A novel form of ciliopathy underlies hyperphagia and obesity in Ankrd26 knockout mice

被引：28

作者：

Acs, Peter ^{[1
]}

Bauer, Peter O. ^{[2
]}

Mayer, Balazs ^{[3
]}

Bera, Tapan ^{[1
]}

Macallister, Rhonda ^{[4
]}

Mezey, Eva ^{[3
]}

Pastan, Ira ^{[1
]}

机构：

[1] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA

[2] NCI, Neurooncol Branch, NINDS, NIH, Bethesda, MD 20892 USA

[3] Natl Inst Dent & Craniofacial Res, Adult Stem Cell Unit, CSDB, NIH, Bethesda, MD 20892 USA

[4] NCI, NIH, Bethesda, MD 20892 USA

来源：

Brain Structure & Function | 2015年 / 220卷 / 03期

关键词：

Obesity; Neuronal cilia; Leptin receptor; ANKRD26; Melanocortin receptor; Feeding behavior; Paraventricular nucleus; Arcuate nucleus; CRH; Ciliary body proteins; BARDET-BIEDL-SYNDROME; CORTICOTROPIN-RELEASING HORMONE; MELANOCYTE-STIMULATING HORMONE; PROTEIN-COUPLED-RECEPTORS; FOOD-INTAKE; MELANOCORTIN-4; RECEPTOR; PARAVENTRICULAR NUCLEUS; CILIARY ROOTLET; LEPTIN RECEPTOR; GENE-EXPRESSION;

D O I：

10.1007/s00429-014-0741-9

中图分类号：

R602 [外科病理学、解剖学]; R32 [人体形态学];

学科分类号：

100101 ;

摘要：

Human ciliopathies are genetic disorders caused by mutations in genes responsible for the formation and function of primary cilia. Some are associated with hyperphagia and obesity (e.g., Bardet-Biedl Syndrome, Alstrom Syndrome), but the mechanisms underlying these problems are not fully understood. The human gene ANKRD26 is located on 10p12, a locus that is associated with some forms of hereditary obesity. Previously, we reported that disruption of this gene causes hyperphagia, obesity and gigantism in mice. In the present study, we looked for the mechanisms that induce hyperphagia in the Ankrd26-/- mice and found defects in primary cilia in regions of the central nervous system that control appetite and energy homeostasis.

引用

页码：1511 / 1528

页数：18

共 60 条

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