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Volume 29(1); March 2014
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Namgok Lecture 2013
Obesity and Metabolism
Ectopic Fat Assessment Focusing on Cardiometabolic and Renal Risk
Soo Lim
Endocrinol Metab. 2014;29(1):1-4.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.1
  • 3,815 View
  • 58 Download
  • 36 Web of Science
  • 36 Crossref
AbstractAbstract PDFPubReader   

It is well known that people with high levels of body fat are at higher risk for developing diabetes mellitus, kidney disease, and cardiovascular disorders. Since individuals who are slightly overweight, or even individuals of normal weight, can vary in body fat distribution, their metabolic profiles and the degree of association of these profiles with cardiometabolic risk factors may differ. Fat distribution might be more of a predictive factor for cardiorenometabolic risk than obesity itself, which has led researchers to investigate whether ectopic fat accumulation may partially account for the development of cardiorenometabolic disorders. In addition to visceral obesity, fat can accumulate in the liver and muscle, and these intrahepatic and intramuscular lipid stores are associated with insulin resistance and adverse metabolic phenotypes. More recently, pericardial fat, perivascular fat, and perirenal fat were found to be associated with coronary atherosclerosis, cardiovascular diseases, and kidney damage, respectively. Thus, regional fat distribution may play a key role in understanding the development of cardiorenometabolic diseases in nonobese people.

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Close layer
Review Articles
Adrenal gland
Differential Diagnosis of Adrenal Mass Using Imaging Modality: Special Emphasis on F-18 Fluoro-2-Deoxy-D-Glucose Positron Emission Tomography/Computed Tomography
Hong Je Lee, Jaetae Lee
Endocrinol Metab. 2014;29(1):5-11.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.5
  • 4,031 View
  • 30 Download
  • 7 Web of Science
  • 6 Crossref
AbstractAbstract PDFPubReader   

Adrenal incidentalomas are adrenal masses serendipitously detected during an imaging study performed for reasons unrelated to suspicion of adrenal disease. The incidence of adrenal incidentalomas has increased because of the widespread use of various imaging modalities. In oncology patients with adrenal incidentalomas, the characterization of the adrenal masses is challenging because nearly 50% of incidental adrenal masses are metastatic lesions that need special medical attention. Although unenhanced computed tomography (CT) densitometry, chemical shift magnetic resonance imaging (MRI), delayed contrast-enhanced CT and CT histogram analysis have been used as sensitive and specific modalities for differentiating benign from malignant adrenal masses, F-18 fluoro-2-deoxy-D-glucose positron emission tomography (F-18 FDG PET)/CT is a highly accurate imaging modality compared to CT or MRI, especially when these two imaging modalities are combined. In addition, a semiquantitative analysis using standardized uptake value ratio further improves the diagnostic accuracy of F-18 FDG PET/CT in differentiating benign from malignant adrenal masses. Thus, F-18 FDG PET/CT is very helpful for determining the best therapeutic management, especially for assessing the need for surgery.

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Close layer
Obesity and Metabolism
Sweet Taste-Sensing Receptors Expressed in Pancreatic β-Cells: Sweet Molecules Act as Biased Agonists
Itaru Kojima, Yuko Nakagawa, Yoshiaki Ohtsu, Anya Medina, Masahiro Nagasawa
Endocrinol Metab. 2014;29(1):12-19.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.12
  • 4,862 View
  • 76 Download
  • 41 Web of Science
  • 38 Crossref
AbstractAbstract PDFPubReader   

The sweet taste receptors present in the taste buds are heterodimers comprised of T1R2 and T1R3. This receptor is also expressed in pancreatic β-cells. When the expression of receptor subunits is determined in β-cells by quantitative reverse transcription polymerase chain reaction, the mRNA expression level of T1R2 is extremely low compared to that of T1R3. In fact, the expression of T1R2 is undetectable at the protein level. Furthermore, knockdown of T1R2 does not affect the effect of sweet molecules, whereas knockdown of T1R3 markedly attenuates the effect of sweet molecules. Consequently, a homodimer of T1R3 functions as a receptor sensing sweet molecules in β-cells, which we designate as sweet taste-sensing receptors (STSRs). Various sweet molecules activate STSR in β-cells and augment insulin secretion. With regard to intracellular signals, sweet molecules act on STSRs and increase cytoplasmic Ca2+ and/or cyclic AMP (cAMP). Specifically, when an STSR is stimulated by one of four different sweet molecules (sucralose, acesulfame potassium, sodium saccharin, or glycyrrhizin), distinct signaling pathways are activated. Patterns of changes in cytoplasmic Ca2+ and/or cAMP induced by these sweet molecules are all different from each other. Hence, sweet molecules activate STSRs by acting as biased agonists.

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Close layer
Thyroid
Prevalence and Risk Factors of Subclinical Thyroid Disease
Ye An Kim, Young Joo Park
Endocrinol Metab. 2014;29(1):20-29.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.20
  • 6,640 View
  • 81 Download
  • 69 Web of Science
  • 70 Crossref
AbstractAbstract PDFPubReader   

Subclinical thyroid disease is defined biochemically by an abnormal thyrotropin (TSH) level and normal serum-free thyroxine level. The prevalence of this condition varies according to the reference range for TSH and geographic or demographic factors. Recently, several studies, including our community-based cohort studies, have reported on the incidence of subclinical thyroid disease in Korea. Using these studies, we reviewed the prevalence and risk factors of subclinical thyroid disease, focusing on subclinical hypothyroidism.

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Editorial
Bone Metabolism
Testosterone Replacement Therapy and Bone Mineral Density in Men with Hypogonadism
Se Hwa Kim
Endocrinol Metab. 2014;29(1):30-32.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.30
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PDFPubReader   

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Original Articles
Thyroid
Diagnostic Whole-Body Scan May Not Be Necessary for Intermediate-Risk Patients with Differentiated Thyroid Cancer after Low-Dose (30 mCi) Radioactive Iodide Ablation
Eon Ju Jeon, Eui Dal Jung
Endocrinol Metab. 2014;29(1):33-39.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.33
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AbstractAbstract PDFPubReader   
Background

A diagnostic whole-body scan (WBS) is recommended 6 to 12 months after total thyroidectomy and radioactive iodide ablation in intermediate- or high-risk patients with differentiated thyroid cancer (DTC). The aim of this study was to evaluate the necessity of a diagnostic WBS after radioactive iodide ablation in intermediate-risk patients with DTC.

Methods

A total of 438 subjects were included in the study: 183 low-risk subjects and 255 intermediate-risk subjects according to the American Thyroid Association guideline. All subjects diagnosed with DTC received 1,100 MBq (30 mCi) activity of radioiodine (I-131) following total thyroidectomy. On follow-up, all subjects underwent a diagnostic I-131 WBS after thyroid hormone withdrawal.

Results

After initial radioactive iodide ablation, 95.1% of low-risk patients and 91.4% of intermediate-risk patients showed no uptake on diagnostic WBS (P=0.135). Intermediate-risk patients with stimulated thyroglobulin (Tg) levels higher than 2.0 ng/mL showed a greater rate of radioactive iodine uptake on diagnostic WBS. Four intermediate-risk patients showed recurrence during the 16 to 80 months follow-up period. Three of the four patients with recurrence showed no uptake on diagnostic WBS and had a stimulated Tg level less than 2.0 ng/mL.

Conclusion

A diagnostic I-131 WBS after radioactive iodide ablation in intermediate-risk patients with DTC may not be necessary. A large prospective study is necessary to determine the necessity of diagnostic WBS in intermediate-risk patients with DTC.

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Obesity and Metabolism
Correlation between Expression of Glucose Transporters in Granulosa Cells and Oocyte Quality in Women with Polycystic Ovary Syndrome
Eunju Kim, Hyun Ha Seok, Su-Yeon Lee, Dong Ryul Lee, Jisook Moon, Tae Ki Yoon, Woo Sik Lee, Kyung-Ah Lee
Endocrinol Metab. 2014;29(1):40-47.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.40
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AbstractAbstract PDFPubReader   
Background

The glucose transporters (GLUTs) exhibit different tissue-specific expression. This study aimed to investigate the types of GLUTs expressed in human granulosa cells (GCs) obtained from women with polycystic ovary syndrome (PCOS) and their relationship with insulin resistance (IR) and the outcomes of in vitro maturation (IVM) of immature oocytes.

Methods

Expression of GLUTs was evaluated in GCs from women with PCOS with or without IR. Thirty-six women with PCOS undergoing an IVM program were included. Differential gene expression between the insulin sensitive (IS) and IR group was measured by reverse transcription polymerase chain reaction.

Results

Expression of GLUTs 1, 3, 5, 8, and 13 was constitutive, whereas expression of GLUTs 2 and 7 was not observed in human GCs. The remaining GLUTs, 4, 6, 9, 10, 11, and 12, were differentially expressed among patients according to metabolic status, such as insulin sensitivity. A higher number of GCs from patients with IR (92%) expressed GLUT6 than GCs from IS PCOS patients (46.3%). Logistic regression showed that expression of GLUTs 9, 11, and 12 correlates with rates of IVM at 48 hours, fertilization, and implantation, respectively.

Conclusion

This is the first report describing the expression pattern of all 13 members of the GLUT family in human GCs. Results of the present study suggest that patients' insulin sensitivity regulates GLUT expression in GCs in PCOS patients, and this may control oocyte quality for IVM and subsequent processes such as fertilization and implantation in patients taking part in an in vitro fertilization program.

Citations

Citations to this article as recorded by  
  • Dysregulation of ferroptosis-related genes in granulosa cells associates with impaired oocyte quality in polycystic ovary syndrome
    Jialyu Huang, Hancheng Fan, Chenxi Li, Kangping Yang, Chaoyi Xiong, Siyi Xiong, Shenghui Feng, Shen Chen, Bangqi Wang, Yufang Su, Boyun Xu, Haiyan Yang, Ni Wang, Jing Zhu
    Frontiers in Endocrinology.2024;[Epub]     CrossRef
  • Chinese herbal medicine alleviates the pathogenesis of polycystic ovary syndrome by improving oxidative stress and glucose metabolism via mitochondrial Sirtuin 3 signaling
    Qing Zhang, Jun Ren, Fangfang Wang, Mingqian Li, Manman Pan, Hui Zhang, Fan Qu
    Phytomedicine.2023; 109: 154556.     CrossRef
  • Essential Role of Granulosa Cell Glucose and Lipid Metabolism on Oocytes and the Potential Metabolic Imbalance in Polycystic Ovary Syndrome
    Chen-Hua Zhang, Xiang-Yi Liu, Jing Wang
    International Journal of Molecular Sciences.2023; 24(22): 16247.     CrossRef
  • Effect of Electro-acupuncture on Expression of IRS-1/PI3K/GLUT4 Pathway in Ovarian Granulosa Cells of Infertile Patients with Polycystic Ovary Syndrome-Insulin Resistance of Phlegm-Dampness Syndrome
    Shan Xiang, Ming-feng Xia, Jing-yan Song, Dan-qi Liu, Fang Lian
    Chinese Journal of Integrative Medicine.2021; 27(5): 330.     CrossRef
  • Comparison of streptozotocin-induced diabetes at different moments of the life of female rats for translational studies
    Yuri K Sinzato, Eduardo Klöppel, Carolina A Miranda, Verônyca G Paula, Larissa F Alves, Lívia LS Nascimento, Ana Paula Campos, Barshana Karki, Václav Hampl, Gustavo T Volpato, Débora C Damasceno
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    Frontiers in Endocrinology.2021;[Epub]     CrossRef
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    Lei Zhao, Qing-Yuan Sun, Zhao-Jia Ge
    Food & Function.2021; 12(21): 10311.     CrossRef
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    XiaoLong Jiang, YunWei Pang, ShanJiang Zhao, HaiSheng Hao, XueMing Zhao, WeiHua Du, YaChun Wang, HuaBin Zhu
    American Journal of Physiology-Endocrinology and Metabolism.2020; 318(3): E405.     CrossRef
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    Valentina Notarstefano, Giorgia Gioacchini, Elisabetta Giorgini, Nina Montik, Andrea Ciavattini, Anna Rita Polidori, Fulvia Antonia Candela, Lisa Vaccari, Maurizio Cignitti, Oliana Carnevali
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    Masoumeh Ghafarzadeh
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    Reproduction, Fertility and Development.2019; 31(8): 1353.     CrossRef
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    Giorgia Gioacchini, Valentina Notarstefano, Elena Sereni, Carlotta Zacà, Giovanni Coticchio, Elisabetta Giorgini, Lisa Vaccari, Oliana Carnevali, Andrea Borini
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    So-Young Kwak, Clara Yongjoo Park, Garam Jo, Oh Yoen Kim, Min-Jeong Shin
    Endocrine Journal.2018; 65(9): 881.     CrossRef
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    Tiantian Li, Hui Mo, Wenfeng Chen, Li Li, Yao Xiao, Jing Zhang, Xiaofang Li, Ying Lu
    Reproductive Sciences.2017; 24(5): 646.     CrossRef
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    Ye Tian, Yu Ding, Juan Liu, Dai Heng, Kaili Xu, Wenbo Liu, Cheng Zhang
    Endocrinology.2017; 158(6): 1898.     CrossRef
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    Liza Margareth Medeiros de Carvalho Sousa, Renata dos Santos Silva, Vanessa Uemura da Fonseca, Rafael Magdanelo Leandro, Thiago Senna Di Vincenzo, Ana Bárbara Alves-Wagner, Ubiratan Fabres Machado, Paula de Carvalho Papa
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    Meghan Ruebel, Kartik Shankar, Dana Gaddy, Forrest Lindsey, Thomas Badger, Aline Andres
    American Journal of Physiology-Endocrinology and Metabolism.2016; 311(1): E269.     CrossRef
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    Joëlle Dupont, Rex J. Scaramuzzi
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
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    YI-MIN CHEN, JIN-FANG ZHAO, YONG-LIN LIU, JIE CHEN, RONG-LIN JIANG
    International Journal of Molecular Medicine.2015; 36(3): 739.     CrossRef
  • Dysregulated hepatic expression of glucose transporters in chronic disease: contribution of semicarbazide-sensitive amine oxidase to hepatic glucose uptake
    Sumera Karim, Evaggelia Liaskou, Janine Fear, Abhilok Garg, Gary Reynolds, Lee Claridge, David H. Adams, Philip N. Newsome, Patricia F. Lalor
    American Journal of Physiology-Gastrointestinal and Liver Physiology.2014; 307(12): G1180.     CrossRef
Close layer
Bone Metabolism
Testosterone Replacement and Bone Mineral Density in Male Pituitary Tumor Patients
Min Jeong Lee, Hyoung Kyu Ryu, So-Yeon An, Ja Young Jeon, Ji In Lee, Yoon-Sok Chung
Endocrinol Metab. 2014;29(1):48-53.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.48
  • 3,490 View
  • 32 Download
  • 11 Web of Science
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AbstractAbstract PDFPubReader   
Background

Hypopituitarism is associated with osteoporosis and osteopenia especially when hypogonadotropic hypogonadism is present. Despite hypopituitarism being an important cause of secondary osteoporosis, osteoporosis in patients receiving surgery for pituitary tumors in Korea has not been studied. In this study, we evaluated the effects of testosterone replacement therapy (TRT) on bone mineral density (BMD) in postoperative hypogonadal patients with pituitary tumors.

Methods

To examine the effect of TRT on BMD, we performed a retrospective observational study in 21 postoperative male patients who underwent pituitary tumor surgery between 2003 and 2012 at the Ajou University Hospital. Testosterone was replaced in postoperative hypogonadal patients by regular intramuscular injection, daily oral medication, or application of transdermal gel. BMD (g/cm2) measurements of central skeletal sites (lumbar spine, femoral neck, and total femur) were obtained using dual-energy X-ray absorptiometry (GE Lunar). For lumbar spine BMD, L1 to L4 values were chosen for analysis. Femur neck and total femur were also analyzed.

Results

During the follow-up period (mean, 56 months; range, 12 to 99 months) serum testosterone levels increased with the administration of TRT (P=0.007). There was significant improvement (4.56%±9.81%) in the lumbar spine BMD compared to baseline BMD. There were no significant changes in the femur neck BMD or total femur BMD. We did not find any statistically significant relationships between changes in testosterone levels and BMD using Spearman correlation analysis.

Conclusion

Our results indicated that TRT used in the postoperative period for hypogonadal pituitary tumor surgery patients may have beneficial effects on the BMD of the spine.

Citations

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Close layer
Thyroid
Curcumin Enhances Docetaxel-Induced Apoptosis of 8505C Anaplastic Thyroid Carcinoma Cells
Jung Min Hong, Chan Sung Park, Il Seong Nam-Goong, Yon Seon Kim, Jong Cheol Lee, Myung Weol Han, Jung Il Choi, Young Il Kim, Eun Sook Kim
Endocrinol Metab. 2014;29(1):54-61.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.54
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  • 26 Web of Science
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AbstractAbstract PDFPubReader   
Background

Anaplastic thyroid cancer (ATC) is one of the most aggressive malignancies in humans, and its progression is poorly controlled by existing therapeutic methods. Curcumin has been shown to suppress inflammation and angiogenesis. In this study, we evaluated whether curcumin could augment docetaxel-induced apoptosis of ATC cells. We also analyzed changes in nuclear factor κB (NF-κB) and cyclooxygenase-2 (COX-2) expression levels to delineate possible mechanisms of their combined action.

Methods

ATC cells were cultured and treated with curcumin and docetaxel alone or in combination. The effects on cell viability were determined by MTS assay. Apoptosis was assessed by annexin V staining and confirmed by flow cytometric analysis. Caspase, COX-2, NF-κB levels were assayed by Western blotting.

Results

Curcumin combined with docetaxel led to lower cell viability than treatment with docetaxel or curcumin alone. Annexin V staining followed by flow cytometric analysis demonstrated that curcumin treatment enhanced the docetaxel-induced apoptosis of ATC cells. Additionally, curcumin inhibited docetaxel-induced p65 activation and COX-2 expression.

Conclusion

We conclude that curcumin may enhance docetaxel's antitumor activity in ATC cells by interfering with NF-κB and COX-2. Our results suggest that curcumin may emerge as an attractive therapeutic candidate to enhance the antitumor activity of taxanes in ATC treatment.

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Close layer
Functional Role of Parkin against Oxidative Stress in Neural Cells
Minyoung Hwang, Ja-Myong Lee, Younghwa Kim, Dongho Geum
Endocrinol Metab. 2014;29(1):62-69.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.62
  • 3,532 View
  • 28 Download
  • 6 Web of Science
  • 5 Crossref
AbstractAbstract PDFPubReader   
Background

Parkinson disease (PD) is caused by selective cell death of dopaminergic neurons in the substantia nigra. An early onset form of PD, autosomal recessive juvenile parkinsonism has been associated with a mutation in the parkin gene. The function of parkin is known to remove misfolding proteins and protect cell death. We aimed to investigate the role of parkin against oxidative stress in neuronal cells.

Methods

Parkin knockout embryonic stem cells (PKO ES cells) were differentiated into neurons by adherent monolayer culture method. Oxidative stress was induced by the treatment of 1-methyl-4-phenylpyridinium (MPP+) in neurons derived from wild type and PKO ES cells, and cell viability was examined by MTT assay. After exposure to MPP+, Tuj1-positive cell population was compared between PKO and wild type cells by fluorescence activated cell sorter (FACS) analysis. The activated caspase3 protein level was also measured by Western blot analysis, FACS and immunocytochemistry.

Results

There was no difference in the efficiency of neuronal differentiation between wild type and PKO ES cells. After exposure to MPP+, no significant differences were found in cell viability and Tuj1-positive cell population between the two groups determined by MTT assay and FACS analysis, respectively. The activated caspase3 protein levels examined by Western blot analysis, FACS and immunocytochemistry were not changed in PKO cells compared with those of wild type cells after MPP+ treatment.

Conclusion

These results suggest that PKO neuronal cells including dopaminergic neurons are not sensitive to caspase3-dependent cell death pathway during the response against MPP+-induced oxidative stress.

Citations

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    Won-Young Lee
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Close layer
Bone Metabolism
Short-Term Caloric Restriction Does Not Reduce Bone Mineral Density in Rats with Early Type 2 Diabetes
Yun Kyung Jeon, Won Jin Kim, Myung Jun Shin, Hae-Young Chung, Sang Soo Kim, Bo Hyun Kim, Seong-Jang Kim, Yong Ki Kim, In Joo Kim
Endocrinol Metab. 2014;29(1):70-76.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.70
  • 3,511 View
  • 27 Download
  • 5 Web of Science
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AbstractAbstract PDFPubReader   
Background

The effect of caloric restriction (CR) in the setting of diabetes on bone metabolism has not yet been fully studied. The aim of this study is to determine if short-term CR alters bone mass and metabolism in Otsuka Long-Evans Tokushima fatty (OLETF) rats, an animal model of type 2 diabetes.

Methods

Four groups (n=5) were created: OLETF rats with food ad libitum (AL), OLETF rats with CR, Long-Evans Tokusima Otsuka (LETO) rats with food AL, and LETO rats with CR. The CR condition was imposed on 24-week-old male rats using a 40% calorie reduction for 4 weeks. The effect of CR on femoral bone mineral density (BMD) was assessed by dual-energy X-ray absorptiometry. Serum markers were measured by immunoassay.

Results

After 4 weeks of CR, body weight decreased in both strains. The BMD decreased in LETO rats and was maintained in OLETF rats. After adjustment for body weight, BMD remained lower in LETO rats (P=0.017) but not OLETF rats (P=0.410). Bone-specific alkaline phosphatase levels decreased in LETO rats (P=0.025) but not in OLEFT rats (P=0.347). Serum leptin levels were reduced after CR in both strains, but hyperleptinemia remained in OLETF rats (P=0.009). CR increased 25-hydroxyvitamin D levels in OLETF rats (P=0.009) but not in LETO rats (P=0.117). Additionally, interleukin-6 and tumor necrosis factor-α levels decreased only in OLETF rats (P=0.009).

Conclusion

Short-term CR and related weight loss were associated with decreases of femoral BMD in LETO rats while BMD was maintained in OLETF rats. Short-term CR may not alter bone mass and metabolism in type 2 diabetic rats.

Citations

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    Junxiong Zhu, Can Liu, Jialin Jia, Chenggui Zhang, Wanqiong Yuan, Huijie Leng, Yingsheng Xu, Chunli Song
    Annals of the New York Academy of Sciences.2020; 1474(1): 47.     CrossRef
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    Tsang‐hai Huang, Gene P. Ables
    Annals of the New York Academy of Sciences.2016; 1363(1): 26.     CrossRef
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
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Case Reports
Thyroid
Hyponatremia after Thyroid Hormone Withdrawal in a Patient with Papillary Thyroid Carcinoma
Hyo Jin Jo, Yong Hyun Kim, Dong Hyun Shin, Mi Jeoung Kim, Sang Jin Lee, Dong Ok Jeon, Sung Gyu Im, Sun Kyung Jang, Jin Young Choi
Endocrinol Metab. 2014;29(1):77-82.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.77
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AbstractAbstract PDFPubReader   

Hyponatremia is an electrolyte abnormality commonly found in clinical practice. It is important to diagnose the underlying etiology of the hyponatremia and correct it appropriately because severe hyponatremia can cause serious complications and substantially increase the risk of mortality. Although hypothyroidism is known to be a cause of hyponatremia, it is rare that hyponatremia occurs in relation to hypothyroidism induced by thyroid hormone withdrawal in patients with differentiated thyroid cancer. We report a case of a 76-year-old woman with papillary thyroid carcinoma presenting with severe hyponatremia related to hypothyroidism induced by thyroid hormone withdrawal for radio-active iodine whole-body scanning, who was treated by thyroid hormone replacement and hydration. Considering that the incidence of differentiated thyroid cancer is rapidly increasing, physicians should be aware that, although uncommon, hyponatremia can occur in patients undergoing radioiodine therapy or diagnostic testing.

Citations

Citations to this article as recorded by  
  • Effect of preparation method for radioactive iodine therapy on serum electrolytes
    Noriko Takata, Masao Miyagawa, Tomohisa Okada, Naoto Kawaguchi, Yutaka Fujimoto, Yoshihiro Kouchi, Shintaro Tsuruoka, Kotaro Uwatsu, Teruhito Kido
    Japanese Journal of Radiology.2023; 41(11): 1247.     CrossRef
  • MANAGEMENT OF ENDOCRINE DISEASE: Hypothyroidism-associated hyponatremia: mechanisms, implications and treatment
    G Liamis, T D Filippatos, A Liontos, M S Elisaf
    European Journal of Endocrinology.2017; 176(1): R15.     CrossRef
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
  • Parathyroid hormone-related protein serves as a prognostic indicator in oral squamous cell carcinoma
    Zhongjing Lv, Xiangbing Wu, Wei Cao, ZongZe Shen, Lizhen Wang, FuRong Xie, JianJun Zhang, Tong Ji, Ming Yan, WanTao Chen
    Journal of Experimental & Clinical Cancer Research.2014;[Epub]     CrossRef
  • Hyponatremia and the Thyroid: Causality or Association?
    Kevin Pantalone, Betul Hatipoglu
    Journal of Clinical Medicine.2014; 4(1): 32.     CrossRef
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Adrenal gland
Pheochromocytoma with Markedly Abnormal Liver Function Tests and Severe Leukocytosis
Chai Ryoung Eun, Jae Hee Ahn, Ji A Seo, Nan Hee Kim
Endocrinol Metab. 2014;29(1):83-90.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.83
  • 3,588 View
  • 34 Download
  • 5 Web of Science
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AbstractAbstract PDFPubReader   

Pheochromocytoma is a rare neuroendocrine tumor arising from the medulla of the adrenal glands, which causes an overproduction of catecholamines. The common symptoms are headache, palpitations, and sweating; however, various other clinical manifestations might also be present. Accurate diagnosis of pheochromocytoma is important because surgical treatment is usually successful, and associated clinical problems are reversible if treated early. A 49-year-old man with a history of uncontrolled hypertension and diabetes mellitus presented with chest pain, fever, and sweating. His liver function tests and white blood cell counts were markedly increased and his echocardiography results suggested stress-induced cardiomyopathy. His abdominal computed tomography showed a 5×5-cm-sized tumor in the left adrenal gland, and laboratory tests confirmed catecholamine overproduction. After surgical resection of the left adrenal gland, his liver function tests and white blood cell counts normalized, and echocardiography showed normal cardiac function. Moreover, his previous antihypertensive regimen was deescalated, and his previously uncontrolled blood glucose levels normalized without medication.

Citations

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  • Liver Transplantation for Fulminant Hepatic Failure Precipitated by Pheochromocytoma Crisis in the Setting of Using Garcinia cambogia Weight Loss Supplement: A Case Report
    Motaz A Selim, Krystal Weierstahl, Calvin Eriksen, Terra Pearson, Harvey Woehlck
    Cureus.2023;[Epub]     CrossRef
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    Mhd Baraa Habib, Mohamed Abdelrazek, Sali Alatasi, Mouhand F. H. Mohamed, Hamda Ali, Mohamad Khair Hamad
    Clinical Case Reports.2021;[Epub]     CrossRef
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    Jay Shah, Zinkal Patel, Shradha Patel, Amit Kumar
    Journal of Pediatric Critical Care.2021; 8(5): 255.     CrossRef
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    Miguel Malespin, Ammar Nassri
    Clinics in Liver Disease.2019; 23(2): 233.     CrossRef
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    Renhua Wu, Nanwei Tong, Xinlei Chen, Shishi Xu, Fang Zhang, Lizhi Tang, Yuwei Zhang
    Medicine.2018; 97(25): e11054.     CrossRef
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
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Thyroid
Hypoparathyroidism and Subclinical Hypothyroidism with Secondary Hemochromatosis
Hyung Ki Jeong, Joon Hwan An, Hyoung Sang Kim, Eun Ae Cho, Min Gui Han, Jung Sik Moon, Hee Kyung Kim, Ho-Cheol Kang
Endocrinol Metab. 2014;29(1):91-95.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.91
  • 4,418 View
  • 45 Download
  • 4 Web of Science
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AbstractAbstract PDFPubReader   

Hemochromatosis is an inherited genetic disorder of iron metabolism which can also occur as a secondary result of iron-overload. It leads to organ damage such as cardiomyopathy, liver cirrhosis, hypogonadism, and diabetes. This paper discusses a case of secondary hemochromatosis associated with repeated transfusions, presenting as asymptomatic hypoparathyroidism and subclinical hypothyroidism with multiple organ involvement. The 29-year-old female, who had severe aplastic anemia, received multiple transfusions totaling approximately 1,400 units of red blood cells over 15 years. During her routine laboratory examination, hypocalcemia was detected with decreased intact parathyroid hormone and increased thyroid stimulating hormone. Serum ferritin, iron, and total iron binding capacity had increased to 27,583.03 ng/mL, 291 µg/dL, and 389 µg/dL, respectively. She had unusually bronze skin and computed tomography revealed iron deposition in the thyroid, liver, and heart. Multiorgan involvement as seen in this case is rare in hemochromatosis associated with secondary transfusions. To the best of the author's knowledge, this is the first case report in Korea of hypoparathyroidism and subclinical hypothyroidism due to iron deposition in the parathyroid and thyroid gland.

Citations

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  • Hypocalcaemic cardiomyopathy: a description of two cases and a literature review
    Martin Válek, Lenka Roblová, Ivan Raška, Dita Schaffelhoferová, Tomáš Paleček
    ESC Heart Failure.2020; 7(3): 1291.     CrossRef
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    Kornkamon Lertsuwan, Ketsaraporn Nammultriputtar, Supanan Nanthawuttiphan, Natnicha Tannop, Jarinthorn Teerapornpuntakit, Jirawan Thongbunchoo, Narattaphol Charoenphandhu, Gianpaolo Papaccio
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    J. Warland, B. Skelly, C. Knudsen, M. Herrtage
    Journal of Veterinary Internal Medicine.2015; 29(1): 400.     CrossRef
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
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Thyroid
Medullary Thyroid Carcinoma with Ectopic Adrenocorticotropic Hormone Syndrome
Hong Seok Choi, Min Joo Kim, Chae Ho Moon, Jong Ho Yoon, Ha Ra Ku, Geon Wook Kang, Im Il Na, Seung-Sook Lee, Byung-Chul Lee, Young Joo Park, Hong Il Kim, Yun Hyi Ku
Endocrinol Metab. 2014;29(1):96-100.   Published online March 14, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.1.96
  • 3,689 View
  • 40 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract PDFPubReader   

Ectopic adrenocorticotropic hormone (ACTH) syndrome is caused most frequently by a bronchial carcinoid tumor or by small cell lung cancer. Medullary thyroid carcinoma (MTC) is a rare etiology of ectopic ACTH syndrome. We describe a case of Cushing syndrome due to ectopic ACTH production from MTC in a 48-year-old male. He was diagnosed with MTC 14 years ago and underwent total thyroidectomy, cervical lymph node dissection and a series of metastasectomies. MTC was confirmed by the pathological examination of the thyroid and metastatic mediastinal lymph node tissues. Two years after his last surgery, he developed Cushingoid features, such as moon face and central obesity, accompanied by uncontrolled hypertension and new-onset diabetes. The laboratory results were compatible with ectopic ACTH syndrome. A bilateral adrenalectomy improved the clinical and laboratory findings that were associated with Cushing syndrome. This is the first confirmed case of ectopic ACTH syndrome caused by MTC in Korea.

Citations

Citations to this article as recorded by  
  • Medullary Thyroid Cancer with Ectopic Cushing's Syndrome: A Case Report and Systematic Review of Detailed Cases from the Literature
    Andrea Corsello, Vittoria Ramunno, Pietro Locantore, Giovanni Pacini, Esther Diana Rossi, Francesco Torino, Alfredo Pontecorvi, Carmela De Crea, Rosa Maria Paragliola, Marco Raffaelli, Salvatore Maria Corsello
    Thyroid.2022; 32(11): 1281.     CrossRef
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    Gyu Gang Choi, Hwan Jin Lee, Hyo Jin Han, Young Beom Jeong, Heung Bum Lee, Ji Hyun Park
    Endocrinology and Metabolism.2021; 36(6): 1312.     CrossRef
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    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
  • Rapid response of hypercortisolism to vandetanib treatment in a patient with advanced medullary thyroid cancer and ectopic Cushing syndrome
    Fabián Pitoia, Fernanda Bueno, Angélica Schmidt, Sabrina Lucas, Graciela Cross
    Archives of Endocrinology and Metabolism.2015; 59(4): 343.     CrossRef
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