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Ji Yun Jeong  (Jeong JY) 2 Articles
Clinical Features and Causes of Endogenous Hyperinsulinemic Hypoglycemia in Korea
Chang-Yun Woo, Ji Yun Jeong, Jung Eun Jang, Jaechan Leem, Chang Hee Jung, Eun Hee Koh, Woo Je Lee, Min-Seon Kim, Joong-Yeol Park, Jung Bok Lee, Ki-Up Lee
Diabetes Metab J. 2015;39(2):126-131.   Published online March 9, 2015
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  • 85 Download
  • 23 Web of Science
  • 20 Crossref
AbstractAbstract PDFPubReader   

Endogenous hyperinsulinemic hypoglycemia (EHH) is characterized by an inappropriately high plasma insulin level, despite a low plasma glucose level. Most of the EHH cases are caused by insulinoma, whereas nesidioblastosis and insulin autoimmune syndrome (IAS) are relatively rare.


To evaluate the relative frequencies of various causes of EHH in Korea, we retrospectively analyzed 84 patients who were diagnosed with EHH from 1998 to 2012 in a university hospital.


Among the 84 EHH patients, 74 patients (88%), five (6%), and five (6%) were diagnosed with insulinoma, nesidioblastosis or IAS, respectively. The most common clinical manifestation of EHH was neuroglycopenic symptoms. Symptom duration before diagnosis was 14.5 months (range, 1 to 120 months) for insulinoma, 1.0 months (range, 6 days to 7 months) for nesidioblastosis, and 2.0 months (range, 1 to 12 months) for IAS. One patient, who was diagnosed with nesidioblastosis in 2006, underwent distal pancreatectomy but was later determined to be positive for insulin autoantibodies. Except for one patient who was diagnosed in 2007, the remaining three patients with nesidioblastosis demonstrated severe hyperinsulinemia (157 to 2,719 µIU/mL), which suggests that these patients might have had IAS, rather than nesidioblastosis.


The results of this study suggest that the prevalence of IAS may be higher in Korea than previously thought. Therefore, measurement of insulin autoantibody levels is warranted for EHH patients, especially in patients with very high plasma insulin levels.


Citations to this article as recorded by  
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  • Use of Translational Science, Continuous Glucose Monitoring in the Primary Care Setting for Management of Nesidioblastosis: A Case Report and Literature Review
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  • Is insulin intoxication still the perfect crime? Analysis and interpretation of postmortem insulin: review and perspectives in forensic toxicology
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  • Insulin autoimmune syndrome induced by exogenous insulin injection: a four-case series
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    BMC Endocrine Disorders.2019;[Epub]     CrossRef
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    S Shao, Z Zeng, S Hu
    QJM: An International Journal of Medicine.2018; 111(4): 237.     CrossRef
  • Anti-tuberculosis Treatment-Induced Insulin Autoimmune Syndrome
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    The Ewha Medical Journal.2016; 39(4): 122.     CrossRef
  • Spontaneous hypoglycemia: diagnostic evaluation and management
    Leelavathy Kandaswamy, Rajeev Raghavan, Joseph M. Pappachan
    Endocrine.2016; 53(1): 47.     CrossRef
  • Hypoglycemia due to Insulin Autoimmune Syndrome: A rare cause not to be forgotten
    Sarah Alam, Maaz Ozair, Jamal Ahmad
    Journal of Clinical and Translational Endocrinology: Case Reports.2016; 2: 7.     CrossRef
Transcriptional Regulation of Pyruvate Dehydrogenase Kinase
Ji Yun Jeong, Nam Ho Jeoung, Keun-Gyu Park, In-Kyu Lee
Diabetes Metab J. 2012;36(5):328-335.   Published online October 18, 2012
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  • 129 Download
  • 111 Crossref
AbstractAbstract PDFPubReader   

The pyruvate dehydrogenase complex (PDC) activity is crucial to maintains blood glucose and ATP levels, which largely depends on the phosphorylation status by pyruvate dehydrogenase kinase (PDK) isoenzymes. Although it has been reported that PDC is phosphorylated and inactivated by PDK2 and PDK4 in metabolically active tissues including liver, skeletal muscle, heart, and kidney during starvation and diabetes, the precise mechanisms by which expression of PDK2 and PDK4 are transcriptionally regulated still remains unclear. Insulin represses the expression of PDK2 and PDK4 via phosphorylation of FOXO through PI3K/Akt signaling pathway. Several nuclear hormone receptors activated due to fasting or increased fat supply, including peroxisome proliferator-activated receptors, glucocorticoid receptors, estrogen-related receptors, and thyroid hormone receptors, also participate in the up-regulation of PDK2 and PDK4; however, the endogenous ligands that bind those nuclear receptors have not been identified. It has been recently suggested that growth hormone, adiponectin, epinephrine, and rosiglitazone also control the expression of PDK4 in tissue-specific manners. In this review, we discuss several factors involved in the expressional regulation of PDK2 and PDK4, and introduce current studies aimed at providing a better understanding of the molecular mechanisms that underlie the development of metabolic diseases such as diabetes.


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