Thyroid hormone T3 counteracts STZ induced diabetes in mouse
Open accessAbstract
This study intended to demonstrate that the thyroid hormone T3 counteracts the onset of a Streptozotocin (STZ) induced diabetes in wild type mice. To test our hypothesis diabetes has been induced in Balb/c male mice by multiple low dose Streptozotocin injection; and a group of mice was contemporaneously injected with T3. After 48 h mice were tested for glucose tolerance test, insulin serum levels and then sacrificed. Whole pancreata were utilized for morphological and biochemical analyses, while protein extracts and RNA were utilized for expression analyses of specific molecules. The results showed that islets from T3 treated mice were comparable to age- and sex-matched control, untreated mice in number, shape, dimension, consistency, ultrastructure, insulin and glucagon levels, Tunel positivity and caspases activation, while all the cited parameters and molecules were altered by STZ alone. The T3-induced pro survival effect was associated with a strong increase in phosphorylated Akt. Moreover, T3 administration prevented the STZ-dependent alterations in glucose blood level, both during fasting and after glucose challenge, as well as in insulin serum level. In conclusion we demonstrated that T3 could act as a protective factor against STZ induced diabetes.
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Physiological T3 treatment promotes beta-cell proliferation.
“Furthermore, excess T3 leads to considerable impairment of the islet function, while physiological T3 treatment promotes beta-cell proliferation (57, 62).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [62]
The Introduction reports that T3 acts as a mitogenic factor in pancreatic β cells, supporting the proliferation part of the claim. But the Results report no increase in Ki67-positive cells in the treated mice, and the Discussion attributes preserved β-cell mass chiefly to prevention of apoptosis. The paper therefore does not show that physiological T3 treatment promoted β-cell proliferation in this study. (LLM, conf=0.86)
Experimental — accuracy not yet measuredExcess T3 leads to considerable impairment of islet function.
“Furthermore, excess T3 leads to considerable impairment of the islet function, while physiological T3 treatment promotes beta-cell proliferation (57, 62).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [62]
The Discussion says excess thyroid hormone can cause systemic side effects, but does not say it impairs islet function. Its findings concern T3-treated mice that did not develop hyperthyroidism; the Results report preservation of islets against STZ damage. Searches for excess or supraphysiological T3 and islet impairment found no passage addressing the claim. (LLM, conf=0.78)
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“Furthermore, excess T3 leads to considerable impairment of the islet function, while physiological T3 treatment promotes beta-cell proliferation (57, 62).”
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- Authors
- Verga Falzacappa, C., Mangialardo, C., Madaro, L., Ranieri, D., Lupoi, L., Stigliano, A., Torrisi, M. R., Bouchè, M., Toscano, V., & Misiti, S.
- Affiliations
- Sapienza University of Rome (IT)
- Università Cattolica del Sacro Cuore (IT)
- Corresponding author
- Misiti, Silvia
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-05-27
- Volume
- 6
- Issue
- 5
- Pages
- e19839
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3103518
- OpenAlex
- W2006638074
- Cited by
- 52
- References
- 35
- Citations by year
- 2026: 1 · 2025: 6 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 1 · 2014: 9 · 2013: 7 · 2012: 2
- FWCI
- 5.90
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- Agenzia Spaziale Italiana
- Sapienza Università di Roma
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- triiodothyronine, thyroid hormones, streptozotocin-induced diabetes, beta-cell survival, pancreatic islets, glucose tolerance, insulin, glucagon, apoptosis, caspase activation, Akt phosphorylation, beta-cell protection
- MeSH terms
- Animals, Cell Survival, Diabetes Mellitus, Experimental, Enzyme Activation, Glucose, Male, Mice, Inbred BALB C, Receptors, Thyroid Hormone, Streptozocin, Triiodothyronine, Apoptosis, Protein Transport, Insulin-Secreting Cells, Proto-Oncogene Proteins c-akt, Glucose Transporter Type 2, 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 ›
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