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Volta, F. ; Gerdes, J.M.

The role of primary cilia in obesity and diabetes.

Ann. NY Acad. Sci. 1391, 71-84 (2017)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
One in 12 people worldwide suffers from diabetes and more than 90% of affected adult individuals are diagnosed with type 2 diabetes mellitus (T2DM). Obesity adds to the personal risk to develop T2DM, and both metabolic diseases are rampantly increasing worldwide. Over recent years, primary cilia have moved into the focus of basic and clinical research, after several human diseases have been identified as ciliopathies (i.e., they are linked to ciliary dysfunction). A subset of ciliopathies presents with obesity and diabetes, either as core symptoms or major complications. Several studies have shown a role for ciliary signaling in the satiety signaling centers of the hypothalamus and in other metabolically active tissues, such as pancreatic islets. Here, we discuss recent advances and perspectives in ciliary metabolic research.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Diabetes ; Insulin Signaling ; Leptin Signaling ; Obesity ; Primary Cilia ; β Cells; Bardet-biedl-syndrome; Nonsyndromic Retinitis-pigmentosa; Neuropeptide Yy2 Receptor; Body-weight; Insulin Sensitivity; Glucose-tolerance; Syndrome Proteins; Joubert Syndrome; Alstrom-syndrome; Kidney-disease
Sprache englisch
Veröffentlichungsjahr 2017
Prepublished im Jahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 0077-8923
e-ISSN 1749-6632
Zeitschrift Annals of the New York Academy of Sciences
Quellenangaben Band: 1391, Heft: 1, Seiten: 71-84 Artikelnummer: , Supplement: ,
Verlag New York Academy of Sciences
Verlagsort Hoboken
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-233
PubMed ID 27706820
DOI 10.1111/nyas.13216
WOS ID WOS:000398806300005
Erfassungsdatum 2016-10-17
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