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Volume 29(2); June 2014
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Review Articles
Obesity and Metabolism
Transcriptional Regulation of Fibroblast Growth Factor 21 Expression
Kwi-Hyun Bae, Jung-Guk Kim, Keun-Gyu Park
Endocrinol Metab. 2014;29(2):105-111.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.105
  • 4,742 View
  • 63 Download
  • 26 Web of Science
  • 24 Crossref
AbstractAbstract PDFPubReader   

Fibroblast growth factor 21 (FGF21) is an attractive target for treating metabolic disease due to its wide-ranging beneficial effects on glucose and lipid metabolism. Circulating FGF21 levels are increased in insulin-resistant states; however, endogenous FGF21 fails to improve glucose and lipid metabolism in obesity, suggesting that metabolic syndrome is an FGF21-resistant state. Therefore, transcription factors for FGF21 are potential drug targets that could increase FGF21 expression in obesity and reduce FGF21 resistance. Despite many studies on the metabolic effects of FGF21, the transcriptional regulation of FGF21 gene expression remains controversial and is not fully understood. As the FGF21 transcription factor pathway is one of the most promising targets for the treatment of metabolic syndrome, further investigation of FGF21 transcriptional regulation is required.

Citations

Citations to this article as recorded by  
  • Glucosamine Enhancement of Learning and Memory Functions by Promoting Fibroblast Growth Factor 21 Production
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  • Serum fibroblast growth factor 21 levels after out of hospital cardiac arrest are associated with neurological outcome
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  • Nutritional Regulation of Hepatic FGF21 by Dietary Restriction of Methionine
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    Frontiers in Endocrinology.2021;[Epub]     CrossRef
  • The Presence of Urinary Ketones according to Metabolic Status and Obesity
    Bo-Reum Kim, Jeong Woo Seo, Sang Man Kim, Kyu-Nam Kim, Nam-Seok Joo
    Journal of Korean Medical Science.2020;[Epub]     CrossRef
  • MS-275 induces hepatic FGF21 expression via H3K18ac-mediated CREBH signal
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  • Spontaneous ketonuria and risk of incident diabetes: a 12 year prospective study
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    Diabetologia.2019; 62(5): 779.     CrossRef
  • Fibroblast Growth Factor 21 and the Adaptive Response to Nutritional Challenges
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    Hormone Molecular Biology and Clinical Investigation.2017;[Epub]     CrossRef
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  • The U-shaped relationship between fibroblast growth factor 21 and microvascular complication in type 2 diabetes mellitus
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  • Hepatic Fgf21 Expression Is Repressed after Simvastatin Treatment in Mice
    Panos Ziros, Zoi Zagoriti, George Lagoumintzis, Venetsana Kyriazopoulou, Ralitsa P. Iskrenova, Evagelia I. Habeos, Gerasimos P. Sykiotis, Dionysios V. Chartoumpekis, Ioannis G Habeos, Kostas Pantopoulos
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  • Association between insulin resistance and impairment of FGF21 signal transduction in skeletal muscles
    Ja Young Jeon, Sung-E Choi, Eun Suk Ha, Tae Ho Kim, Jong Gab Jung, Seung Jin Han, Hae Jin Kim, Dae Jung Kim, Yup Kang, Kwan-Woo Lee
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  • Fibroblast growth factor 21 deficiency exacerbates chronic alcohol-induced hepatic steatosis and injury
    Yanlong Liu, Cuiqing Zhao, Jian Xiao, Liming Liu, Min Zhang, Cuiling Wang, Guicheng Wu, Ming-Hua Zheng, Lan-Man Xu, Yong-Ping Chen, Moosa Mohammadi, Shao-Yu Chen, Matthew Cave, Craig McClain, Xiaokun Li, Wenke Feng
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  • The Impact of Organokines on Insulin Resistance, Inflammation, and Atherosclerosis
    Kyung Mook Choi
    Endocrinology and Metabolism.2016; 31(1): 1.     CrossRef
  • Physiological and Pharmacological Roles of FGF21 in Cardiovascular Diseases
    Peng Cheng, Fangfang Zhang, Lechu Yu, Xiufei Lin, Luqing He, Xiaokun Li, Xuemian Lu, Xiaoqing Yan, Yi Tan, Chi Zhang
    Journal of Diabetes Research.2016; 2016: 1.     CrossRef
  • Minireview: Roles of Fibroblast Growth Factors 19 and 21 in Metabolic Regulation and Chronic Diseases
    Fangfang Zhang, Lechu Yu, Xiufei Lin, Peng Cheng, Luqing He, Xiaokun Li, Xuemian Lu, Yi Tan, Hong Yang, Lu Cai, Chi Zhang
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  • AMP-activated protein kinase suppresses the expression of LXR/SREBP-1 signaling-induced ANGPTL8 in HepG2 cells
    Jinmi Lee, Seok-Woo Hong, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee
    Molecular and Cellular Endocrinology.2015; 414: 148.     CrossRef
  • Articles in 'Endocrinology and Metabolism' in 2014
    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
Close layer
Obesity and Metabolism
Neurocognitive Changes and Their Neural Correlates in Patients with Type 2 Diabetes Mellitus
Junghyun H Lee, Yera Choi, Chansoo Jun, Young Sun Hong, Han Byul Cho, Jieun E Kim, In Kyoon Lyoo
Endocrinol Metab. 2014;29(2):112-121.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.112
  • 5,141 View
  • 49 Download
  • 34 Web of Science
  • 31 Crossref
AbstractAbstract PDFPubReader   

As the prevalence and life expectancy of type 2 diabetes mellitus (T2DM) continue to increase, the importance of effective detection and intervention for the complications of T2DM, especially neurocognitive complications including cognitive dysfunction and dementia, is receiving greater attention. T2DM is thought to influence cognitive function through an as yet unclear mechanism that involves multiple factors such as hyperglycemia, hypoglycemia, and vascular disease. Recent developments in neuroimaging methods have led to the identification of potential neural correlates of T2DM-related neurocognitive changes, which extend from structural to functional and metabolite alterations in the brain. The evidence indicates various changes in the T2DM brain, including global and regional atrophy, white matter hyperintensity, altered functional connectivity, and changes in neurometabolite levels. Continued neuroimaging research is expected to further elucidate the underpinnings of cognitive decline in T2DM and allow better diagnosis and treatment of the condition.

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Close layer
Obesity and Metabolism
Regulation of Adipocyte Differentiation via MicroRNAs
You Hwa Son, Sojeong Ka, A Young Kim, Jae Bum Kim
Endocrinol Metab. 2014;29(2):122-135.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.122
  • 7,237 View
  • 114 Download
  • 75 Web of Science
  • 73 Crossref
AbstractAbstract PDFPubReader   

Adipocyte differentiation, termed adipogenesis, is a complicated process in which pluripotent mesenchymal stem cells differentiate into mature adipocytes. The process of adipocyte differentiation is tightly regulated by a number of transcription factors, hormones and signaling pathway molecules. Recent studies have demonstrated that microRNAs, which belong to small noncoding RNA species, are also involved in adipocyte differentiation. In vivo and in vitro studies have revealed that various microRNAs affect adipogenesis by targeting several adipogenic transcription factors and key signaling molecules. In this review, we will summarize the roles of microRNAs in adipogenesis and their target genes associated with each stage of adipocyte differentiation.

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Bone Metabolism
Diagnostic Modalities for FGF23-Producing Tumors in Patients with Tumor-Induced Osteomalacia
Seiji Fukumoto
Endocrinol Metab. 2014;29(2):136-143.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.136
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AbstractAbstract PDFPubReader   

Fibroblast growth factor 23 (FGF23) is a hormone that is produced by osteocytes and regulates phosphate and vitamin D metabolism through binding to the Klotho-FGF receptor complex. Excessive actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia. Tumor-induced rickets/osteomalacia (TIO) is a paraneoplastic syndrome caused by overproduction of FGF23 from the responsible tumors. Because TIO is cured by complete resection of the causative tumors, it is of great clinical importance to locate these tumors. Several imaging methods including skeletal survey by magnetic resonance imaging and octreotide scintigraphy have been used to identify the tumors that cause TIO. However, none of these imaging studies indicate that the detected tumors are actually producing FGF23. Recently, systemic venous sampling was conducted for locating FGF23-producing tumor in suspected patients with TIO and demonstrated that this test might be beneficial to a subset of patient. Further studies with more patients are necessary to establish the clinical utility of venous sampling in patients with TIO.

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Editorial
Thyroid
The Biochemical Prognostic Factors of Subclinical Hypothyroidism
You Jin Lee
Endocrinol Metab. 2014;29(2):144-145.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.144
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PDFPubReader   
Close layer
Original Articles
Adrenal gland
Genetic Analysis of Multiple Endocrine Neoplasia Type 1 (MEN1) Leads to Misdiagnosis of an Extremely Rare Presentation of Intrasellar Cavernous Hemangioma as MEN1
Dong Min Lee, Seung Hee Yu, Hyun Hwa Yoon, Kang Lock Lee, Young Sil Eom, Kiyoung Lee, Byung-Joon Kim, Yeun Sun Kim, Ie Byung Park, Kwang-Won Kim, Sihoon Lee
Endocrinol Metab. 2014;29(2):146-153.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.146
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AbstractAbstract PDFPubReader   
Background

Multiple endocrine neoplasia type 1 (MEN1) is a rare inherited disorder characterized by the simultaneous occurrence of endocrine tumors in target tissues (mainly the pituitary, endocrine pancreas, and parathyroid glands). MEN1 is caused by mutations in the MEN1 gene, which functions as a tumor suppressor and consists of one untranslated exon and nine exons encoding the menin protein. This condition is usually suspected when we encounter patients diagnosed with tumors in multiple endocrine organs, as mentioned above.

Methods

A 65-year-old woman who underwent surgery for a pancreatic tumor (serous cystadenoma) 5 years previously was referred to our hospital due to neurologic symptoms of diplopia and left ptosis. Brain magnetic resonance imaging revealed a 3.4-cm lesion originating from the cavernous sinus wall and extending into the sellar region. It was thought to be a nonfunctioning tumor from the results of the combined pituitary function test. Incidentally, we found that she also had a pancreatic tumor, indicating the necessity of genetic analysis for MEN1.

Results

Genomic analysis using peripheral leukocytes revealed a heterozygous c.1621G>A mutation in the MEN1 gene that was previously reported to be either a pathogenic mutation or a simple polymorphism. We pursued a stereotactic approach to the pituitary lesion, and microscopic findings of the tumor revealed it to be an intrasellar cavernous hemangioma, a rare finding in the sellar region and even rarer in relation to oculomotor palsy. The patient recovered well from surgery, but refused further evaluation for the pancreatic lesion.

Conclusion

There is great emphasis placed on genetic testing in the diagnosis of MEN1, but herein we report a case where it did not assist in diagnosis, hence, further discussion on the role of genetic testing in this disease is needed. Also, in cases of pituitary tumor with cranial nerve palsy, despite its low prevalence, intrasellar cavernous hemangioma could be suspected.

Citations

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  • Diffuse cavernous hemangioma of the skull misdiagnosed as skull metastasis in breast cancer patient: one case report and literature review
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    Won-Young Lee
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Close layer
Thyroid
The Biochemical Prognostic Factors of Subclinical Hypothyroidism
Myung Won Lee, Dong Yeob Shin, Kwang Joon Kim, Sena Hwang, Eun Jig Lee
Endocrinol Metab. 2014;29(2):154-162.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.154
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AbstractAbstract PDFPubReader   
Background

Patients with subclinical hypothyroidism (SHT) are common in clinical practice. However, the clinical significance of SHT, including prognosis, has not been established. Further clarifying SHT will be critical in devising a management plan and treatment guidelines for SHT patients. Thus, the aim of this study was to investigate the prognostic factors of SHT.

Methods

We reviewed the medical records of Korean patients who visited the endocrinology outpatient clinic of Severance Hospital from January 2008 to September 2012. Newly-diagnosed patients with SHT were selected and reviewed retrospectively. We compared two groups: the SHT maintenance group and the spontaneous improvement group.

Results

The SHT maintenance group and the spontaneous improvement group had initial thyroid-stimulating hormone (TSH) levels that were significantly different (P=0.035). In subanalysis for subjects with TSH levels between 5 to 10 µIU/mL, the spontaneous improvement group showed significantly lower antithyroid peroxidase antibody (anti-TPO-Ab) titer than the SHT maintenance group (P=0.039). Regarding lipid profiles, only triglyceride level, unlike total cholesterol and low density lipoprotein cholesterol, was related to TSH level, which is correlated with the severity of SHT. Diffuse thyroiditis on ultrasonography only contributed to the severity of SHT, not to the prognosis. High sensitivity C-reactive protein and urine iodine excretion, generally regarded as possible prognostic factors, did not show any significant relation with the prognosis and severity of SHT.

Conclusion

Only initial TSH level was a definite prognostic factor of SHT. TPO-Ab titer was also a helpful prognostic factor for SHT in cases with mildly elevated TSH. Other than TSH and TPO-Ab, we were unable to validate biochemical prognostic factors in this retrospective study for Korean SHT patients.

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Close layer
Obesity and Metabolism
Insulin Phosphorylates Tyrosine Residue 464 of Tub and Translocates Tubby into the Nucleus in HIRcB Cells
Jin Wook Kim, Hyeon Soo Kim, Sang Dae Kim, Jung Yul Park
Endocrinol Metab. 2014;29(2):163-168.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.163
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AbstractAbstract PDFPubReader   
Background

The tubby protein has a motif that might be relevant for its action in the insulin signaling pathway. Previous studies have indicated that tubby undergoes phosphorylation on tyrosine residues in response to several stimuli and is known to localize in the nucleus as well as in the plasma membrane. However, the relationship between phosphorylation and nuclear translocation is not well understood. Here, we report that insulin directly phosphorylates tubby, which translocates into the nucleus.

Methods

The effects of insulin on Tubby were performed with Western blot. The immunoprecipitation and confocal microscopy were performed to prove phosphorylation and nuclear translocation.

Results

Mutation study reveals that tyrosine residue 464 of tubby gene (Tub) is a phosphorylation site activated by insulin. In addition, major portions of tubby protein in the plasma membrane are translocated into the nucleus after insulin treatment. Tyrosine kinase inhibitor pretreatment blocked insulin-induced tubby translocation, suggesting that phosphorylation is important for nuclear translocation. Moreover, mutant tyrosine residue 464 did not translocate into the nucleus in respond to insulin. These findings demonstrate that insulin phosphorylates tyrosine residue 464 of Tub, and this event is important for insulin-induced tubby nuclear translocation.

Conclusion

Insulin phosphorylates tyrosine residue 464 of Tub and translocates tubby into the nuclei of HIRcB cells.

Citations

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    Sendi Mejia, Jose Lorenzo B. Santos, Christos Noutsos
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Close layer
Adrenal gland
Highly Palatable Food during Adolescence Improves Anxiety-Like Behaviors and Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Rats that Experienced Neonatal Maternal Separation
Jong-Ho Lee, Jin Young Kim, Jeong Won Jahng
Endocrinol Metab. 2014;29(2):169-178.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.169
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AbstractAbstract PDFPubReader   
Background

This study was conducted to examine the effects of ad libitum consumption of highly palatable food (HPF) during adolescence on the adverse behavioral outcome of neonatal maternal separation.

Methods

Male Sprague-Dawley pups were separated from dam for 3 hours daily during the first 2 weeks of birth (maternal separation, MS) or left undisturbed (nonhandled, NH). Half of MS pups received free access to chocolate cookies in addition to ad libitum chow from postnatal day 28 (MS+HPF). Pups were subjected to behavioral tests during young adulthood. The plasma corticosterone response to stress challenge was analyzed by radioimmunoassay.

Results

Daily caloric intake and body weight gain did not differ among the experimental groups. Ambulatory activities were decreased defecation activity and rostral grooming were increased in MS controls (fed with chow only) compared with NH rats. MS controls spent less time in open arms, and more time in closed arms during the elevated plus maze test, than NH rats. Immobility duration during the forced swim test was increased in MS controls compared with NH rats. Cookie access normalized the behavioral scores of ambulatory and defecation activities and grooming, but not the scores during the elevated plus maze and swim tests in MS rats. Stress-induced corticosterone increase was blunted in MS rats fed with chow only, and cookie access normalized it.

Conclusion

Prolonged access to HPF during adolescence and youth partly improves anxiety-related, but not depressive, symptoms in rats that experienced neonatal maternal separation, possibly in relation with improved function of the hypothalamic-pituitary-adrenal (HPA) axis.

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Close layer
Gene Expression Regulation by Agonist-Independent Constitutive Signaling of Melanocortin-1 Receptor
Ikjoo Seong, Jaesang Kim
Endocrinol Metab. 2014;29(2):179-184.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.179
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AbstractAbstract PDFPubReader   
Background

Melanocortin-1 receptor (Mc1r), a key signaling receptor for melanogenesis, has been reported to mediate migration of B16F10 melanoma cells. Interestingly, this activity appears to be a part of the constitutive signaling of Mc1r.

Methods

We carried out small interfering RNA-mediated knock-down of Mc1r on murine melanoma B16F10 cells and performed microarray analysis to characterize changes in the gene expression profile.

Results

We isolated 22 and four genes whose expression decreased and increased, respectively, by 2.5-fold or higher as the result of Mc1r knock-down. Several down-regulated genes have been proposed to be involved in cell migration. Among these genes are several members of the chemokine gene family.

Conclusion

We provide a gene set for further functional analyses of Mc1r. The Mc1r target genes we present may be particularly relevant for understanding the ligand-independent activity of Mc1r. Further examination of the mode of action may lead to novel strategies in regulating the migration and metastasis of melanoma cells.

Citations

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  • NRF2 and Key Transcriptional Targets in Melanoma Redox Manipulation
    Evan L. Carpenter, Alyssa L. Becker, Arup K. Indra
    Cancers.2022; 14(6): 1531.     CrossRef
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    Won-Young Lee
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Close layer
A Novel Cytosolic Isoform of Mitochondrial Trans-2-Enoyl-CoA Reductase Enhances Peroxisome Proliferator-Activated Receptor α Activity
Dong-Gyu Kim, Jae Cheal Yoo, Eunju Kim, Young-Sun Lee, Oleg V. Yarishkin, Da Yong Lee, Kun Ho Lee, Seong-Geun Hong, Eun Mi Hwang, Jae-Yong Park
Endocrinol Metab. 2014;29(2):185-194.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.185
  • 4,569 View
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AbstractAbstract PDFPubReader   
Background

Mitochondrial trans-2-enoyl-CoA reductase (MECR) is involved in mitochondrial synthesis of fatty acids and is highly expressed in mitochondria. MECR is also known as nuclear receptor binding factor-1, which was originally reported with yeast two-hybrid screening as a binding protein of the nuclear hormone receptor peroxisome proliferator-activated receptor α (PPARα). However, MECR and PPARα are localized at different compartment, mitochondria, and the nucleus, respectively. Therefore, the presence of a cytosolic or nuclear isoform of MECR is necessary for functional interaction between MECR and PPARα.

Methods

To identify the expression pattern of MECR and the cytosolic form of MECR (cMECR), we performed reverse transcription polymerase chain reaction (RT-PCR) with various tissue samples from Sprague-Dawley rats. To confirm the interaction between cMECR and PPARα, we performed several binding assays such as yeast two-hybrid, coimmunoprecipitation, and bimolecular fluorescence complementation. To observe subcellular localization of these proteins, immunocytochemistry was performed. A luciferase assay was used to measure PPARα activity.

Results

We provide evidence of an alternatively spliced variant of the rat MECR gene that yields cMECR. The cMECR lacks the N-terminal 76 amino acids of MECR and shows uniform distribution in the cytoplasm and nucleus of HeLa cells. cMECR directly bound PPARα in the nucleus and increased PPARα-dependent luciferase activity in HeLa cells.

Conclusion

We found the cytosolic form of MECR (cMECR) was expressed in the cytosolic and/or nuclear region, directly binds with PPARα, and enhances PPARα activity.

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Close layer
Case Reports
Bone Metabolism
A Novel PHEX Gene Mutation in a Patient with Sporadic Hypophosphatemic Rickets
Yea Eun Kang, Jun Hwa Hong, Jimin Kim, Kyong Hye Joung, Hyun Jin Kim, Bon Jeong Ku, Koon Soon Kim
Endocrinol Metab. 2014;29(2):195-201.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.195
  • 4,006 View
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AbstractAbstract PDFPubReader   

Phosphate regulating gene with homologies to endopeptidases on the X-chromosome (PHEX) is a common cause of X-linked hypophosphatemic (XLH) rickets. Diverse PHEX gene mutations have been reported; however, gene mutations in sporadic rickets are less common than in XLH rickets. Herein, we describe a 50-year-old female patient with sporadic hypophosphatemic rickets harboring a novel splicing-site mutation in the PHEX gene (c.663+1G>A) at the exon 5-intron 5 boundary. The patient had recently suffered from right thigh pain and an aggravated waddling gait. She also presented with very short stature, generalized bone pain, and muscle weakness. Despite low serum phosphate levels, her phosphate reabsorption rate was lower than normal. Additionally, her 1,25-dihydroxyvitamin D3 concentration was lower than normal, although FGF23 level was normal. After treatment with alfacalcidol and elemental phosphate, her rachitic symptoms subsided, and callus formation was observed in the fracture site on the right femur.

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Obesity and Metabolism
Recurrent Hypoglycemia Triggered by Sorafenib Therapy in a Patient with Hemangiopericytoma
Si Won Lee, Eun Kyung Lee, Tak Yun, Young-Woong Won, Eun Jeong Ko, Mihong Choi, Sang Il Choi, Sun Seob Park, Eun Kyung Hong
Endocrinol Metab. 2014;29(2):202-205.   Published online June 26, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.2.202
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AbstractAbstract PDFPubReader   

Targeted therapy has been proven to be one of the most effective cancer treatments. However, some endocrine disorders can occur during treatment with targeted agents. We report the case of a patient who exhibited a wax and wane pattern of hypoglycemia that was attributed to sorafenib therapy. A 32-year-old woman with metastatic hemangiopericytoma visited the emergency department in a stuporous state. Nonhyperinsulinemic hypoglycemia was diagnosed, was exacerbated shortly after sorafenib therapy, and was improved by the cessation of sorafenib with additional glucocorticoid therapy. Patients with metastatic hemangiopericytoma should be carefully monitored with particular attention to hypoglycemia when sorafenib therapy is initiated.

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