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Tae-Seo Sohn  (Sohn TS) 3 Articles
Basic Research
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Mitochondrial TFAM as a Signaling Regulator between Cellular Organelles: A Perspective on Metabolic Diseases
Jin-Ho Koh, Yong-Woon Kim, Dae-Yun Seo, Tae-Seo Sohn
Diabetes Metab J. 2021;45(6):853-865.   Published online November 22, 2021
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  • 294 Download
  • 17 Web of Science
  • 19 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
Tissues actively involved in energy metabolism are more likely to face metabolic challenges from bioenergetic substrates and are susceptible to mitochondrial dysfunction, leading to metabolic diseases. The mitochondria receive signals regarding the metabolic states in cells and transmit them to the nucleus or endoplasmic reticulum (ER) using calcium (Ca2+) for appropriate responses. Overflux of Ca2+ in the mitochondria or dysregulation of the signaling to the nucleus and ER could increase the incidence of metabolic diseases including insulin resistance and type 2 diabetes mellitus. Mitochondrial transcription factor A (Tfam) may regulate Ca2+ flux via changing the mitochondrial membrane potential and signals to other organelles such as the nucleus and ER. Since Tfam is involved in metabolic function in the mitochondria, here, we discuss the contribution of Tfam in coordinating mitochondria-ER activities for Ca2+ flux and describe the mechanisms by which Tfam affects mitochondrial Ca2+ flux in response to metabolic challenges.


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    Journal of Pharmaceutical Analysis.2024; 14(2): 225.     CrossRef
  • Mitochondrial damage‐associated molecular patterns: A new insight into metabolic inflammation in type 2 diabetes mellitus
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    Diabetes/Metabolism Research and Reviews.2024;[Epub]     CrossRef
  • Altered Energy Metabolism, Mitochondrial Dysfunction, and Redox Imbalance Influencing Reproductive Performance in Granulosa Cells and Oocyte During Aging
    Hiroshi Kobayashi, Chiharu Yoshimoto, Sho Matsubara, Hiroshi Shigetomi, Shogo Imanaka
    Reproductive Sciences.2024; 31(4): 906.     CrossRef
  • The Protective Mechanism of TFAM on Mitochondrial DNA and its Role in Neurodegenerative Diseases
    Ying Song, Wenjun Wang, Beibei Wang, Qiwen Shi
    Molecular Neurobiology.2024; 61(7): 4381.     CrossRef
  • When Our Best Friend Becomes Our Worst Enemy: The Mitochondrion in Trauma, Surgery, and Critical Illness
    May-Kristin Torp, Kåre-Olav Stensløkken, Jarle Vaage
    Journal of Intensive Care Medicine.2024;[Epub]     CrossRef
  • Attenuating mitochondrial dysfunction and morphological disruption with PT320 delays dopamine degeneration in MitoPark mice
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    Journal of Biomedical Science.2024;[Epub]     CrossRef
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    Yan Zhou, Xiaoyi Huang, Yinglu Jin, Minhao Qiu, Peter C. Ambe, Zarrin Basharat, Wandong Hong
    Biomedicine & Pharmacotherapy.2024; 175: 116690.     CrossRef
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    International Journal of Molecular Sciences.2023; 24(6): 5498.     CrossRef
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    Experimental Eye Research.2023; 231: 109498.     CrossRef
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    Yu-Ling Hsu, Hui-Jye Chen, Jia-Xin Gao, Ming-Yang Yang, Ru-Huei Fu
    Antioxidants.2023; 12(9): 1782.     CrossRef
  • TBBPA causes apoptosis in grass carp hepatocytes involving destroyed ER-mitochondrial function
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  • Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women
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    Antioxidants.2022; 11(7): 1302.     CrossRef
  • The Effects of Galgunhwanggumhwangryun-tang on Glucose and Energy Metabolism in C2C12 Myotubes
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Angiotensin II Inhibits Insulin Binding to Endothelial Cells
Su-Jin Oh, Won-Chul Ha, Jee-In Lee, Tae-Seo Sohn, Ji-Hyun Kim, Jung-Min Lee, Sang-Ah Chang, Oak-Kee Hong, Hyun-Shik Son
Diabetes Metab J. 2011;35(3):243-247.   Published online June 30, 2011
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  • 24 Download
  • 6 Crossref
AbstractAbstract PDFPubReader   

Insulin-mediated glucose uptake in insulin target tissues is correlated with interstitial insulin concentration, rather than plasma insulin concentration. Therefore, insulin delivery to the interstitium of target tissues is very important, and the endothelium may also play an important role in the development of insulin resistance.


After treating bovine aortic endothelial cells with angiotensin II (ATII), we observed the changes in insulin binding capacity and the amounts of insulin receptor (IR) on the cell membranes and in the cytosol.


After treatment of 10-7M ATII, insulin binding was decreased progressively, up to 60% at 60 minutes (P<0.05). ATII receptor blocker (eprosartan) dose dependently improved the insulin binding capacity which was reduced by ATII (P<0.05). At 200 µM, eprosartan fully restored insulin binding capacity, althogh it resulted in only a 20% to 30% restoration at the therapeutic concentration. ATII did not affect the total amount of IR, but it did reduce the amount of IR on the plasma membrane and increased that in the cytosol.


ATII decreased the insulin binding capacity of the tested cells. ATII did not affect the total amount of IR but did decrease the amount of IR on the plasma membrane. Our data indicate that ATII decreases insulin binding by translocating IR from the plasma membrane to the cytosol. The binding of insulin to IR is important for insulin-induced vasodilation and transendothelial insulin transport. Therefore, ATII may cause insulin resistance through this endothelium-based mechanism.


Citations to this article as recorded by  
  • Acute, local infusion of angiotensin II impairs microvascular and metabolic insulin sensitivity in skeletal muscle
    Dino Premilovac, Emily Attrill, Stephen Rattigan, Stephen M Richards, Jeonga Kim, Michelle A Keske
    Cardiovascular Research.2019; 115(3): 590.     CrossRef
  • Angiotensin II type 2 receptor inhibits expression and function of insulin receptor in rat renal proximal tubule cells
    Yang Yang, Caiyu Chen, Chunjiang Fu, Zaicheng Xu, Cong Lan, Yongchun Zeng, Zhi Chen, Pedro A. Jose, Ye Zhang, Chunyu Zeng
    Journal of the American Society of Hypertension.2018; 12(2): 135.     CrossRef
  • Endothelial function, its relation to arterial hypertension and the possibility of its modulation
    Vladislav Biel, Jan Novák, Luděk Pluháček, Jiří Špác
    Vnitřní lékařství.2018; 64(7-8): 762.     CrossRef
  • Evidence to Consider Angiotensin II Receptor Blockers for the Treatment of Early Alzheimer’s Disease
    Juan M. Saavedra
    Cellular and Molecular Neurobiology.2016; 36(2): 259.     CrossRef
  • Ameliorative effect of eprosartan on high-fat diet/streptozotocin-induced early diabetic nephropathy in rats
    Mohamed A. Morsy, Gehan H. Heeba, Magda E. Mahmoud
    European Journal of Pharmacology.2015; 750: 90.     CrossRef
  • Metabolic actions of angiotensin II and insulin: A microvascular endothelial balancing act
    Ranganath Muniyappa, Sahzene Yavuz
    Molecular and Cellular Endocrinology.2013; 378(1-2): 59.     CrossRef
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Diabetic Ketoacidosis as an Effect of Sodium-Glucose Cotransporter 2 Inhibitor: Real World Insights
Han-Sang Baek, Chaiho Jeong, Yeoree Yang, Joonyub Lee, Jeongmin Lee, Seung-Hwan Lee, Jae Hyoung Cho, Tae-Seo Sohn, Hyun-Shik Son, Kun-Ho Yoon, Eun Young Lee
Received January 22, 2024  Accepted May 13, 2024  Published online June 10, 2024  
DOI:    [Epub ahead of print]
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  • 37 Download
AbstractAbstract PDFPubReader   ePub   
One of the notable adverse effects of sodium-glucose cotransporter 2 (SGLT2) inhibitor is diabetic ketoacidosis (DKA) often characterized by euglycemia. In this retrospective review of patients with DKA from 2015 to 2023, 21 cases of SGLT2 inhibitorassociated DKA were identified. Twelve (57.1%) exhibited euglycemic DKA (euDKA) while nine (42.9%) had hyperglycemic DKA (hyDKA). More than 90% of these cases were patients with type 2 diabetes mellitus. Despite similar age, sex, body mass index, and diabetes duration, individuals with hyDKA showed poorer glycemic control and lower C-peptide levels compared with euDKA. Renal impairment and acidosis were worse in the hyDKA group, requiring hemodialysis in two patients. Approximately one-half of hyDKA patients had concurrent hyperosmolar hyperglycemic state. Common symptoms included nausea, vomiting, general weakness, and dyspnea. Seizure was the initial manifestation of DKA in two cases. Infection and volume depletion were major contributors, while carbohydrate restriction and inadequate insulin treatment also contributed to SGLT2 inhibitor-associated DKA. Despite their beneficial effects, clinicians should be vigilant for SGLT2 inhibitor risk associated with DKA.

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