Prolactin treatment increases GLUT2 but not the G protein subunit content in cell membranes from cultured neonatal rat islets

FEBS Letters

Carneiro, Everardo M.¹  de Mazancourt, Philippe²  Atwater, Illani¹  Boschero, A.Carlos¹ 

[1] Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA;Laboratoire Central de Biologie, Centre Hospitalier Intercommunal Leon Touhladjian, 78303 Poissy, France

关键词: Islet;    Neonatal rat;    GLUT2;    G protein;    Prolactin;    DTT;    dithiotreitol;    EGTA;    (ethylene glycol-bis[β-ami-noethyl ether]-N;    N;    N';    N;    -tetraa cetic acid;    NEM;    N-ethylmaleimide;    PMSF;    phenylmethylsulfonil fluoride;    PVDF;    polyvinylidene difluoride;    SDS;    sodium dodecyl sulfate;    TTBS;    tris-bufferd saline;   

DOI  :  10.1016/0014-5793(94)80305-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Neonatal rat islets exhibit a reduced secretory response to glucose, compared to adult rat islets. The maturation of the secretory response is stimulated by prolactin (PRL). We show here by immunoblot analysis that PRL increases the β-cell/liver glucose transporter GLUT2 in membrane fractions from cultured neonatal rat islets. This increase (+86%) may explain, at least in part, the development of a mature glucose response. G proteins modulate insulin secretion from pancreatic β-cells. We show here by immunoblot analysis that, in contrast to the effect on GLUT2, PRL treatment does not modify the G protein subunits αi2, αi3, αo, αs, αq and β35 and β36, in cultured neonatal islets.

【 授权许可】

Unknown