Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 30, Pages 11133-11138Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1411413111
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Funding
- Wellcome Trust [088357, 084210, 095515]
- Medical Research Council (MRC) Programme Grant [G9824984]
- MRC Centre for Obesity and Related Metabolic Disease (MRC CORD) [G0600717]
- subsequently MRC Metabolic Diseases Unit [4050281695]
- National Institute for Health Research Cambridge Biomedical Research Centre [CG50826]
- Victorian Government's Operational Infrastructure Support Program
- Australian Research Council Linkage Grant [LP120100654]
- MRC [G0900554, G0600717, MC_UU_12012/1, MC_UU_12012/3, G9824984, MC_UU_12012/5] Funding Source: UKRI
- Medical Research Council [G0900554, MC_UU_12012/3, MC_UU_12012/5, MC_UU_12012/5/B, G9824984, G0600717B, MC_UU_12012/1, G0600717] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0507-10380] Funding Source: researchfish
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The gut endocrine system is emerging as a central player in the control of appetite and glucose homeostasis, and as a rich source of peptides with therapeutic potential in the field of diabetes and obesity. In this study we have explored the physiology of insulin-like peptide 5 (Insl5), which we identified as a product of colonic enteroendocrine L-cells, better known for their secretion of glucagon-like peptide-1 and peptideYY. i.p. Insl5 increased food intake in wild-type mice but not mice lacking the cognate receptor Rxfp4. Plasma Insl5 levels were elevated by fasting or prolonged calorie restriction, and declined with feeding. We conclude that Insl5 is an orexigenic hormone released from colonic L-cells, which promotes appetite during conditions of energy deprivation.
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