The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Gastric Inhibitory Polypeptide as an Endogenous Factor Promoting New Bone Formation after Food Ingestion
Open accessAbstract
Calcium plays a fundamental role as second messenger in intracellular signaling and bone serves as the body’s calcium reserve to tightly maintain blood calcium levels. Calcium in ingested meal is the main supply and inadequate calcium intake causes osteoporosis and bone fracture. Here, we describe a novel mechanism of how ingested calcium is deposited on bone. Meal ingestion elicits secretion of the gut hormone gastric inhibitory polypeptide (GIP) from endocrine K cells in the duodenum. Bone histomorphometrical analyses revealed that bone formation parameters in the mice lacking GIP receptor (GIPR−/−) were significantly lower than those of wild-type (GIPR+/+) mice, and that the number of osteoclasts, especially multinuclear osteoclasts, was significantly increased in GIPR−/− mice, indicating that GIPR−/− mice have high-turnover osteoporosis. In vitro examination showed the percentage of osteoblastic cells undergoing apoptosis to be significantly decreased in the presence of GIP. Because GIPR−/− mice exhibited an increased plasma calcium concentration after meal ingestion, GIP directly links calcium contained in meal to calcium deposition on bone.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“GIP also stimulates bone formation by inhibiting osteoclast apoptosis [52].”
From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [52]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“These findings suggest that liraglutide specifically reduces bone resorption without influencing bone formation.368”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [368]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
PARFITT, A. M., Drezner, M. K., Glorieux, F. H., Kanis, J. А., Malluche, H. H., Meunier, P. J., Ott, S. M., & Recker, R. R. (1987) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.5650020617 · Cited by 5,344
Neer, R. M., Arnaud, C. D., Zanchetta, J. R., Prince, R., Gaich, G. A., Reginster, J.-Y., Hodsman, A. B., Eriksen, E. F., Ish-Shalom, S., Genant, H. K., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200105103441904 · Cited by 4,602
Suda, T., Takahashi, N., Udagawa, N., Jimi, E., Gillespie, M. T., & Martin, T. J. (1999) · Endocrine Reviews · doi:10.1210/edrv.20.3.0367 · Cited by 2,345
Self-citationDawson‐Hughes, B., Harris, S. S., Krall, E. A., & Dallal, G. E. (1997) · New England Journal of Medicine · doi:10.1056/nejm199709043371003 · Cited by 2,276
Lips, P. (2001) · Endocrine reviews · doi:10.1210/edrv.22.4.0437 · Cited by 2,203
Genetic regulation of osteoclast development and function
Teitelbaum, S. L., & Ross, F. P. (2003) · Nature Reviews Genetics · doi:10.1038/nrg1122 · Cited by 1,720
The Osteoblast: A Sophisticated Fibroblast under Central Surveillance
Ducy, P. F., Schinke, T., & Karsenty, G. (2000) · Science · doi:10.1126/science.289.5484.1501 · Cited by 1,137
Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
Jilka, R. L., Weinstein, R. S., Bellido, T., Roberson, P. K., PARFITT, A. M., & Manolagas, S. C. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6610 · Cited by 1,042
Inhibition of gastric inhibitory polypeptide signaling prevents obesity
Miyawaki, K., Yamada, Y., Ban, N., Ihara, Y., Tsukiyama, K., Zhou, H., Fujimoto, S., Oku, A., Tsuda, K., Toyokuni, S., et al. (2002) · Nature Medicine · doi:10.1038/nm727 · Cited by 963
Self-citationA Controlled Trial of the Effect of Calcium Supplementation on Bone Density in Postmenopausal Women
Dawson‐Hughes, B., Dallal, G. E., Krall, E. A., Sadowski, L., Sahyoun, N. R., & Tannenbaum, S. (1990) · New England Journal of Medicine · doi:10.1056/nejm199009273231305 · Cited by 945
Cited by
Sorted by citations
Pharmacology, physiology, and mechanisms of incretin hormone action.
Campbell, J. E., & Drucker, D. J. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.04.008 · Cited by 1,500
Glucagon-like peptide-1 receptor: mechanisms and advances in therapy
Zheng, Z., Zong, Y., Ma, Y., Tian, Y., Pang, Y., Zhang, C., & Gao, J. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01931-z · Cited by 1,036
“368 Since GLP-1R is expressed in thyroid C cells and GLP-1 directly stimulates the secretion of calcitonin, which is a potent inhibitor of bone resorption in osteoclasts, GLP-1 may contribute to the nutrient-mediated reduction in bone resorption.”
BackgroundIncretin hormones: Their role in health and disease
Nauck, M. A., & Meier, J. J. (2018) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.13129 · Cited by 950
The role of incretins in glucose homeostasis and diabetes treatment
Kim, W., & Egan, J. M. (2008) · Pharmacological Reviews · doi:10.1124/pr.108.000604 · Cited by 824
GIP and GLP-1, the two incretin hormones: Similarities and differences
Seino, Y., Fukushima, M., & Yabe, D. (2010) · Journal of Diabetes Investigation · doi:10.1111/j.2040-1124.2010.00022.x · Cited by 746
Self-citation
Metadata
- Authors
- Tsukiyama, K., Yamada, Y., Yamada, C., Harada, N., Kawasaki, Y., Ogura, M., Bessho, K., Li, M., Amizuka, N., Sato, M., Udagawa, N., Takahashi, N., Tanaka, K., Oiso, Y., & Seino, Y.
- Affiliations
- Nagoya University (JP)
- Departments of Diabetes and Clinical Nutrition (K.Ts., Y.Y., C.Y., N.H., Y.K., M.O., Y.S.), Kyoto 606-8507, Japan;
- Kyoto University (JP)
- Niigata University (JP)
- Department of Biochemistry (M.S., N.U.), Nagano 399-0781, Japan;
- Matsumoto Dental University (JP)
- Kyoto Women's University (JP)
- Kansai Electric Power Hospital (JP)
- Corresponding author
- Yamada, Yuichiro
- ORCID
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2006-07-01
- Volume
- 20
- Issue
- 7
- Pages
- 1644-1651
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W2103318165
- Cited by
- 198
- References
- 33
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 7 · 2023: 5 · 2022: 9 · 2021: 6 · 2020: 8 · 2019: 17 · 2018: 15 · 2017: 11 · 2016: 12 · 2015: 15 · 2014: 12 · 2013: 18 · 2012: 6
- FWCI
- 3.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Japan Society for the Promotion of Science
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Keywords
- glucose-dependent insulinotropic polypeptide, GIP receptor, bone formation, calcium homeostasis, meal ingestion, gastrointestinal hormones, K cells, osteoclasts, osteoblast apoptosis, plasma calcium, bone histomorphometry
- MeSH terms
- Animals, Bone Resorption, Calcium, Eating, Gastric Inhibitory Polypeptide, Male, Mice, Transgenic, Models, Biological, Osteoblasts, Osteoclasts, Osteogenesis, Osteoporosis, Tibia, Signal Transduction, Apoptosis Regulatory Proteins, Mice
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 ›
Are you an author, or do you see a problem with this page? Request a review
