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Seung Hee Lee  (Lee SH) 2 Articles
APOA5 Polymorphism Is Associated with Metabolic Syndrome in Korean Postmenopausal Women.
Doh Hee Kim, Seung Hee Lee, Kyung Hoon Han, Chae Bong Kim, Kwan Young Song, Sook Cho, Kye Heui Lee
Endocrinol Metab. 2012;27(4):276-281.   Published online December 20, 2012
DOI: https://doi.org/10.3803/EnM.2012.27.4.276
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  • 23 Download
  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Menopause is an independent risk factor in metabolic syndrome which induced an alteration of the lipid metabolism by hormonal changes. Apolipoprotein A5 gene (APOA5) was related to the regulation of triglyceride and high density lipoprotein cholesterol (HDL-C) level with biosynthesis and decomposition. This study was conducted to investigate the relationship between APOA5 polymorphism and metabolic syndrome in Korean postmenopausal women. METHODS: This study included 307 postmenopausal women with anthropometric and biochemical measurement in 2010-2011. The polymorphism of APOA5 was analyzed by polymerase chain reaction-restriction fragment length polymorphism method with MseI restriction enzyme. RESULTS: The metabolic syndrome prevalence with TT genotype was significantly lower than the frequency in those with TC/CC (27.09%, 38.46%, and 45.71% for TT, TC, and CC, respectively; P < 0.05). Multiple regression analysis of metabolic syndrome risk factors indicated that postmenopausal women with CC genotype had a higher risk with 3 times than that in TT genotype (P < 0.05). APOA5 C carriers showed an increased risk of triglyceride level (odd ratio, 2.93 and 1.85 for CC and TC+CC, respectively; P < 0.05). Interestingly, HDL-C was related to triglyceride directly in comparison to APOA5. CONCLUSION: The results of this study indicate that APOA5 has an influence on serum triglyceride and HDL-C, which contribute to metabolic syndrome in Korean postmenopausal women.

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  • Effects of a 3-year dietary intervention on age-related changes in triglyceride and apolipoprotein A-V levels in patients with impaired fasting glucose or new-onset type 2 diabetes as a function of the APOA5 -1131 T > C polymorphism
    Minjoo Kim, Jey Sook Chae, Miri Kim, Sang-Hyun Lee, Jong Ho Lee
    Nutrition Journal.2014;[Epub]     CrossRef
  • APOA5Polymorphism Is Associated with Metabolic Syndrome in Korean Postmenopausal Women
    Mi Hae Seo, Won Young Lee
    Endocrinology and Metabolism.2012; 27(4): 274.     CrossRef
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A Case of Bilateral Macronodular Adrenocortical Hyperplasia Accompanied by Hyperresponsiveness to Vasopressin.
Deok In Kim, Seung Hee Lee, Eun A Kim, Hwi La Park, Gyeong Ug Lee, Seong Bin Hong, Moon Suk Nam, Seok Hwan Shin, Yong Seong Kim
J Korean Endocr Soc. 2005;20(4):390-394.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.390
  • 1,531 View
  • 17 Download
AbstractAbstract PDF
Cushing's syndrome associated with nodular adrenal hyperplasia glands is divided into 4 main categories: adrenal adenoma, adrenal carcinoma, primary pigmented nodular adrenal dysplasia and macronodular adrenal hyperplasia(MAH). The mechanism of bilateral MAH, when ACTH is suppressed, was previously unknown, and referred to as being "autonomous". Recently, several reports have shown MAH to be under the control of ectopic or eutopic membrane hormone. Here, a case of Cushing's syndrome, caused by bilateral MAH, is reported. A 62-year-old woman presented with Cushingoid features, hypertension and diabetes mellitus. In her case, abnormal adrenal stimulation of cortisol secretion in response to exogenous vasopression stimulation was shown. Her urine free cortisol was 726.0microgram/dL, which was not suppressed after administration of high-dose dexamethasone. Her plasma cortisol level was elevated, but without circadian rhythm. ACTH was undetectable. An abdomen CT scan demonstrated bilaterally enlarged multinodular adrenal glands. A Sella MRI revealed no alteration of the pituitary gland. The patient underwent a laparoscopic bilateral adrenalectomy. Histological examination revealed bilateral macronodular hyperplasia. After having recovered, the patient showed progressive regression of the Cushingoid status.
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