Endocrinology and Metabolism

Review Article

Thyroid
Deiodinases and the Three Types of Thyroid Hormone Deiodination Reactions: Laura Sabatino, Cristina Vassalle, Cristina Del Seppia, Giorgio Iervasi; Endocrinol Metab. 2021;36(5):952-964. Published online October 21, 2021; DOI: https://doi.org/10.3803/EnM.2021.1198

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Thyroid hormone (TH) signaling is strictly regulated by iodothyronine deiodinase activity, which both preserves the circulating levels of the biologically active triiodothyronine (T3) and regulates TH homeostasis at the local level, in a cell- and time-dependent manner. Three deiodinases have been identified—namely iodothyronine deiodinase 1 (DIO1), DIO2, and DIO3—that differ in their catalytic properties and tissue distribution. The deiodinases represent a dynamic system that changes in the different stages of life according to their functions and roles in various cell types and tissues. Deiodinase activity at the tissue level permits cell-targeted fine regulation of TH homeostasis, mediating the activation (DIO1 and DIO2) and inactivation (DIO3) of THs. Deiodinase homeostasis is the driving force that leads T3-target cells towards customized TH signaling, which takes into account both the hormonal circulating levels and the tissue-specific response. This review analyzes the complex role of deiodinases in physiological and pathological contexts, exploring new challenges and opportunities deriving from a deeper knowledge of the dynamics underlying their roles and functions.

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Original Articles

Adrenal Gland
Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor: Jin Young Lee, Da Ae Kim, Eunah Choi, Yun Sun Lee, So Jeong Park, Beom-Jun Kim; Endocrinol Metab. 2021;36(4):865-874. Published online July 30, 2021; DOI: https://doi.org/10.3803/EnM.2021.1108

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Background
Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it.
Methods
Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reversetranscription polymerase chain reaction, Western blot, viability, and migration analyses were performed for experimental research.
Results
Recombinant aldosterone treatment suppressed muscle differentiation from mouse C2C12 myoblasts in a dose-dependent manner, and consistently reduced the expression of myogenic differentiation markers. Furthermore, aldosterone significantly increased intracellular reactive oxygen species (ROS) levels in myotubes, and treatment with N-acetyl cysteine, a potent biological thiol antioxidant, reversed the decrease of myotube area, myotube area per myotube, nucleus number per myotube, and fusion index due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone.
Conclusion
These findings support the hypothesis that hypersecretion of aldosterone, like PA, directly contributes to muscular deterioration and suggest that antioxidants and/or MR antagonists could be effective therapeutic options to reduce the risk of sarcopenia in these patients.

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Endocrine Research
The Role of Nuclear Factor-E2-Related Factor 1 in the Oxidative Stress Response in MC3T3-E1 Osteoblastic Cells: So Young Park, Sung Hoon Kim, Hyun Koo Yoon, Chang Hoon Yim, Sung-Kil Lim; Endocrinol Metab. 2016;31(2):336-342. Published online April 25, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.2.336

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Background

Reactive oxygen species (ROS) and antioxidants are associated with maintenance of cellular function and metabolism. Nuclear factor-E2-related factor 1 (NFE2L1, Nrf1) is known to regulate the expression of a number of genes involved in oxidative stress and inflammation. The purpose of this study was to examine the effects of NFE2L1 on the response to oxidative stress in osteoblastic MC3T3-E1 cells.

Methods

The murine calvaria-derived MC3T3-E1 cell line was exposed to lipopolysaccharide (LPS) for oxidative stress induction. NFE2L1 effects were evaluated using small interfering RNA (siRNA) for NFE2L1 mRNA. ROS generation and the levels of known antioxidant enzyme genes were assayed.

Results

NFE2L1 expression was significantly increased 2.4-fold compared to the control group at 10 µg/mL LPS in MC3T3-E1 cells (P<0.05). LPS increased formation of intracellular ROS in MC3T3-E1 cells. NFE2L1 knockdown led to an additional increase of ROS (20%) in the group transfected with NFE2L1 siRNA compared with the control group under LPS stimulation (P<0.05). RNA interference of NFE2L1 suppressed the expression of antioxidant genes including metallothionein 2, glutamatecysteine ligase catalytic subunit, and glutathione peroxidase 1 in LPS-treated MC3T3-E1 cells.

Conclusion

Our results suggest that NFE2L1 may have a distinct role in the regulation of antioxidant enzymes under inflammation-induced oxidative stress in MC3T3-E1 osteoblastic cells.

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Obesity and Metabolism
Lipid Accumulation Product Is Associated with Insulin Resistance, Lipid Peroxidation, and Systemic Inflammation in Type 2 Diabetic Patients: Parvin Mirmiran, Zahra Bahadoran, Fereidoun Azizi; Endocrinol Metab. 2014;29(4):443-449. Published online December 29, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.4.443

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Background

Lipid accumulation product (LAP) is a novel biomarker of central lipid accumulation related to risk of diabetes and cardiovascular disease. In this study, we assessed the association of LAP with glucose homeostasis, lipid and lipid peroxidation, and subclinical systemic inflammation in diabetic patients.

Methods

Thirty-nine male and 47 female type 2 diabetic patients were assessed for anthropometrics and biochemical measurements. LAP was calculated as [waist circumference (cm)-65]×[triglycerides (mmol/L)] in men, and [waist circumference (cm)-58]×[triglycerides (mmol/L)] in women. Associations of LAP with fasting glucose, insulin, insulin resistance index, lipid and lipoprotein levels, malondialdehyde, and high-sensitive C-reactive protein (hs-CRP) were assessed.

Results

Mean age and LAP index were 53.6±9.6 and 51.9±31.2 years, respectively. After adjustments for age, sex and body mass index status, a significant positive correlation was observed between LAP index and fasting glucose (r=0.39, P<0.001), and homeostasis model assessment of insulin resistance (r=0.31, P<0.05). After additional adjustment for fasting glucose levels, antidiabetic and antilipidemic drugs, the LAP index was also correlated to total cholesterol (r=0.45, P<0.001), high density lipoprotein cholesterol (HDL-C) levels (r=-0.29, P<0.05), triglycerides to HDL-C ratio (r=0.89, P<0.001), malondialdehyde (r=0.65, P<0.001), and hs-CRP levels (r=0.27, P<0.05).

Conclusion

Higher central lipid accumulation in diabetic patients was related to higher insulin resistance, oxidative stress and systemic inflammation.

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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

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Abstract PDF PubReader

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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A Modified Differentiation Protocol In Vitro to Generate Dopaminergic Neurons from Pluripotent Stem Cells
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Nianping Zhang, Ying Lyu, Xuebing Pan, Liping Xu, Aiguo Xuan, Xiaosong He, Wandan Huang, Dahong Long
International Journal of Molecular Medicine.2017; 40(3): 814. CrossRef
Increased susceptibility to fundus camera-delivered light-induced retinal degeneration in mice deficient in oxidative stress response proteins
Yi Ding, Bogale Aredo, Xin Zhong, Cynthia X. Zhao, Rafael L. Ufret-Vincenty
Experimental Eye Research.2017; 159: 58. CrossRef
Articles in 'Endocrinology and Metabolism' in 2014
Won-Young Lee
Endocrinology and Metabolism.2015; 30(1): 47. CrossRef
Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression
Jaclyn Nicole Le Grand, Laura Gonzalez-Cano, Maria Angeliki Pavlou, Jens C. Schwamborn
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Effects of S-allylcysteine on Oxidative Stress in Streptozotocin-Induced Diabetic Rats.: Chul Ho Shin, Jahei Ihm; J Korean Endocr Soc. 2008;23(2):129-136. Published online April 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.2.129

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Abstract PDF

BACKGROUND
An increase in oxidative stress is postulated to contribute to the development of diabetic complications and the use of antioxidant therapy could be protective against these processes. This study was performed to investigate the role of the antioxidant S-allylcysteine (SAC), a water-soluble component of aged garlic, for reducing levels of oxidative stress that occurs in diabetic rats. METHODS: SAC (100 mg/head/day) was administered orally to streptozotocin-induced diabetic rats for eight weeks. The effects of SAC on the levels of markers of oxidative stress (malondialdehyde and glutathione) and mRNA expression of antioxidant enzymes were measured in the liver and kidney. RESULTS: SAC-fed rats showed lower cholesterol and triacylglyceride levels than untreated diabetic rats. Malondialdehyde levels were increased in the liver and kidney of diabetic rats and SAC administration lowered the levels in both organs. Glutathione levels were lower in the liver and kidney of diabetic rats, and SAC administration restored the glutathione to a level similar in non-diabetic rats. In the liver and kidney of untreated diabetic rats, mRNA expression of catalase, superoxide dismutase and glutathione reductase were down regulated, and administration of SAC increased expression of these enzymes. CONCLUSION: Our results have shown that administration of SAC to diabetic rats can lower blood lipid levels and alleviate oxidative stress in the diabetic tissues, suggesting that SAC might have beneficial effects in a prevention trial for diabetic complications.

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Effect of Garlic and Aged Black Garlic on Hyperglycemia and Dyslipidemia in Animal Model of Type 2 Diabetes Mellitus
Yeong-Ju Seo, Oh-Cheon Gweon, Ji-Eun Im, Young-Min Lee, Min-Jung Kang, Jung-In Kim
Preventive Nutrition and Food Science.2009; 14(1): 1. CrossRef
Antioxidant effect of garlic and aged black garlic in animal model of type 2 diabetes mellitus
Young-Min Lee, Oh-Cheon Gweon, Yeong-Ju Seo, Jieun Im, Min-Jung Kang, Myo-Jeong Kim, Jung-In Kim
Nutrition Research and Practice.2009; 3(2): 156. CrossRef
Effects of Adenophora triphylla Ethylacetate Extract on mRNA Levels of Antioxidant Enzymes in Human HepG2 Cells
Hyun-Jin Choi, Soo-Hyun Kim, Hyun-Taek Oh, Mi-Ja Chung, Cheng-Bi Cui, Seung-Shi Ham
Journal of the Korean Society of Food Science and Nutrition.2008; 37(10): 1238. CrossRef

Review Article

Mechanism of Developing Diabetic Vascular Complication by Oxidative Stress.: Bo Hyun Kim, Seok Man Son; J Korean Endocr Soc. 2006;21(6):448-459. Published online December 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.6.448

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Abstract PDF

Macrovascular and microvascular diseases are currently the principal causes of morbidity and mortality in the patients with diabetes mellitus. Oxidative stress has been postulated to be a major contributor to the pathogenesis of these events. There is considerable evidence that many biochemical pathways that are adversely affected by hyperglycemia are associated with the generation of reactive oxygen species, and this ultimately leads to increased oxidative stress in a variety of tissues. In the absence of appropriate compensation by the endogenous antioxidant defense network, increased oxidative stress leads to the activation of stress-sensitive intracellular signaling pathways and the formation of gene products that cause cellular damage and contribute to the late complications of diabetes. Hyperglycemia increases oxidant production by multiple pathways rather than by a single dominant pathway. Glucose can undergo nonenzymatic reactions to form gluco-oxidants and glycated products, which can be oxidants. Metabolism of excessive intracellular glucose can occur by several processes such as aldose reductase, mitochondrial oxidative phosphorylation, activation of NAD(P)H oxidases, and the alteration of the NADPH/NADP ratios. Reactive oxygen species participate in vascular smooth muscle cell growth and migration, modulation of endothelial function, including abnormal endothelium-dependent relaxation and the expression of a proinflammatory phenotype, and modification of the extracellular matrix. All of these events contribute to the development of diabetic microvascular and macrovascular complications, suggesting that the sources of reactive oxygen species and the signaling pathways that they modify may represent important therapeutic targets.

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Original Articles

The Effect of Oxidative Stress on the Proliferation and Differentiation of Human Bone Marrow Stromal Cell-Derived Osteoblasts.: Eun Sook Oh, Ki Hyun Baek, Won Young Lee, Ki Won Oh, Hye Soo Kim, Je Ho Han, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Moo Il Kang; J Korean Endocr Soc. 2006;21(3):222-232. Published online June 1, 2006; DOI: https://doi.org/10.3803/jkes.2006.21.3.222

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Abstract PDF

BACKGROUND
The objectives of our study were to assess the effects of oxidative stress on the proliferation, differentiation and apoptosis of human bone marrow stromal cell (BMSC)-derived osteoblasts and to explore pathways by which osteoblast cell apoptosis was induced. METHODS: Mononuclear cells including BMSCs were cultured to osteoblastic lineage. Different doses of hydrogen peroxide (H2O2) were added to the culture media. The colony forming units-fibroblastic (CFU-Fs) were stained with crystal violet and alkaline phosphatase (ALP). The MTT assay was done to see the effect of H2O2 on cell viability. The effect of H2O2 on osteocalcin gene expression was determined by RT-PCR. The matrix calcification measurement was performed. FACS analysis was performed to determine the osteoblasts apoptosis. Caspase-3, -8 and 9 activity assay and cytochrome c release were measured. RESULTS: The size and number of ALP (+) CFU-Fs were also decreased by H2O2 treatment. When compared with the control group, H2O2 significantly decreased the total number of cells of each culture well during MTT assay. H2O2 significantly diminished expression of osteocalcin mRNA. N-acetylcystein (NAC) blocked the diminution of cell viability and the inhibition of osteocalcin mRNA expression by H2O2. H2O2 reduced matrix calcification. FACS analysis revealed H2O2 increased percentage of apoptotic cells. Addition of H2O2 resulted in the increase of caspase-9 and -3 activity but not caspase-8, and release of cytochrome c to the cytosol. CONCLUSION: These data suggest that, in primary human BMSCs, oxidative stress inhibits proliferation of stromal cells and inhibits the differentiation to osteoblastic lineage. In addition, oxidative stress induces apoptosis of human BMSC-derived osteoblasts and this may be mediated by mitochondrial pathway of apoptotic signal.

Citations

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Antioxidaitve and Differentiation Effects of Artemisia capillaris T. Extract on Hydrogen Peroxide-induced Oxidative Damage of MC3T3-E1 Osteoblast Cells
Jee-Eun Seo, Eun-Sun Hwang, Gun-Hee Kim
Journal of the Korean Society of Food Science and Nutrition.2011; 40(11): 1532. CrossRef

Effects of alpha-Lipoic Acid on Bone Metabolism in Rats with Low Bone Mass.: Jung Min Koh, Hee Sook Lee, Duk Jae Kim, Ghi Su Kim; J Korean Endocr Soc. 2005;20(5):476-487. Published online October 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.5.476

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Abstract PDF: BACKGROUND
Growing evidence has shown a biochemical link between increased oxidative stress and reduced bone density. In our previous study, alpha-lipoic acid (alpha-LA), a thiol antioxidant, suppressed both osteoclastogenesis and bone resorption, and also prevented TNF-alpha-induced apoptosis of osteoblast lineages. The effects of alpha-LA were investigated on bone metabolism in rats with a low bone mass. METHODS: An ovariectomy (OVX) or Talc injection (inflammation-mediated osteopenia, IMO) was performed in 12 week old female Sprague-Dawley rats. Diets containing either 0.3%, 0.5% or 1.0% alpha-LA were administered to the OVX rats for 16 weeks, and to the IMO rats for 21 days. The bone mineral densities (BMD) of the anterior-posterior lumbar spine and total femur were measured using dual-energy X-ray absorptiometry (Hologic QDR 4500-A), with small animal software. The plasma bone specific alkaline phosphatase activity (BSAP) and urinary free deoxypyridinoline concentration (DPD) were determined using enzyme immunoassay methods. RESULTS: The body weights were significantly decreased in the OVX rats on the diets containing 0.3 and 0.5% alpha-LA than in the OVX control. No significant differences in the BMD at either site were noted between rats administered the diets with or without alpha-LA. However, the administration of various doses of alpha-LA noticeably decreased the level of urinary DPD in both the OVX and IMO rats. High doses of alpha-LA (0.5% and/or 1.0%) also decreased the levels of plasma BSAP in both models. CONCLUSION: Although no increase in BMD was demonstrated by the administration of alpha-LA, these results suggest that alpha-LA suppresses the rates of bone turnover in rats with a low bone mass

Sex Hormone-Binding Globulin and Oxidative Stress in Korean Premenopausal Women.: Young Ju Choi, Jee Young Oh, Young Sun Hong, Yeon Ah Sung; J Korean Endocr Soc. 2004;19(1):48-57. Published online February 1, 2004

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Abstract PDF: BACKGROUND
Low levels of sex hormone-binding globulin(SHBG), an indirect index of androgenicity, are associated with insulin resistance and cardiovascular risk factors. The risk factors of the cardiovascular disease are known to be related to oxidative stress. In recent reports, sex hormones were associated with oxidative stress in women with polycystic ovarian syndrome(PCOS), which is characterized by increased androgenicity and insulin resistance. METHODS: To investigate the relationship between sex hormones and oxidative stress, we examined the association of malondialdehyde(MDA), total antioxidant status(TAS), oxidized low density lipoprotein cholesterol(ox-LDL), and SHBG in 46 Korean premenopausal women. RESULTS: 1. SHBG and MDA levels were not significantly different among the women with NGT and IGT. But, TAS was significantly lower(p=0.034) in the subjects with IGT than in the subjects with NGT. 2. The SHBG level was significantly lower(p=0.036) in obese women than in non-obese women. 3.The SHBG level was significantly inversely correlated with BMI(r=-0.394, p=0.007), post challenge glucose(r=-0.326, p=0.027), waist size(r=-0.323, p=0.029), waist-to-thigh ratio(WTR) (r=-0.308, p=0.037), fasting insulin level(r=-0.387, p=0.008), visceral fat area(VFA)(r=-0.339, p=0.021), and was significantly positively correlated with SI(r=0.397, p=0.008). 4. The SHBG level was significantly inversely correlated with levels of MDA(r=-0.357, p=0.015) and ox-LDL(r=-0.367, p=0.014). 5. In a multiple linear regression analysis, the SHBG level was a significant and independent factor for both MDA and ox-LDL. For TAS, the fasting insulin level and post challenge glucose were significant and independent factors. CONCLUSION: Increased androgenicity assessed by the decrease in serum SHBG levels is associated with the increase in MDA and ox-LDL. These results suggest that increased androgenicity in premenopausal women can contribute to the development of cardiovascular diseases via increased oxidative stress.

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