Clusterin and LRP2 are critical components of the hypothalamic feeding regulatory pathway

So Young Gil, Byung-Soo Youn, Kyunghee Byun, Hu Huang, Churl Namkoong, Pil-Geum Jang, Joo-Yong Lee, Young-Hwan Jo, Gil Myoung Kang, Hyun-Kyong Kim, Mi-Seon Shin, Claus U. Pietrzik, Bonghee Lee, Young-Bum Kim and Min-Seon Kim ()
Additional contact information
So Young Gil: Asan Institute for Life Science, University of Ulsan College of Medicine
Byung-Soo Youn: AdipoGen Inc.
Kyunghee Byun: Lee Gil Ya Cancer and Diabetes Institute, Gachon University
Hu Huang: Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School
Churl Namkoong: Asan Institute for Life Science, University of Ulsan College of Medicine
Pil-Geum Jang: Asan Institute for Life Science, University of Ulsan College of Medicine
Joo-Yong Lee: Asan Institute for Life Science, University of Ulsan College of Medicine
Young-Hwan Jo: Albert Einstein College of Medicine
Gil Myoung Kang: Asan Institute for Life Science, University of Ulsan College of Medicine
Hyun-Kyong Kim: Asan Institute for Life Science, University of Ulsan College of Medicine
Mi-Seon Shin: Asan Medical Center, University of Ulsan College of Medicine
Claus U. Pietrzik: Institute of Pathobiochemistry, University Medical Center of the Johannes Gutenberg-University Mainz
Bonghee Lee: Lee Gil Ya Cancer and Diabetes Institute, Gachon University
Young-Bum Kim: Lee Gil Ya Cancer and Diabetes Institute, Gachon University
Min-Seon Kim: Asan Institute for Life Science, University of Ulsan College of Medicine

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: Abstract Hypothalamic feeding circuits are essential for the maintenance of energy balance. There have been intensive efforts to discover new biological molecules involved in these pathways. Here we report that central administration of clusterin, also called apolipoprotein J, causes anorexia, weight loss and activation of hypothalamic signal transduction-activated transcript-3 in mice. In contrast, inhibition of hypothalamic clusterin action results in increased food intake and body weight, leading to adiposity. These effects are likely mediated through the mutual actions of the low-density lipoprotein receptor-related protein-2, a potential receptor for clusterin, and the long-form leptin receptor. In response to clusterin, the low-density lipoprotein receptor-related protein-2 binding to long-form leptin receptor is greatly enhanced in cultured neuronal cells. Furthermore, long-form leptin receptor deficiency or hypothalamic low-density lipoprotein receptor-related protein-2 suppression in mice leads to impaired hypothalamic clusterin signalling and actions. Our study identifies the hypothalamic clusterin–low-density lipoprotein receptor-related protein-2 axis as a novel anorexigenic signalling pathway that is tightly coupled with long-form leptin receptor-mediated signalling.

Date: 2013
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DOI: 10.1038/ncomms2896

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