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Gutierrez-Aguilar, R.* ; Kim, D.* ; Casimir, M.* ; Dai, X.* ; Pfluger, P.T. ; Park, J.* ; Haller, A.* ; Donelan, E.* ; D'Alessio, D.* ; Woods, S.C.* ; MacDonald, P.E.* ; Seeley, R.J.*

The role of the transcription factor ETV5 in insulin exocytosis.

Diabetologia 57, 383-391 (2014)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Genome-wide association studies have revealed an association of the transcription factor ETS variant gene 5 (ETV5) with human obesity. However, its role in glucose homeostasis and energy balance is unknown. Etv5 knockout (KO) mice were monitored weekly for body weight (BW) and food intake. Body composition was measured at 8 and 16 weeks of age. Glucose metabolism was studied, and glucose-stimulated insulin secretion was measured in vivo and in vitro. Etv5 KO mice are smaller and leaner, and have a reduced BW and lower fat mass than their wild-type controls on a chow diet. When exposed to a high-fat diet, KO mice are resistant to diet-induced BW gain. Despite a greater insulin sensitivity, KO mice have profoundly impaired glucose tolerance associated with impaired insulin secretion. Morphometric analysis revealed smaller islets and a reduced beta cell size in the pancreatic islets of Etv5 KO mice. Knockdown of ETV5 in an insulin-secreting cell line or beta cells from human donors revealed intact mitochondrial and Ca2+ channel activity, but reduced insulin exocytosis. This work reveals a critical role for ETV5 in specifically regulating insulin secretion both in vitro and in vivo.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Beta Cell ; Etv5 ; Genome-wide Association Study ; Glucose Homeostasis ; Insulin Exocytosis ; Insulin Secretion ; Insulin Sensitivity ; Transcription Factor; Target Genes; Factor Erm; Ets; Expression; Secretion; Family; Domain; Mouse; Mechanisms; Growth
ISSN (print) / ISBN 0012-186X
e-ISSN 1432-0428
Zeitschrift Diabetologia
Quellenangaben Band: 57, Heft: 2, Seiten: 383-391 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Berlin ; Heidelberg [u.a.]
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)