Cooperation between HMGA1, PDX-1, and MafA is essential for glucose- induced insulin transcription in pancreatic beta cells
Open accessAbstract
The high-mobility group AT-hook 1 (HMGA1) protein is a nuclear architectural factor that can organize chromatin structures. It regulates gene expression by controlling the formation of stereospecific multiprotein complexes called "enhanceosomes" on the AT-rich regions of target gene promoters. Previously, we reported that defects in HMGA1 caused decreased insulin receptor expression and increased susceptibility to type 2 diabetes mellitus in humans and mice. Interestingly, mice with disrupted HMGA1 gene had significantly smaller islets and decreased insulin content in their pancreata, suggesting that HMGA1 may have a direct role in insulin transcription and secretion. Herein, we investigate the regulatory roles of HMGA1 in insulin transcription. We provide evidence that HMGA1 physically interacts with PDX-1 and MafA, two critical transcription factors for insulin gene expression and beta-cell function, both in vitro and in vivo. We then show that the overexpression of HMGA1 significantly improves the transactivating activity of PDX-1 and MafA on human and mouse insulin promoters, while HMGA1 knockdown considerably decreased this transactivating activity. Lastly, we demonstrate that high glucose stimulus significantly increases the binding of HMGA1 to the insulin (INS) gene promoter, suggesting that HMGA1 may act as a glucose-sensitive element controlling the transcription of the INS gene. Together, our findings provide evidence that HMGA1, by regulating PDX-1- and MafA-induced transactivation of the INS gene promoter, plays a critical role in pancreatic beta-cell function and insulin production.
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In obese individuals destined to become diabetics, pancreatic beta-cells may compensate for impaired peripheral insulin responsiveness by secreting more insulin, leading to hyperinsulinemia, a biological marker of insulin resistance often indicative of pre-diabetic status.
“At first, in obese individuals destined to become diabetics, pancreatic β-cells may compensate for the impaired peripheral insulin responsiveness by secreting more insulin into the bloodstream in an effort to reduce blood glucose levels, thus leading to hyperinsulinemia, a biological marker of IR, often indicative of a pre-diabetic status [29,30].”
From Mediterranean diet nutrients to turn the tide against insulin resistance and related diseases (2020) · cites this paper as [30]
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- Authors
- Arcidiacono, B., Iiritano, S., Chiefari, E., Brunetti, F. S., Gu, G., Foti, D. P., & Brunetti, A.
- Affiliations
- Magna Graecia University (IT)
- Vanderbilt University (US)
- Corresponding author
- Brunetti, Antonio
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2015-01-13
- Volume
- 5
- Pages
- 237-237
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC4292585
- OpenAlex
- W2075481792
- Cited by
- 68
- References
- 62
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 25 · 2017: 11 · 2016: 3 · 2015: 5
- FWCI
- 14.78
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca (2007–2013, GGP04245, protocol 2004062059-002 Italy, 2004062059-002, 2004062059)
- Regione Calabria
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK065949)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- HMGA1, PDX1, MafA, pancreatic beta cells, insulin gene promoter, transcription factor interaction, chromatin structure, enhanceosome, type 2 diabetes, insulin secretion
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