Haematopoietic cells produce BDNF and regulate appetite upon migration to the hypothalamus

Hiroshi Urabe, Hideto Kojima (), Lawrence Chan, Tomoya Terashima, Nobuhiro Ogawa, Miwako Katagi, Kazunori Fujino, Asako Kumagai, Hiromichi Kawai, Akihiro Asakawa, Akio Inui, Hitoshi Yasuda, Yutaka Eguchi, Kazuhiro Oka, Hiroshi Maegawa, Atsunori Kashiwagi and Hiroshi Kimura
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Hiroshi Urabe: Shiga University of Medical Science
Hideto Kojima: Shiga University of Medical Science
Lawrence Chan: and Molecular and Cellular Biology, Baylor College of Medicine
Tomoya Terashima: Shiga University of Medical Science
Nobuhiro Ogawa: Shiga University of Medical Science
Miwako Katagi: Shiga University of Medical Science
Kazunori Fujino: Shiga University of Medical Science
Asako Kumagai: Shiga University of Medical Science
Hiromichi Kawai: Shiga University of Medical Science
Akihiro Asakawa: Kagoshima University Graduate School of Medical and Dental Sciences
Akio Inui: Kagoshima University Graduate School of Medical and Dental Sciences
Hitoshi Yasuda: Shiga University of Medical Science
Yutaka Eguchi: Shiga University of Medical Science
Kazuhiro Oka: and Molecular and Cellular Biology, Baylor College of Medicine
Hiroshi Maegawa: Shiga University of Medical Science
Atsunori Kashiwagi: Shiga University of Medical Science
Hiroshi Kimura: Shiga University of Medical Science

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

Abstract: Abstract Brain-derived neurotrophic factor (BDNF) suppresses food intake by acting on neurons in the hypothalamus. Here we show that BDNF-producing haematopoietic cells control appetite and energy balance by migrating to the hypothalamic paraventricular nucleus. These haematopoietic-derived paraventricular nucleus cells produce microglial markers and make direct contacts with neurons in response to feeding status. Mice with congenital BDNF deficiency, specifically in haematopoietic cells, develop hyperphagia, obesity and insulin resistance. These abnormalities are ameliorated by bone marrow transplantation with wild-type bone marrow cells. Furthermore, when injected into the third ventricle, wild-type bone marrow mononuclear cells home to the paraventricular nucleus and reverse the hyperphagia of BDNF-deficient mice. Our results suggest a novel mechanism of feeding control based on the production of BDNF by haematopoietic cells and highlight a potential new therapeutic route for the treatment of obesity.

Date: 2013
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DOI: 10.1038/ncomms2536

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