRNA encoding
a glucose transporter protein (GTIII) localized exclusively to muscle and adipose tissue is undetectable in fibroblasts but
present in adipocytes. GTIII mRNA is first expressed three days after differentiation of 3T3-L1 cells has begun. Similarly,
it is not until 3 days following the initiation of differentiation that GTIII protein can be detected, as assayed either by
Western immunoblot or indirect immunofluorescence. The latter technique localizes GTIII predominantly to the perinuclear region
of the adipocyte. The appearance of GTIII in developing fat cells correlates temporally with the acquisition of an increased
stimulation of hexose uptake by maximal concentrations of insulin. These data support the concept that the marked increase
in hexose transport in adipocytes in response to insulin is dependent on the expression in these cells of a specific, hormone-regulatable
transport protein. |
---|---|
ISSN: | 0021-9258 1083-351X |
DOI: | 10.1016/S0021-9258(19)47209-8 |