Control of lipid metabolism by tachykinin in Drosophila
Cell Reports. 2014-10-01; 9(1): 40-47
DOI: 10.1016/j.celrep.2014.08.060
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Song W(1), Veenstra JA(2), Perrimon N(3).
Author information:
(1)Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Howard
Hughes Medical Institute, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Electronic address: .
(2)Université de Bordeaux, INCIA UMR 5287 CNRS, 33405 Talence, France.
(3)Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Howard
Hughes Medical Institute, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Electronic address: .
Erratum in
Cell Rep. 2020 Feb 18;30(7):2461.
The intestine is a key organ for lipid uptake and distribution, and abnormal
intestinal lipid metabolism is associated with obesity and hyperlipidemia.
Although multiple regulatory gut hormones secreted from enteroendocrine cells
(EEs) regulate systemic lipid homeostasis, such as appetite control and energy
balance in adipose tissue, their respective roles regarding lipid metabolism in
the intestine are not well understood. We demonstrate that tachykinins (TKs), one
of the most abundant secreted peptides expressed in midgut EEs, regulate
intestinal lipid production and subsequently control systemic lipid homeostasis
in Drosophila and that TKs repress lipogenesis in enterocytes (ECs) associated
with TKR99D receptor and protein kinase A (PKA) signaling. Interestingly,
nutrient deprivation enhances the production of TKs in the midgut. Finally,
unlike the physiological roles of TKs produced from the brain, gut-derived TKs do
not affect behavior, thus demonstrating that gut TK hormones specifically
regulate intestinal lipid metabolism without affecting neuronal functions.
Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.