Endocrinology and Metabolism

Original Article

Miscellaneous
AM1638, a GPR40-Full Agonist, Inhibited Palmitate- Induced ROS Production and Endoplasmic Reticulum Stress, Enhancing HUVEC Viability in an NRF2-Dependent Manner: Hwan-Jin Hwang, Joo Won Kim, SukHwan Yun, Min Jeong Park, Eyun Song, Sooyeon Jang, Ahreum Jang, Kyung Mook Choi, Sei Hyun Baik, Hye Jin Yoo; Endocrinol Metab. 2023;38(6):760-769. Published online November 2, 2023; DOI: https://doi.org/10.3803/EnM.2023.1774

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Abstract PDF PubReader ePub: Background
G protein-coupled receptor 40 (GPR40) is a key molecule in diabetes and fatty liver, but its role in endothelial dysfunction remains unclear. Our objective in this study was to determine whether GPR40 agonists protect endothelial cells against palmitatemediated oxidative stress.
Methods
Human umbilical vein endothelial cells (HUVECs) were used to investigate effects of various GPR40 agonists on vascular endothelium.
Results
In HUVECs, AM1638, a GPR40-full agonist, enhanced nuclear factor erythroid 2–related factor 2 (NRF2) translocation to the nucleus and heme oxygenase-1 (HO-1) expression, which blocked palmitate-induced superoxide production. Those antioxidant effects were not detected after treatment with LY2922470 or TAK875, GPR40-partial agonists, suggesting that GPR40 regulates reactive oxygen species (ROS) removal in a ligand-dependent manner. We also found that palmitate-induced CCAAT/enhancer‐binding protein homologous protein expression; X-box binding protein-1 splicing, nuclear condensation, and fragmentation; and caspase-3 cleavage were all blocked in an NRF2-dependent manner after AM1638 treatment. Both LY2922470 and TAK875 also improved cell viability independent of the NRF2/ROS pathway by reducing palmitate-mediated endoplasmic reticulum stress and nuclear damage. GPR40 agonists thus have beneficial effects against palmitate in HUVECs. In particular, AM1638 reduced palmitate-induced superoxide production and cytotoxicity in an NRF2/HO-1 dependent manner.
Conclusion
GPR40 could be developed as a good therapeutic target to prevent or treat cardiovascular diseases such as atherosclerosis.

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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Abstract PDF PubReader ePub

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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Diabetes
Pioglitazone Attenuates Palmitate-Induced Inflammation and Endoplasmic Reticulum Stress in Pancreatic β-Cells: Seok-Woo Hong, Jinmi Lee, Jung Hwan Cho, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee; Endocrinol Metab. 2018;33(1):105-113. Published online March 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.1.105

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Background

The nuclear receptor peroxisome proliferator-activator gamma (PPARγ) is a useful therapeutic target for obesity and diabetes, but its role in protecting β-cell function and viability is unclear.

Methods

To identify the potential functions of PPARγ in β-cells, we treated mouse insulinoma 6 (MIN6) cells with the PPARγ agonist pioglitazone in conditions of lipotoxicity, endoplasmic reticulum (ER) stress, and inflammation.

Results

Palmitate-treated cells incubated with pioglitazone exhibited significant improvements in glucose-stimulated insulin secretion and the repression of apoptosis, as shown by decreased caspase-3 cleavage and poly (adenosine diphosphate [ADP]-ribose) polymerase activity. Pioglitazone also reversed the palmitate-induced expression of inflammatory cytokines (tumor necrosis factor α, interleukin 6 [IL-6], and IL-1β) and ER stress markers (phosphor-eukaryotic translation initiation factor 2α, glucose-regulated protein 78 [GRP78], cleaved-activating transcription factor 6 [ATF6], and C/EBP homologous protein [CHOP]), and pioglitazone significantly attenuated inflammation and ER stress in lipopolysaccharide- or tunicamycin-treated MIN6 cells. The protective effect of pioglitazone was also tested in pancreatic islets from high-fat-fed KK-Ay mice administered 0.02% (wt/wt) pioglitazone or vehicle for 6 weeks. Pioglitazone remarkably reduced the expression of ATF6α, GRP78, and monocyte chemoattractant protein-1, prevented α-cell infiltration into the pancreatic islets, and upregulated glucose transporter 2 (Glut2) expression in β-cells. Moreover, the preservation of β-cells by pioglitazone was accompanied by a significant reduction of blood glucose levels.

Conclusion

Altogether, these results support the proposal that PPARγ agonists not only suppress insulin resistance, but also prevent β-cell impairment via protection against ER stress and inflammation. The activation of PPARγ might be a new therapeutic approach for improving β-cell survival and insulin secretion in patients with diabetes mellitus

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Review Articles

Diabetes-Related Cardiac Dysfunction: Lamario J. Williams, Brenna G. Nye, Adam R. Wende; Endocrinol Metab. 2017;32(2):171-179. Published online June 23, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.2.171

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Abstract PDF PubReader ePub

The proposal that diabetes plays a role in the development of heart failure is supported by the increased risk associated with this disease, even after correcting for all other known risk factors. However, the precise mechanisms contributing to the condition referred to as diabetic cardiomyopathy have remained elusive, as does defining the disease itself. Decades of study have defined numerous potential factors that each contribute to disease susceptibility, progression, and severity. Many recent detailed reviews have been published on mechanisms involving insulin resistance, dysregulation of microRNAs, and increased reactive oxygen species, as well as causes including both modifiable and non-modifiable risk factors. As such, the focus of the current review is to highlight aspects of each of these topics and to provide specific examples of recent advances in each area.

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Thyroid
Clinical Relevance of Environmental Factors in the Pathogenesis of Autoimmune Thyroid Disease: Wilmar M. Wiersinga; Endocrinol Metab. 2016;31(2):213-222. Published online May 13, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.2.213

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Genetic factors contribute for about 70% to 80% and environmental factors for about 20% to 30% to the pathogenesis of autoimmune thyroid disease (AITD). Relatives of AITD patients carry a risk to contract AITD themselves. The 5-year risk can be quantified by the so-called Thyroid Events Amsterdam-score, based on serum thyroid-stimulating hormone, thyroid peroxidase (TPO)-antibodies and family history. Subjects at risk may ask what they can do to prevent development of AITD. This review summarizes what is known about modulation of exposure to environmental factors in terms of AITD prevention. To stop smoking decreases the risk on Graves disease but increases the risk on Hashimoto disease. Moderate alcohol intake provides some protection against both Graves and Hashimoto disease. Low selenium intake is associated with a higher prevalence of thyroid autoimmunity, but evidence that selenium supplementation may lower TPO antibodies and prevent subclinical hypothyroidism remains inconclusive. Low serum vitamin D levels are associated with a higher prevalence of TPO antibodies, but intervention studies with extra vitamin D have not been done yet. Stress may provoke Graves hyperthyroidism but not Hashimoto thyroiditis. Estrogen use have been linked to a lower prevalence of Graves disease. The postpartum period is associated with an increased risk of AITD. Taking together, preventive interventions to diminish the risk of AITD are few, not always feasible, and probably of limited efficacy.

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Original Articles

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.

Citations

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SDH5 down-regulation mitigates the damage of osteoporosis via inhibiting the MyD88/NF-κB signaling pathway
Hongzi Wu, Dehua Zhang, Haijun Xia, Yongqi Li, Feng Mao, Yi Liao
Immunopharmacology and Immunotoxicology.2023; 45(3): 317. CrossRef
N-acetyl Cysteine Inhibits Cell Proliferation and Differentiation of LPSInduced MC3T3-E1 Cells Via Regulating Inflammatory Cytokines
Wangyang Li, Hui Zhang, Junchi Chen, Yujie Tan, Ailing Li, Ling Guo
Current Pharmaceutical Biotechnology.2023; 24(3): 450. CrossRef
Unravelling the role of NFE2L1 in stress responses and related diseases
Xingzhu Liu, Chang Xu, Wanglong Xiao, Nianlong Yan
Redox Biology.2023; 65: 102819. CrossRef
Nfe2l1 deficiency mitigates streptozotocin-induced pancreatic β-cell destruction and development of diabetes in male mice
Simeng Bao, Hongzhi Zheng, Chengjie Chen, Yuhang Zhang, Lina Bao, Bei Yang, Yongyong Hou, Yanyan Chen, Qiang Zhang, Jingbo Pi, Jingqi Fu
Food and Chemical Toxicology.2021; 158: 112633. CrossRef
Long isoforms of NRF1 negatively regulate adipogenesis via suppression of PPARγ expression
Peng Xue, Yongyong Hou, Zhuo Zuo, Zhendi Wang, Suping Ren, Jian Dong, Jingqi Fu, Huihui Wang, Melvin E. Andersen, Qiang Zhang, Yuanyuan Xu, Jingbo Pi
Redox Biology.2020; 30: 101414. CrossRef
Protracted rosiglitazone treatment exacerbates inflammation in white adipose tissues of adipocyte-specific Nfe2l1 knockout mice
Suping Ren, Yongyong Hou, Zhuo Zuo, Zhiyuan Liu, Huihui Wang, Yuanyuan Xu, Masayuki Yamamoto, Qiang Zhang, Jingqi Fu, Jingbo Pi
Food and Chemical Toxicology.2020; 146: 111836. CrossRef
Nrf1 is paved as a new strategic avenue to prevent and treat cancer, neurodegenerative and other diseases
Jianxin Yuan, Shuwei Zhang, Yiguo Zhang
Toxicology and Applied Pharmacology.2018; 360: 273. CrossRef
Silencing of long isoforms of nuclear factor erythroid 2 like 1 primes macrophages towards M1 polarization
Huihui Wang, Jiayu Zhu, Zhiyuan Liu, Hang Lv, Peng Lv, Feng Chen, Jingqi Fu, Yongyong Hou, Rui Zhao, Yuanyuan Xu, Qiang Zhang, Jingbo Pi
Free Radical Biology and Medicine.2018; 117: 37. CrossRef
Costunolide increases osteoblast differentiation via ATF4-dependent HO-1 expression in C3H10T1/2 cells
Wan-Jin Jeon, Kyeong-Min Kim, Eun-Jung Kim, Won-Gu Jang
Life Sciences.2017; 178: 94. CrossRef

Obesity and Metabolism
Exendin-4 Inhibits the Expression of SEPP1 and Fetuin-A via Improvement of Palmitic Acid-Induced Endoplasmic Reticulum Stress by AMPK: Jinmi Lee, Seok-Woo Hong, Se Eun Park, Eun-Jung Rhee, Cheol-Young Park, Ki-Won Oh, Sung-Woo Park, Won-Young Lee; Endocrinol Metab. 2015;30(2):177-184. Published online June 30, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.2.177

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Background

Selenoprotein P (SEPP1) and fetuin-A, both circulating liver-derived glycoproteins, are novel biomarkers for insulin resistance and nonalcoholic fatty liver disease. However, the effect of exendin-4 (Ex-4), a glucagon-like peptide-1 receptor agonist, on the expression of hepatokines, SEPP1, and fetuin-A, is unknown.

Methods

The human hepatoma cell line HepG2 was treated with palmitic acid (PA; 0.4 mM) and tunicamycin (tuni; 2ug/ml) with or without exendin-4 (100 nM) for 24 hours. The change in expression of PA-induced SEPP1, fetuin-A, and endoplasmic reticulum (ER) stress markers by exendin-4 treatment were evaluated using quantitative real-time reverse transcription polymerase chain reaction and Western blotting. Transfection of cells with AMP-activated protein kinase (AMPK) small interfering RNA (siRNA) was performed to establish the effect of exendin-4-mediated AMPK in the regulation of SEPP1 and fetuin-A expression.

Results

Exendin-4 reduced the expression of SEPP1, fetuin-A, and ER stress markers including PKR-like ER kinase, inositol-requiring kinase 1α, activating transcription factor 6, and C/EBP homologous protein in HepG2 cells. Exendin-4 also reduced the expression of SEPP1 and fetuin-A in cells treated with tunicamycin, an ER stress inducer. In cells treated with the AMPK activator 5-aminoidazole-4-carboxamide ribonucleotide (AICAR), the expression of hepatic SEPP1 and fetuin-A were negatively related by AMPK, which is the target of exendin-4. In addition, exendin-4 treatment did not decrease SEPP1 and fetuin-A expression in cells transfected with AMPK siRNA.

Conclusion

These data suggest that exendin-4 can attenuate the expression of hepatic SEPP1 and fetuin-A via improvement of PA-induced ER stress by AMPK.

Citations

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Improvement of β-Cell Function After Switching From DPP-4 Inhibitors to Oral Semaglutide: SWITCH-SEMA2 Post Hoc Analysis
Hiroshi Nomoto, Sho Furusawa, Hiroki Yokoyama, Yuka Suzuki, Rimi Izumihara, Yuki Oe, Kiyohiko Takahashi, Aika Miya, Hiraku Kameda, Kyu Yong Cho, Jun Takeuchi, Yoshio Kurihara, Akinobu Nakamura, Tatsuya Atsumi
The Journal of Clinical Endocrinology & Metabolism.2024;[Epub] CrossRef
Maternal Organic Selenium Supplementation Relieves Intestinal Endoplasmic Reticulum Stress in Piglets by Enhancing the Expression of Glutathione Peroxidase 4 and Selenoprotein S
Dajiang Ding, Daolin Mou, Heng Zhu, Xuemei Jiang, Lianqiang Che, Zhengfeng Fang, Shengyu Xu, Yan Lin, Yong Zhuo, Jian Li, Chao Huang, Yuanfeng Zou, Lixia Li, De Wu, Bin Feng
Frontiers in Nutrition.2022;[Epub] CrossRef
Alliin, capsaicin, and gingerol attenuate endoplasmic reticulum stress-induced hepatic steatosis in HepG2 cells and C57BL/6N mice
Ye-Rang Yun, Ji-Eun Lee
Journal of Functional Foods.2022; 95: 105186. CrossRef
PNPLA3 I148M is involved in the variability in anti-NAFLD response to exenatide
Yunzhi Chen, Xuemei Yan, Xiao Xu, Shuhua Yuan, Fen Xu, Hua Liang
Endocrine.2020; 70(3): 517. CrossRef
Green tea extracts reduce leukocyte cell–Derived chemotaxin 2 and selenoprotein P levels in the livers of C57BL/6J mice fed a high-fat diet
Shintaro Onishi, Hidefumi Kitazawa, Shinichi Meguro, Ichiro Tokimitsu
Bioscience, Biotechnology, and Biochemistry.2018; 82(9): 1568. CrossRef
Melatonin improves insulin resistance and hepatic steatosis through attenuation of alpha‐2‐HS‐glycoprotein
Jee‐In Heo, Dae Wui Yoon, Ji Hee Yu, Nam Hoon Kim, Hye Jin Yoo, Ji A. Seo, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Dong Seop Choi, Nan Hee Kim
Journal of Pineal Research.2018;[Epub] CrossRef
Palmitic acid induces ceramide accumulation, mitochondrial protein hyperacetylation, and mitochondrial dysfunction in porcine oocytes†
Nobuhiko Itami, Koumei Shirasuna, Takehito Kuwayama, Hisataka Iwata
Biology of Reproduction.2018; 98(5): 644. CrossRef
Astragaloside IV attenuates free fatty acid-induced ER stress and lipid accumulation in hepatocytes via AMPK activation
Bing Zhou, Dan-li Zhou, Xiao-hong Wei, Rong-yu Zhong, Jie Xu, Liao Sun
Acta Pharmacologica Sinica.2017; 38(7): 998. CrossRef
New Potential Targets of Glucagon-Like Peptide 1 Receptor Agonists in Pancreatic β-Cells and Hepatocytes
Won-Young Lee
Endocrinology and Metabolism.2017; 32(1): 1. CrossRef
Selenoprotein P neutralizes lipopolysaccharide and participates in hepatic cell endoplasmic reticulum stress response
Yongzhong Zhao, Shuvojit Banerjee, Ping Huang, Xinning Wang, Candece L. Gladson, Warren D. Heston, Charles B. Foster
FEBS Letters.2016; 590(24): 4519. CrossRef
Novel phenotypes of prediabetes?
Hans-Ulrich Häring
Diabetologia.2016; 59(9): 1806. CrossRef

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.

Citations

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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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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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Adolescent nonpharmacological interventions for early-life stress and their mechanisms
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Martin Viktorov, Matthew P. Wilkinson, Victoria C. E. Elston, Medi Stone, Emma S. J. Robinson
Brain and Neuroscience Advances.2022; 6: 239821282210816. CrossRef
Impact of preweaning stress on long-term neurobehavioral outcomes in Sprague-Dawley rats: Differential effects of barren cage rearing, pup isolation, and the combination
Jenna L.N. Sprowles, Charles V. Vorhees, Michael T. Williams
Neurotoxicology and Teratology.2021; 84: 106956. CrossRef
Maternal separation in rodents: a journey from gut to brain and nutritional perspectives
Marion Rincel, Muriel Darnaudéry
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Systematic review and meta-analysis: effects of maternal separation on anxiety-like behavior in rodents
Daniel Wang, Jessica L. S. Levine, Victor Avila-Quintero, Michael Bloch, Arie Kaffman
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Maternal Deprivation and Sex Alter Central Levels of Neurotrophins and Inflammatory Cytokines in Rats Exposed to Palatable Food in Adolescence
Roberta Ströher, Carla de Oliveira, Dirson João Stein, Isabel Cristina de Macedo, Jéferson Ferraz Goularte, Lisiane Santos da Silva, Gabriela Gregory Regner, Helouise Richardt Medeiros, Wolnei Caumo, Iraci L.S. Torres
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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.

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Adrenal gland
Effects of Chronic Restraint Stress on Body Weight, Food Intake, and Hypothalamic Gene Expressions in Mice: Joo Yeon Jeong, Dong Hoon Lee, Sang Soo Kang; Endocrinol Metab. 2013;28(4):288-296. Published online December 12, 2013; DOI: https://doi.org/10.3803/EnM.2013.28.4.288

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Abstract PDF PubReader

Background

Stress affects body weight and food intake, but the underlying mechanisms are not well understood.

Methods

We evaluated the changes in body weight and food intake of ICR male mice subjected to daily 2 hours restraint stress for 15 days. Hypothalamic gene expression profiling was analyzed by cDNA microarray.

Results

Daily body weight and food intake measurements revealed that both parameters decreased rapidly after initiating daily restraint stress. Body weights of stressed mice then remained significantly lower than the control body weights, even though food intake slowly recovered to 90% of the control intake at the end of the experiment. cDNA microarray analysis revealed that chronic restraint stress affects the expression of hypothalamic genes possibly related to body weight control. Since decreases of daily food intake and body weight were remarkable in days 1 to 4 of restraint, we examined the expression of food intake-related genes in the hypothalamus. During these periods, the expressions of ghrelin and pro-opiomelanocortin mRNA were significantly changed in mice undergoing restraint stress. Moreover, daily serum corticosterone levels gradually increased, while leptin levels significantly decreased.

Conclusion

The present study demonstrates that restraint stress affects body weight and food intake by initially modifying canonical food intake-related genes and then later modifying other genes involved in energy metabolism. These genetic changes appear to be mediated, at least in part, by corticosterone.

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Oxytocin involves in chronic stress-evoked melanoma metastasis via β-arrestin 2-mediated ERK signaling pathway
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Anxiolytic effects of γ-oryzanol in chronically- stressed mice are related to monoamine levels in the brain
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Centella asiaticaPrevents Increase of Hippocampal Tumor Necrosis Factor-αIndependently of Its Effect on Brain-Derived Neurotrophic Factor in Rat Model of Chronic Stress
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Ghrelin is a persistent biomarker for chronic stress exposure in adolescent rats and humans
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GLP-1 Can Protect Proinflammatory Cytokines Induced Beta Cell Apoptosis through the Ubiquitination.: Dong Mee Lim, Ju Young Kim, Kang Woo Lee, Keun Young Park, Byung Joon Kim; Endocrinol Metab. 2011;26(2):142-149. Published online June 1, 2011; DOI: https://doi.org/10.3803/EnM.2011.26.2.142

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Abstract PDF: BACKGROUND
Proinflammatory cytokines are one of the causes of diabetes mellitus. However, the exact molecular mechanism by which proinflammatory cytokines induce beta-cell death remains to be clearly elucidated. Glucagon-like peptide-1 (GLP-1) affects the stimulation of insulin secretion and the preservation of beta-cells. Additionally, it may exert an antiapoptotic effect on beta cells; however, the mechanism underlying this effect has yet to be demonstrated. Therefore, we investigated the protective effects of GLP-1 in endoplasmic reticulum (ER)-mediated beta-cell apoptosis using proinflammatory cytokines. METHODS: To induce ER stress, hamster insulin-secreting tumor (HIT)-T15 cells were treated using a mixture of cytokines. Apoptosis was evaluated via MTT assay, Hoechst 33342 staining, and annexin/propidium iodide (PI) flow cytometry. The mRNA and protein expression levels of ER stress-related molecules were determined via PCR and Western blotting, respectively. Nitric oxide was measured with Griess reagent. The levels of inducible nitric oxide synthase (iNOS) mRNA and protein were analyzed via real-time PCR and Western blot, respectively. iNOS protein degradation was evaluated via immunoprecipitation. We pretreated HIT-T15 cells with exendin (Ex)-4 for 1 hour prior to the induction of stress. RESULTS: We determined that Ex-4 exerted a protective effect through nitric oxide and the modulation of ER stress-related molecules (glucose-regulated protein [GRP]78, GRP94, and CCAAT/enhancer-binding protein homologous protein [CHOP]) and that Ex-4 stimulates iNOS protein degradation via the ubiquitination pathway. Additionally, Ex-4 also induced the recovery of insulin2 mRNA expression in beta cells. CONCLUSION: The results of this study indicate that GLP-1 may protect beta cells against apoptosis through the ubiquitination pathway.

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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