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Defective insulin secretion in hepatocyte nuclear factor 1alpha-deficient mice.
Open accessAbstract
Mutations in the gene for the transcription factor hepatocyte nuclear factor (HNF) 1alpha cause maturity-onset diabetes of the young (MODY) 3, a form of diabetes that results from defects in insulin secretion. Since the nature of these defects has not been defined, we compared insulin secretory function in heterozygous [HNF-1alpha (+/-)] or homozygous [HNF-1alpha (-/-)] mice with null mutations in the HNF-1alpha gene with their wild-type littermates [HNF-1alpha (+/+)]. Blood glucose concentrations were similar in HNF-1alpha (+/+) and (+/-) mice (7.8+/-0.2 and 7.9+/-0.3 mM), but were significantly higher in the HNF-1alpha (-/-) mice (13.1+/-0.7 mM, P < 0.001). Insulin secretory responses to glucose and arginine in the perfused pancreas and perifused islets from HNF-1alpha (-/-) mice were < 15% of the values in the other two groups and were associated with similar reductions in intracellular Ca2+ responses. These defects were not due to a decrease in glucokinase or insulin gene transcription. beta cell mass adjusted for body weight was not reduced in the (-/-) animals, although pancreatic insulin content adjusted for pancreas weight was slightly lower (0.06+/-0.01 vs. 0.10+/-0.01 microg/mg, P < 0.01) than in the (+/+) animals. In summary, a null mutation in the HNF-1alpha gene in homozygous mice leads to diabetes due to alterations in the pathways that regulate beta cell responses to secretagogues including glucose and arginine. These results provide further evidence in support of a key role for HNF-1alpha in the maintenance of normal beta cell function.
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“it is the loss of HNF1α resulting in an almost abolished insulin secretion, likely due to a decreased response to intracellular calcium.”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [176]
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“These findings support the importance of HNF1α in maintaining β-cell function176 and its involvement in maturity-onset diabetes of the young (MODY3).177”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [176]
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Mutations in the hepatocyte nuclear factor-1α gene in maturity-onset diabetes of the young (MODY3)
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Self-citationInteraction of a Liver-Specific Nuclear Factor with the Fibrinogen and α 1 -Antitrypsin Promoters
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Self-citationCharacterization of the MODY3 phenotype. Early-onset diabetes caused by an insulin secretion defect.
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Cited by
Sorted by citations
Molecular mechanisms and clinical pathophysiology of maturity-onset diabetes of the young
Fajans, S. S., Bell, G. I., & Polonsky, K. S. (2001) · New England Journal of Medicine · doi:10.1056/nejmra002168 · Cited by 1,123
Self-citationPancreatic regulation of glucose homeostasis.
Röder, P. V., Wu, B., Liu, Y., & Han, W. (2016) · Experimental & Molecular Medicine · doi:10.1038/emm.2016.6 · Cited by 985
Mitochondrial function in normal and diabetic β-cells
Maechler, P., & Wollheim, C. B. (2001) · Nature · doi:10.1038/414807a · Cited by 519
“Suppression of the HNF-1α gene in mice results in diabetes and impairment of glucose-induced insulin secretion assessed in vitro”
BackgroundGenetic cause of hyperglycaemia and response to treatment in diabetes
Pearson, E. R., Starkey, B. J., Powell, R. J., Gribble, F. M., Clark, P. M., & Hattersley, A. T. (2003) · The Lancet · doi:10.1016/s0140-6736(03)14571-0 · Cited by 607
Regulation of pancreatic β-cell growth and survival by the serine/threonine protein kinase Akt1/PKBα
Tuttle, R. L., Gill, N. S., Pugh, W., Lee, J.-P., Koeberlein, B., Furth, E. E., Polonsky, K. S., Naji, A., & Birnbaum, M. J. (2001) · Nature Medicine · doi:10.1038/nm1001-1133 · Cited by 511
“The pancreas was perfused using a slightly modified protocol as describe”
MethodSelf-citation
Metadata
- Authors
- Pontoglio, M., Sreenan, S., Roe, M., Pugh, W., Ostrega, D., Doyen, A., Pick, A. J., Baldwin, A., Velho, G., Froguel, P., Levisetti, M., Bonner-Weir, S., Bell, G. I., Yaniv, M., & Polonsky, K. S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Institut Pasteur de Lille (FR)
- Inserm (FR)
- Howard Hughes Medical Institute (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1998-05-15
- Volume
- 101
- Issue
- 10
- Pages
- 2215-2222
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC508809
- OpenAlex
- W2095311108
- Cited by
- 321
- References
- 23
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 4 · 2023: 3 · 2022: 14 · 2021: 11 · 2020: 7 · 2019: 7 · 2018: 5 · 2017: 8 · 2016: 7 · 2015: 16 · 2014: 7 · 2013: 4 · 2012: 11
- FWCI
- 21.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p01dk044840-10)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 44840, DK-31842, DK 20595)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- HNF1A, maturity-onset diabetes of the young, MODY3, insulin secretion, beta-cell function, glucose-stimulated insulin secretion, arginine-stimulated insulin secretion, intracellular calcium, hyperglycemia, insulin content, glucokinase, insulin gene transcription
- MeSH terms
- Insulin Secretion, Animals, Arginine, Blood Glucose, Body Weight, Calcium, Diabetes Mellitus, Type 2, DNA-Binding Proteins, Gene Expression Regulation, Glucose, Heterozygote, Homozygote, Immunohistochemistry, Insulin, Islets of Langerhans, Nuclear Proteins, Organ Size, Pancreas, RNA, Messenger, Transcription Factors, Mice, Knockout, Mice, Hepatocyte Nuclear Factor 1, Hepatocyte Nuclear Factor 1-alpha, Hepatocyte Nuclear Factor 1-beta
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