RETRACTED: Betatrophin: A Hormone that Controls Pancreatic β Cell Proliferation
Open accessAbstract
Replenishing insulin-producing pancreatic β cell mass will benefit both type I and type II diabetics. In adults, pancreatic β cells are generated primarily by self-duplication. We report on a mouse model of insulin resistance that induces dramatic pancreatic β cell proliferation and β cell mass expansion. Using this model, we identify a hormone, betatrophin, that is primarily expressed in liver and fat. Expression of betatrophin correlates with β cell proliferation in other mouse models of insulin resistance and during gestation. Transient expression of betatrophin in mouse liver significantly and specifically promotes pancreatic β cell proliferation, expands β cell mass, and improves glucose tolerance. Thus, betatrophin treatment could augment or replace insulin injections by increasing the number of endogenous insulin-producing cells in diabetics.
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Betatrophin was first identified as a factor that drives β-cell proliferation and increases β-cell mass in a murine model of insulin resistance.
“The hepatokine betatrophin, also known as TD26, re-feeding induced fat and liver (RIFL), lipasin or angiopoietin-like (ANGPTL) 8, was first identified as a factor that drives β-cell proliferation and thus increases β-cell mass in a murine model of insulin resistance.178”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [178]
In the ACCORD, VADT, ORIGIN, and ADVANCE trials, intensive glucose lowering did not reduce cardiovascular events.
“In none of these studies did intensive glucose lowering reduce cardiovascular events”
From Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future (2014) · cites this paper as [123]
ORIGIN showed no evidence of increased risk of cancer with glargine.
“Noteworthy from the ORIGIN study was the lack of evidence of an increased risk of cancer with glargine123”
From Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future (2014) · cites this paper as [123]
Only reports of troglitazone in the DPP and glargine in ORIGIN suggest a residual benefit after prolonged withdrawal of the intervention.
“Only reports of the effects of troglitazone in the DPP149 and glargine in ORIGIN123 suggest a residual benefit after prolonged withdrawal of the intervention.”
From Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future (2014) · cites this paper as [123]
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- Authors
- Yi, P., Park, J.-S., & Melton, D. A.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Melton, Douglas A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 153
- Issue
- 4
- Pages
- 747-758
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3756510
- OpenAlex
- W2104584321
- Cited by
- 449
- References
- 57
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 10 · 2022: 18 · 2021: 20 · 2020: 24 · 2019: 17 · 2018: 30 · 2017: 49 · 2016: 72 · 2015: 76 · 2014: 82 · 2013: 40 · 2012: 1
- FWCI
- 88.00
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- Howard Hughes Medical Institute
- Helen Hay Whitney Foundation
- National Institutes of Health
- Harvard Stem Cell Institute
- National Institute of Diabetes and Digestive and Kidney Diseases (RC4DK090781)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- betatrophin, pancreatic beta-cell proliferation, beta-cell mass expansion, insulin resistance, glucose tolerance, type 1 diabetes, type 2 diabetes, liver hormone, gestation, retraction
- MeSH terms
- Angiopoietin-like Proteins, Angiopoietin-Like Protein 8, Amino Acid Sequence, Animals, Female, Glucose, Humans, Insulin Resistance, Liver, Male, Mice, Inbred C57BL, Molecular Sequence Data, Pancreas, Peptides, Receptor, Insulin, Sequence Alignment, Peptide Hormones, Cell Proliferation, Insulin-Secreting Cells, Mice, Adipose Tissue, White
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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