Inhibitors of RNA and protein synthesis cause Glut4 translocation and increase glucose uptake in adipocytes.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
19 09 2022
Historique:
received: 25 03 2022
accepted: 30 08 2022
entrez: 19 9 2022
pubmed: 20 9 2022
medline: 23 9 2022
Statut: epublish

Résumé

Insulin stimulates glucose uptake in adipocytes by triggering translocation of glucose transporter 4-containg vesicles to the plasma membrane. Under basal conditions, these vesicles (IRVs for insulin-responsive vesicles) are retained inside the cell via a "static" or "dynamic" mechanism. We have found that inhibitors of RNA and protein synthesis, actinomycin D and emetine, stimulate Glut4 translocation and glucose uptake in adipocytes without engaging conventional signaling proteins, such as Akt, TBC1D4, or TUG. Actinomycin D does not significantly affect endocytosis of Glut4 or recycling of transferrin, suggesting that it specifically increases exocytosis of the IRVs. Thus, the intracellular retention of the IRVs in adipocytes requires continuous RNA and protein biosynthesis de novo. These results point out to the existence of a short-lived inhibitor of IRV translocation thus supporting the "static" model.

Identifiants

pubmed: 36123369
doi: 10.1038/s41598-022-19534-5
pii: 10.1038/s41598-022-19534-5
pmc: PMC9485115
doi:

Substances chimiques

Insulin 0
Transferrins 0
Dactinomycin 1CC1JFE158
RNA 63231-63-0
Proto-Oncogene Proteins c-akt EC 2.7.11.1
Glucose IY9XDZ35W2
Emetine X8D5EPO80M

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

15640

Subventions

Organisme : NIH HHS
ID : RO1DK52057
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK129466
Pays : United States
Organisme : NIH HHS
ID : RO1DK129466
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK045735
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK052057
Pays : United States

Informations de copyright

© 2022. The Author(s).

Références

Cell. 2018 Oct 18;175(3):605-614
pubmed: 30340032
Cell Metab. 2008 May;7(5):421-33
pubmed: 18460333
Methods Mol Biol. 2008;456:307-15
pubmed: 18516571
Mol Biol Cell. 2017 Jun 15;28(12):1667-1675
pubmed: 28450454
J Clin Invest. 2000 Jul;106(2):171-6
pubmed: 10903330
Dev Cell. 2005 Jul;9(1):99-108
pubmed: 15992544
J Biol Chem. 1999 Feb 5;274(6):3253-6
pubmed: 9920861
AIDS. 2002 Apr 12;16(6):859-63
pubmed: 11919487
J Clin Invest. 1999 Sep;104(6):733-41
pubmed: 10491408
Biochim Biophys Acta. 2014 Dec;1846(2):342-52
pubmed: 25109892
Mol Metab. 2019 Oct;28:1-13
pubmed: 31444134
Sci STKE. 2003 Feb 11;2003(169):PE5
pubmed: 12582199
Biochem J. 2022 Feb 11;479(3):445-462
pubmed: 35147164
J Biol Chem. 2007 Mar 9;282(10):7710-22
pubmed: 17202135
J Biol Chem. 2008 Oct 31;283(44):30311-21
pubmed: 18713752
EMBO J. 2006 Dec 13;25(24):5648-58
pubmed: 17139247
Mol Endocrinol. 2008 Feb;22(2):226-33
pubmed: 17717074
J Biol Chem. 2003 Sep 5;278(36):33609-12
pubmed: 12788932
Mol Biol Cell. 2003 Mar;14(3):973-86
pubmed: 12631717
J Biol Chem. 2012 Jul 6;287(28):23932-47
pubmed: 22610098
Nat Rev Mol Cell Biol. 2002 Apr;3(4):267-77
pubmed: 11994746
J Clin Endocrinol Metab. 2021 Mar 25;106(4):e1631-e1646
pubmed: 33382888
J Biol Chem. 2002 Mar 15;277(11):9133-8
pubmed: 11782457
Mol Cell Biol. 2007 May;27(9):3456-69
pubmed: 17339344
Nat Rev Mol Cell Biol. 2006 Feb;7(2):85-96
pubmed: 16493415
Physiology (Bethesda). 2022 May 1;37(3):115-127
pubmed: 34779282
J Biol Chem. 2019 Jul 26;294(30):11369-11381
pubmed: 31175156
Nature. 2003 Oct 16;425(6959):727-33
pubmed: 14562105
Horm Metab Res. 2007 Oct;39(10):717-21
pubmed: 17952832
Biosci Rep. 2009 Feb;29(1):1-11
pubmed: 19143591
Annu Rev Biochem. 2012;81:507-32
pubmed: 22482906
J Cell Biol. 1991 Apr;113(1):123-35
pubmed: 2007617
J Biol Chem. 2016 Dec 2;291(49):25629-25640
pubmed: 27738101
Nat Metab. 2021 Mar;3(3):378-393
pubmed: 33686286
Diabetes. 2006 May;55(5):1283-8
pubmed: 16644684
Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E581-91
pubmed: 18728222
J Cell Biol. 2011 May 16;193(4):643-53
pubmed: 21555461
Curr Opin Cell Biol. 2010 Aug;22(4):506-12
pubmed: 20417083
J Biol Chem. 2018 Jul 6;293(27):10466-10486
pubmed: 29773651
Cell Metab. 2010 Jan;11(1):84-92
pubmed: 20074531

Auteurs

A B Meriin (AB)

Department of Biochemistry, Boston University School of Medicine, Boston, MA, 02118, USA.

N Zaarur (N)

Department of Biochemistry, Boston University School of Medicine, Boston, MA, 02118, USA.

J S Bogan (JS)

Department of Internal Medicine and Cell Biology, Yale University School of Medicine, New Haven, CO, 06520, USA.

K V Kandror (KV)

Department of Biochemistry, Boston University School of Medicine, Boston, MA, 02118, USA. kkandror@bu.edu.

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