Diabetes & Metabolism Journal

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T-Cell Senescence in Human Metabolic Diseases: Ha Thi Nga, Thi Linh Nguyen, Hyon-Seung Yi; Diabetes Metab J. 2024;48(5):864-881. Published online August 28, 2024; DOI: https://doi.org/10.4093/dmj.2024.0140

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Immunosenescence denotes a state of dysregulated immune cell function characterized by a confluence of factors, including arrested cell cycle, telomere shortening, markers of cellular stress, mitochondrial dysfunction, loss of proteostasis, epigenetic reprogramming, and secretion of proinflammatory mediators. This state primarily manifests during the aging process but can also be induced in various pathological conditions, encompassing chronic viral infections, autoimmune diseases, and metabolic disorders. Age-associated immune system alterations extend to innate and adaptive immune cells, with T-cells exhibiting heightened susceptibility to immunosenescence. In particular, senescent T-cells have been identified in the context of metabolic disorders such as obesity, diabetes, and cardiovascular diseases. Recent investigations suggest a direct link between T-cell senescence, inflammation, and insulin resistance. The perturbation of biological homeostasis by senescent T-cells appears intricately linked to the initiation and progression of metabolic diseases, particularly through inflammation-mediated insulin resistance. Consequently, senescent T-cells are emerging as a noteworthy therapeutic target. This review aims to elucidate the intricate relationship between metabolic diseases and T-cell senescence, providing insights into the potential roles of senescent T-cells in the pathogenesis of metabolic disorders. Through a comprehensive examination of current research findings, this review seeks to contribute to a deeper understanding of the complex interplay between immunosenescence and metabolic health.

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Immune cell dysfunction: A critical player in development of diabetes complications
Mohamed J. Saadh, Omer Qutaiba B. Allela, Radhwan Abdul Kareem, Ashishkumar Kyada, H. Malathi, Deepak Nathiya, Deepak Bhanot, Hayder Naji Sameer, Atheer Khdyair Hamad, Zainab H. Athab, Mohaned Adil
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Oxidative stress, senescence and mRNA decay in peripheral blood mononuclear cells of women with gestational diabetes mellitus‐link to increased cardiovascular disease risk
Tove Lekva, Marie Cecilie Paasche Roland, Elisabeth Qvigstad, Yusuf Khan, Kristin Godang, Annika E. Michelsen, Thor Ueland
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Immune-mediated renal injury in diabetic kidney disease: from mechanisms to therapy
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Single-cell sequencing reveals dysregulated cell type perturbations and critical mediator communication remodelling in colorectal cancer
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Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges
Hubert Klepacki, Krystyna Kowalczuk, Natalia Łepkowska, Justyna Magdalena Hermanowicz
Cells.2025; 14(13): 942. CrossRef
Red ginseng extract enhances mitochondrial function and alleviates immunosenescence in T cells
Ho Yeop Lee, Jingwen Tian, Ha Thi Nga, Thi Linh Nguyen, Ji Sun Moon, Hyo Ju Jang, Alfin Mohammad Abdillah, Jieun Lee, Sang Hyeon Ju, Seung Ho Lee, Hun Kun Ko, Minho Shong, Hyon-Seung Yi
Journal of Ginseng Research.2025; 49(5): 564. CrossRef
Immunosenescence and the Geriatric Giants: Molecular Insights into Aging and Healthspan
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Medical Sciences.2025; 13(3): 100. CrossRef
Immunosenescence and Ageing: An Entangled Web of Senescence and Declining Immunity
Afsar U. Ahmed
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Immunosenescence and cancer: molecular hallmarks, tumor microenvironment remodeling, and age-specific immunotherapy challenges
Qianwen Liu, Jingfeng Li, Xiuqiao Sun, Jiayu Lin, Zhengwei Yu, Yue Xiao, Dan Li, Baofa Sun, Haili Bao, Yihao Liu
Journal of Hematology & Oncology.2025;[Epub] CrossRef
Correlation Between the Proportion of Senescence-Associated β-Galactosidase-Stained CD8+ T Cells and Age: A Cross-Sectional Study in Japan
Masaya Tsubokawa, Yoshiki Shimizu, Misato Yazaki, Shieri Shimodan, Masayuki Noguchi, Arisa Yamazaki, Tomomichi Watanabe, Makoto Ocho, Tsuyoshi Sakurada, Yoshie Hirose, Jiro Saito, Yuri Ishii
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From Steatosis to Immunosenescence: The Impact of Metabolic Dysfunction on Immune Aging in HIV and Non-HIV Populations
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Junyan Jin, Qianqian Xu, Xin Zhang, Aiwei Zhu, Wei Xia, Christiane Moog, Alex Siu Wing Chan, Tong Zhang, Bin Su
BMC Medicine.2025;[Epub] CrossRef
“Dissecting the role of T cell exhaustion in cancer progression: a multifaceted approach“
Xinyang Li, Shiwen Song
Frontiers in Immunology.2025;[Epub] CrossRef
The immune health assessment technique of the elderly population and its application and promotion in the prevention and treatment of common aged diseases
Qing Li, Ling-bing Meng
Journal of Aging and Rehabilitation.2024; 1(4): 93. CrossRef

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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Mitochondrial stress and the dysregulated mitochondrial unfolded protein response (UPR^mt) are linked to various diseases, including metabolic disorders, neurodegenerative diseases, and cancer. Mitokines, signaling molecules released by mitochondrial stress response and UPR^mt, 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.

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Original Article

Drug/Regimen
Comparative Efficacy of Rosuvastatin Monotherapy and Rosuvastatin/Ezetimibe Combination Therapy on Insulin Sensitivity and Vascular Inflammatory Response in Patients with Type 2 Diabetes Mellitus: Ji Hye Han, Kyong Hye Joung, Jun Choul Lee, Ok Soon Kim, Sorim Choung, Ji Min Kim, Yea Eun Kang, Hyon-Seung Yi, Ju Hee Lee, Bon Jeong Ku, Hyun Jin Kim; Diabetes Metab J. 2024;48(1):112-121. Published online January 3, 2024; DOI: https://doi.org/10.4093/dmj.2022.0402

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Background
Type 2 diabetes mellitus (T2DM) induces endothelial dysfunction and inflammation, which are the main factors for atherosclerosis and cardiovascular disease. The present study aimed to compare the effects of rosuvastatin monotherapy and rosuvastatin/ezetimibe combination therapy on lipid profile, insulin sensitivity, and vascular inflammatory response in patients with T2DM.
Methods
A total of 101 patients with T2DM and dyslipidemia were randomized to either rosuvastatin monotherapy (5 mg/day, n=47) or rosuvastatin/ezetimibe combination therapy (5 mg/10 mg/day, n=45) and treated for 12 weeks. Serum lipids, glucose, insulin, soluble intercellular adhesion molecule-1 (sICAM-1), and peroxiredoxin 4 (PRDX4) levels were determined before and after 12 weeks of treatment.
Results
The reduction in low density lipoprotein cholesterol (LDL-C) by more than 50% from baseline after treatment was more in the combination therapy group. The serum sICAM-1 levels increased significantly in both groups, but there was no difference between the two groups. The significant changes in homeostasis model assessment of insulin resistance (HOMA-IR) and PRDX4 were confirmed only in the subgroup in which LDL-C was reduced by 50% or more in the combination therapy group. However, after adjusting for diabetes mellitus duration and hypertension, the changes in HOMA-IR and PRDX4 were not significant between the two groups.
Conclusion
Although rosuvastatin/ezetimibe combination therapy had a greater LDL-C reduction effect than rosuvastatin monotherapy, it had no additional effects on insulin sensitivity and vascular inflammatory response. Further studies are needed on the effect of long-term treatment with ezetimibe on insulin sensitivity and vascular inflammatory response.

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Sujung Lee, Dae-Soon Son, Jae-In Kim, Jungmin Lee
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Komal Thapa, Neha Kanojia, Heena Khan, Amarjot Kaur, Thakur Gurjeet Singh
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Combining Ezetimibe and Rosuvastatin: Impacts on Insulin Sensitivity and Vascular Inflammation in Patients with Type 2 Diabetes Mellitus
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Does Rosuvastatin/Ezetimibe Combination Therapy Offer Potential Benefits for Glucose Metabolism beyond Lipid-Lowering Efficacy in T2DM?
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Editorials

Implication of Sex Differences in Visceral Fat for the Assessment of Incidence Risk of Type 2 Diabetes Mellitus: Sang Hyeon Ju, Hyon-Seung Yi; Diabetes Metab J. 2022;46(3):414-416. Published online May 25, 2022; DOI: https://doi.org/10.4093/dmj.2022.0089

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The Role of Carnitine Orotate Complex in Fatty Liver: Hyon-Seung Yi; Diabetes Metab J. 2021;45(6):866-867. Published online November 22, 2021; DOI: https://doi.org/10.4093/dmj.2021.0272

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Structural and systems characterization of phosphorylation on metabolic enzymes identifies sex-specific metabolic reprogramming in obesity
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Original Articles

Others
Serum R-Spondin 1 Is a New Surrogate Marker for Obesity and Insulin Resistance: Yea Eun Kang, Ji Min Kim, Hyon-Seung Yi, Kyong Hye Joung, Ju Hee Lee, Hyun Jin Kim, Bon Jeong Ku; Diabetes Metab J. 2019;43(3):368-376. Published online October 23, 2018; DOI: https://doi.org/10.4093/dmj.2018.0066

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Background

Recent in vivo studies indicated that R-spondin 1 (RSPO1) regulates food intake and increases insulin secretion, but its role in humans remains unknown. This study investigated the association between serum levels of RSPO1 and diverse metabolic parameters in humans.

Methods

The study population consisted of 43 subjects with newly diagnosed diabetes mellitus, and 79 non-diabetic participants. Serum levels of RSPO1 were measured using the enzyme-linked immunosorbent assay. The relationships between circulating RSPO1 and diverse metabolic parameters were analyzed.

Results

Circulating RSPO1 levels increased to a greater extent in the obese group than in the lean group. Moreover, serum levels of RSPO1 were higher in the insulin-resistant group than in the insulin-sensitive group. Serum levels of RSPO1 were significantly correlated with a range of metabolic parameters including body mass index, fasting C-peptide, homeostasis model assessment of insulin resistance index, and lipid profile. Moreover, levels were significantly associated with insulin resistance and obesity in non-diabetic subjects.

Conclusion

This study demonstrated the association between serum levels of RSPO1 and a range of metabolic parameters in humans. Serum levels of RSPO1 are significantly related to obesity and insulin resistance, although the precise mechanisms remain unknown.

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Effect of Atorvastatin on Growth Differentiation Factor-15 in Patients with Type 2 Diabetes Mellitus and Dyslipidemia: Ji Min Kim, Min Kyung Back, Hyon-Seung Yi, Kyong Hye Joung, Hyun Jin Kim, Bon Jeong Ku; Diabetes Metab J. 2016;40(1):70-78. Published online February 19, 2016; DOI: https://doi.org/10.4093/dmj.2016.40.1.70

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Background

Elevated serum levels of growth differentiation factor-15 (GDF-15) are associated with type 2 diabetes. Therefore, the effects of atorvastatin on metabolic parameters and GDF-15 levels in patients with type 2 diabetes and dyslipidemia were evaluated.

Methods

In this prospective randomized trial from February 2013 to March 2014, 50 consecutive type 2 diabetic patients with a low density lipoprotein cholesterol (LDL-C) levels ≥100 mg/dL were enrolled. The patients were divided into two groups based on the amount of atorvastatin prescribed, 10 mg/day (n=23) or 40 mg/day (n=27). The effect of atorvastatin on metabolic parameters, including lipid profiles and GDF-15 levels, at baseline and after 8 weeks of treatment were compared.

Results

The baseline metabolic parameters and GDF-15 levels were not significantly different between the two groups. After 8 weeks of treatment, the total cholesterol (TC) and LDL-C levels were significantly decreased in both groups. The mean changes in TC and LDL-C levels were more significant in the 40 mg atorvastatin group. The GDF-15 level was decreased in the 10 mg atorvastatin group, from 1,460.6±874.8 to 1,451.0±770.8 pg/mL, and was increased in the 40 mg atorvastatin group, from 1,271.6±801.0 to 1,341.4±855.2 pg/mL. However, the change in the GDF-15 level was not statistically significant in the 10 or 40 mg atorvastatin group (P=0.665 and P=0.745, respectively).

Conclusion

The GDF-15 levels were not significantly changed after an 8-week treatment with atorvastatin in type 2 diabetic patients.

Citations

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