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Cell Rep. 2014 Oct 9;9(1):40-47. doi: 10.1016/j.celrep.2014.08.060. Epub 2014 Sep 25.

Control of lipid metabolism by tachykinin in Drosophila.

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: rsong@genetics.med.harvard.edu.
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: perrimon@receptor.med.harvard.edu.

Abstract

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.

PMID:
25263556
PMCID:
PMC4325997
DOI:
10.1016/j.celrep.2014.08.060
[Indexed for MEDLINE]
Free PMC Article

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