Energy Homeostasis and Gastrointestinal Endocrine Differentiation Do Not Require the Anorectic Hormone Peptide YY
Open accessAbstract
The gastrointestinal hormone peptide YY is a potent inhibitor of food intake and is expressed early during differentiation of intestinal and pancreatic endocrine cells. In order to better understand the role of peptide YY in energy homeostasis and development, we created mice with a targeted deletion of the peptide YY gene. All intestinal and pancreatic endocrine cells developed normally in the absence of peptide YY with the exception of pancreatic polypeptide (PP) cells, indicating that peptide YY expression was not required for terminal differentiation. We used recombination-based cell lineage trace to determine if peptide YY cells were progenitors for gastrointestinal endocrine cells. Peptide YY(+) cells gave rise to all L-type enteroendocrine cells and to islet partial differential and PP cells. In the pancreas, approximately 40% of pancreatic alpha and rare beta cells arose from peptide YY(+) cells, suggesting that most beta cells and surprisingly the majority of alpha cells are not descendants of peptide YY(+)/glucagon-positive/insulin-positive cells that appear during early pancreagenesis. Despite the anorectic effects of exogenous peptide YY(3-36) following intraperitoneal administration, mice lacking peptide YY showed normal growth, food intake, energy expenditure, and responsiveness to peptide YY(3-36). These observations suggest that targeted disruption of the peptide YY gene does not perturb terminal endocrine cell differentiation or the control of food intake and energy homeostasis.
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Deletion of Pyy in mice does not reveal any obvious defects in endoderm patterning.
“Deletion of Pyy in mice does not reveal any obvious defects in endoderm patterning [46,47].”
From A systematic screen for genes expressed in definitive endoderm by Serial Analysis of Gene Expression (SAGE) (2007) · cites this paper as [46]
The Discussion reports that Pyy-null mice largely retain endocrine differentiation in the colon and pancreas, supporting a narrower finding about these endoderm-derived tissues. It also notes an exception for pancreatic PP cells. The paper does not establish that endoderm patterning overall is unaffected. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGenetic lineage tracing using Pyy-Cre and a ROSA26 reporter mouse strain demonstrated that in the adult, descendants of Pyy-expressing cells can contribute to the periphery of pancreatic islets and the L-type cells of the distal intestine.
“However, genetic lineage tracing using Pyy-Cre and a ROSA26 reporter mouse strain demonstrated that in the adult, descendants of Pyy-expressing cells can contribute to the periphery of pancreatic islets and the L-type cells of the distal intestine [46].”
From A systematic screen for genes expressed in definitive endoderm by Serial Analysis of Gene Expression (SAGE) (2007) · cites this paper as [46]
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PYY in the Expanding Pancreatic Epithelium
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Peptide YY: obesity's cause and cure?
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The role of PYY in improving insulin resistance
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The role of gut hormones in controlling the food intake. What is their role in emerging diseases?
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THE ROLE OF THE INTESTINAL MICROBIOTA IN THE MODULATION OF FOOD INTAKE AND BODY WEIGHTPreprint
Dalby, M. J. (2017) · doi:10.31237/osf.io/rqz2p
Gastrointestinal Hormones and the Control of Food Intake and Energy Metabolism
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(2006) · Current Opinion in Endocrinology & Diabetes · doi:10.1097/01.med.0000202323.44809.4f
- Authors
- Schonhoff, S., Baggio, L., Ratineau, C., Ray, S. K., Lindner, J., Magnuson, M. A., Drucker, D. J., & Leiter, A. B.
- Affiliations
- Tufts Medical Center (US)
- University of Toronto (CA)
- Vanderbilt University (US)
- Tufts University (US)
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2005-05-01
- Volume
- 25
- Issue
- 10
- Pages
- 4189-4199
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC1087718
- OpenAlex
- W2113114436
- Cited by
- 53
- References
- 53
- Citations by year
- 2026: 1 · 2025: 2 · 2022: 1 · 2021: 2 · 2018: 2 · 2017: 5 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 1 · 2012: 9
- FWCI
- 6.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p60dk020593-31, DK 20593, DK42502)
- Canadian Institutes of Health Research
- National Cancer Institute (T32 CA65441, T32CA065441)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60-DK020593, DK67166, R01DK067166, P01DK042502, R01DK052870, P30 DK-34928, DK42502, DK 20593, P30DK034928, DK43673, R01DK043673, U19DK042502, DK52870, P30DK020593)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- peptide YY, energy homeostasis, gastrointestinal endocrine cells, endocrine differentiation, pancreatic endocrine cells, intestinal endocrine cells, pancreatic polypeptide cells, alpha cells, pancreatic beta cells, dietary intake, gene deletion mice, lineage tracing, energy expenditure
- MeSH terms
- Animals, Cell Differentiation, Digestive System, Digestive System Physiological Phenomena, Eating, Endocrine System, Energy Metabolism, Homeostasis, Islets of Langerhans, Mice, Transgenic, Weight Gain, Gene Deletion, Gene Expression Regulation, Developmental, Cell Lineage, Transgenes, Peptide YY, Mice
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