ArticleJournal of clinical research in pediatric endocrinology2012
Early onset of liver steatosis in a Japanese girl with maturity-onset diabetes of the young type 3 (MODY3).
Article in Journal of clinical research in pediatric endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Dominant-negative HNF1α mutant promotes liver steatosis and inflammation by regulating hepatic complement factor D.iScience · 2023Article
- Loss of HNF1α Function Contributes to Hepatocyte Proliferation and Abnormal Cholesterol Metabolism via Downregulating miR-122: A Novel Mechanism of MODY3.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Maturity-onset diabetes of the young type 3 (MODY3) is caused by heterozygous mutation in the HNF1A gene. Liver adenomatosis has been reported in MODY3 patients. The patient reported in this paper is a Japanese girl who first developed hepatomegaly, fatty liver, and hepatic dysfunction at age 5 years. Liver biopsy demonstrated steatosis and degeneration of hepatocytes. At that time, blood glucose and HbA1c levels were within normal ranges. Elevated HbA1c was noticed 4 years later, but islet cell and glutamic acid decarboxylase antibodies were not detected in the serum. Therefore, MODY3 was suspected and subsequent analysis of the HNF1A gene identified a heterozygous germline splice donor-site mutation in intron 9. MODY3 patients should be screened by non-invasive liver imaging, and careful follow-up of liver disease should be performed.
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