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Basic Research
Mitochondrial Stress and Mitokines: Therapeutic Perspectives for the Treatment of Metabolic Diseases
Benyuan Zhang, Joon Young Chang, Min Hee Lee, Sang-Hyeon Ju, Hyon-Seung Yi, Minho Shong
Diabetes Metab J. 2024;48(1):1-18.   Published online January 3, 2024
DOI: https://doi.org/10.4093/dmj.2023.0115
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  • 267 Download
AbstractAbstract PDFPubReader   ePub   
Mitochondrial stress and the dysregulated mitochondrial unfolded protein response (UPRmt) are linked to various diseases, including metabolic disorders, neurodegenerative diseases, and cancer. Mitokines, signaling molecules released by mitochondrial stress response and UPRmt, are crucial mediators of inter-organ communication and influence systemic metabolic and physiological processes. In this review, we provide a comprehensive overview of mitokines, including their regulation by exercise and lifestyle interventions and their implications for various diseases. The endocrine actions of mitokines related to mitochondrial stress and adaptations are highlighted, specifically the broad functions of fibroblast growth factor 21 and growth differentiation factor 15, as well as their specific actions in regulating inter-tissue communication and metabolic homeostasis. Finally, we discuss the potential of physiological and genetic interventions to reduce the hazards associated with dysregulated mitokine signaling and preserve an equilibrium in mitochondrial stress-induced responses. This review provides valuable insights into the mechanisms underlying mitochondrial regulation of health and disease by exploring mitokine interactions and their regulation, which will facilitate the development of targeted therapies and personalized interventions to improve health outcomes and quality of life.
Sulwon Lecture 2019
Pathophysiology
The Role of Growth Differentiation Factor 15 in Energy Metabolism
Joon Young Chang, Hyun Jung Hong, Seul Gi Kang, Jung Tae Kim, Ben Yuan Zhang, Minho Shong
Diabetes Metab J. 2020;44(3):363-371.   Published online June 29, 2020
DOI: https://doi.org/10.4093/dmj.2020.0087
  • 8,339 View
  • 229 Download
  • 15 Web of Science
  • 14 Crossref
AbstractAbstract PDFPubReader   

Growth differentiation factor 15 (GDF15) is receiving great interest beyond its role as an aging and disease-related biomarker. Recent discovery of its receptor, glial cell line-derived neurotrophic factor (GDNF) family receptor α-like (GFRAL), suggests a central role in appetite regulation. However, there is also considerable evidence that GDF15 may have peripheral activity through an as-of-yet undiscovered mode of action. This raises the question as to whether increased GDF15 induction during pathophysiologic conditions also suppresses appetite. The present review will briefly introduce the discovery of GDF15 and describe the different contexts under which GDF15 is induced, focusing on its induction during mitochondrial dysfunction. We will further discuss the metabolic role of GDF15 under various pathophysiological conditions and conclude with possible therapeutic applications.

Citations

Citations to this article as recorded by  
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    Jojo Reyes, Yanlin Zhao, Krushang Pandya, George S. Yap
    Brain, Behavior, and Immunity.2024; 116: 24.     CrossRef
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    Maria-Elizabeth Baeva, Isabelle Tottenham, Marcus Koch, Carlos Camara-Lemarroy
    Journal of Neuroimmunology.2024; 387: 578268.     CrossRef
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    Natalia Kurhaluk
    Biomolecules.2024; 14(3): 260.     CrossRef
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    Songmao Zheng, David Polidori, Yuanping Wang, Brian Geist, Xiefan Lin‐Schmidt, Jennifer L. Furman, Serena Nelson, Andrea R. Nawrocki, Simon A. Hinke
    Clinical and Translational Science.2023; 16(8): 1431.     CrossRef
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    Samuel N. Breit, Rakesh Manandhar, Hong-Ping Zhang, Michelle Lee-Ng, David A. Brown, Vicky Wang-Wei Tsai
    Cell Metabolism.2023; 35(8): 1341.     CrossRef
  • Serum growth differentiation factor-15 (GDF-15) is a biomarker of cardiac manifestations in children with COVID-19
    Sally Raafat Ishak, Mona Mostafa El Ganzoury, Eman Mahmoud Fouda, Maha Ahmad Anwar, Amany Moustafa Kamal, Heba Mostafa Hamza, Nehad Ahmed Bakry
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    Experimental & Molecular Medicine.2022; 54(4): 426.     CrossRef
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    Wan-Hsuan Lu, Kelly Virecoulon Giudici, John E. Morley, Sophie Guyonnet, Angelo Parini, Geetika Aggarwal, Andrew D. Nguyen, Yan Li, Randall J. Bateman, Bruno Vellas, Philipe de Souto Barreto, Bruno Vellas, Sophie Guyonnet, Isabelle Carrié, Lauréane Brigit
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    Ahmad O. Babalghith, Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Michel De Waard, Jean-Marc Sabatier, Hebatallah M. Saad, Gaber El-Saber Batiha
    Diagnostics.2022; 12(9): 2051.     CrossRef
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    Jae Seung Chang, Jun Namkung
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    Melissa Olivar-Villanueva, Mindong Ren, Colin K.L. Phoon
    Mitochondrion.2021; 61: 188.     CrossRef
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    Yanee Choksomngam, Sintip Pattanakuhar, Nipon Chattipakorn, Siriporn C. Chattipakorn
    Obesity Research & Clinical Practice.2021; 15(4): 315.     CrossRef
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    Kornelia Johann, Maximilian Kleinert, Susanne Klaus
    Cells.2021; 10(11): 2990.     CrossRef
Review
Pathophysiology
Regulation of Systemic Glucose Homeostasis by T Helper Type 2 Cytokines
Yea Eun Kang, Hyun Jin Kim, Minho Shong
Diabetes Metab J. 2019;43(5):549-559.   Published online October 24, 2019
DOI: https://doi.org/10.4093/dmj.2019.0157
  • 6,855 View
  • 94 Download
  • 10 Web of Science
  • 10 Crossref
AbstractAbstract PDFPubReader   

Obesity results in an inflammatory microenvironment in adipose tissue, leading to the deterioration of tissue protective mechanisms. Although recent studies suggested the importance of type 2 immunity in an anti-inflammatory microenvironment in adipose tissue, the regulatory effects of T helper 2 (Th2) cytokines on systemic metabolic regulation are not fully understood. Recently, we identified the roles of the Th2 cytokine (interleukin 4 [IL-4] and IL-13)-induced adipokine, growth differentiation factor 15 (GDF15), in adipose tissue in regulating systemic glucose metabolism via signal transducer and activator of transcription 6 (STAT6) activation. Moreover, we showed that mitochondrial oxidative phosphorylation is required to maintain these macrophage-regulating autocrine and paracrine signaling pathways via Th2 cytokine-induced secretion of GDF15. In this review, we discuss how the type 2 immune response and Th2 cytokines regulate metabolism in adipose tissue. Specifically, we review the systemic regulatory roles of Th2 cytokines in metabolic disease and the role of mitochondria in maintenance of type 2 responses in adipose tissue homeostasis.

Citations

Citations to this article as recorded by  
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    Liwen Wang, Jie Hu, Haiyan Zhou
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    Seul-Gi Kang, Seong-Eun Lee, Min-Jeong Choi, Joon-Young Chang, Jung-Tae Kim, Ben-Yuan Zhang, Yea-Eun Kang, Ju-Hee Lee, Hyon-Seung Yi, Minho Shong
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Response
Response: GDF15 Is a Novel Biomarker for Impaired Fasting Glucose (Diabetes Metab J 2014;38:472-9)
Jun Hwa Hong, Bon Jeong Ku, Minho Shong
Diabetes Metab J. 2015;39(1):84-86.   Published online February 16, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.1.84
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  • 27 Download
PDFPubReader   
Original Articles
GDF15 Is a Novel Biomarker for Impaired Fasting Glucose
Jun Hwa Hong, Hyo Kyun Chung, Hye Yoon Park, Kyong-Hye Joung, Ju Hee Lee, Jin Gyu Jung, Koon Soon Kim, Hyun Jin Kim, Bon Jeong Ku, Minho Shong
Diabetes Metab J. 2014;38(6):472-479.   Published online December 15, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.6.472
  • 5,645 View
  • 78 Download
  • 69 Web of Science
  • 64 Crossref
AbstractAbstract PDFPubReader   
Background

Growth differentiation factor-15 (GDF15) is a protein that belongs to the transforming growth factor β superfamily. An elevated serum level of GDF15 was found to be associated with type 2 diabetes mellitus (T2DM). T2DM is an inflammatory disease that progresses from normal glucose tolerance (NGT) to impaired fasting glucose (IFG). Hence, we aimed to validate the relationship between GDF15 and IFG.

Methods

The participants were divided into the following three groups: NGT (n=137), IFG (n=29), and T2DM (n=75). The controls and T2DM outpatients visited the hospital for routine health check-ups. We used fasting blood glucose to detect IFG in nondiabetic patients. We checked the body mass index (BMI), C-reactive protein level, metabolic parameters, and fasting serum GDF15 level.

Results

Age, BMI, triglyceride, insulin, glucose, homeostatic model assessment-insulin resistance (HOMA-IR), and GDF15 levels were elevated in the IFG and T2DM groups compared to the NGT group. In the correlation analysis between metabolic parameters and GDF15, age and HOMA-IR had a significant positive correlation with GDF15 levels. GDF15 significantly discriminated between IFG and NGT, independent of age, BMI, and HOMA-IR. The serum levels of GDF15 were more elevated in men than in women. As a biomarker for IFG based on the receiver operating characteristic curve analysis, the cutoff value of GDF15 was 510 pg/mL in males and 400 pg/mL in females.

Conclusion

GDF15 had a positive correlation with IR independent of age and BMI, and the serum level of GDF15 was increased in the IFG and T2DM groups. GDF15 may be a novel biomarker for detecting IFG in nondiabetic patients.

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    Alexander E. Berezin, Alexander A. Berezin
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    Myung Haeng Hur, Mi-Kyoung Lee, Kayeon Seong, Jun Hwa Hong
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  • Regulation of Systemic Glucose Homeostasis by T Helper Type 2 Cytokines
    Yea Eun Kang, Hyun Jin Kim, Minho Shong
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Bone Mineral Density in Prediabetic Men
Ju Hee Lee, Yun Hyeong Lee, Kyoung Hye Jung, Min Kyeong Kim, Hye Won Jang, Tae Kyun Kim, Hyun Jin Kim, Young Suk Jo, Minho Shong, Tae Yong Lee, Bon Jeong Ku
Korean Diabetes J. 2010;34(5):294-302.   Published online October 31, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.5.294
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AbstractAbstract PDFPubReader   
Background

There are many studies regarding the effects of insulin on bone metabolism and changes in bone mineral density (BMD) in the setting of diabetes. The effect of prediabetes on BMD is not known.

Methods

A total of 802 men participated in the Korea Rural Genomic Cohort Study (in Geumsan County). According to the results of an oral glucose tolerance test, subjects were classified into normal, prediabetic, and diabetic categories. One hundred twenty-four subjects diagnosed with type 2 diabetes were excluded, leaving 678 subjects for the study inclusion. BMD was estimated with a quantitative ultrasonometer.

Results

The average BMD T scores of normal and prediabetic subjects were -1.34 ± 1.42 and -1.33 ± 1.30, respectively; there was no significant difference in the BMD T scores between these groups. The BMD T score was inversely associated with age and positively correlated with body weight, body mass index, total cholesterol, low density lipoprotein cholesterol, and HbA1c. On multiple linear regression analysis, low density lipoprotein cholesterol was the only statistically significant variable for prediabetes (β = 0.007, P = 0.005). On the stepwise regression analysis, age (β = -0.026, P < 0.001), the body mass index (β = 0.079, P < 0.001), and low density lipoprotein cholesterol (β = 0.004, P = 0.016) were significant variables for prediabetes.

Conclusions

There was no significant difference in the BMD T score between the normal and prediabetic subjects. Further studies are needed regarding the association of fracture risk and changes in BMD with the development of overt diabetes.

Citations

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    Korean Diabetes Journal.2010; 34(6): 386.     CrossRef
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    Chul-Hee Kim
    Korean Diabetes Journal.2010; 34(6): 384.     CrossRef

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