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Yoon Jung Choi  (Choi YJ) 2 Articles
COVID-19
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Does Diabetes Increase the Risk of Contracting COVID-19? A Population-Based Study in Korea
Sung-Youn Chun, Dong Wook Kim, Sang Ah Lee, Su Jung Lee, Jung Hyun Chang, Yoon Jung Choi, Seong Woo Kim, Sun Ok Song
Diabetes Metab J. 2020;44(6):897-907.   Published online December 23, 2020
DOI: https://doi.org/10.4093/dmj.2020.0199
  • 8,755 View
  • 164 Download
  • 11 Web of Science
  • 10 Crossref
AbstractAbstract PDFPubReader   ePub   
Background
This study aimed to determine the infection risk of coronavirus disease 2019 (COVID-19) in patients with diabetes (according to treatment method).
Methods
Claimed subjects to the Korean National Health Insurance claims database diagnosed with COVID-19 were included. Ten thousand sixty-nine patients with COVID-19 between January 28 and April 5, 2020, were included. Stratified random sampling of 1:5 was used to select the control group of COVID-19 patients. In total 50,587 subjects were selected as the control group. After deleting the missing values, 60,656 subjects were included.
Results
Adjusted odds ratio (OR) indicated that diabetic insulin users had a higher risk of COVID-19 than subjects without diabetes (OR, 1.25; 95% confidence interval [CI], 1.03 to 1.53; P=0.0278). In the subgroup analysis, infection risk was higher among diabetes male insulin users (OR, 1.42; 95% CI, 1.07 to 1.89), those between 40 and 59 years (OR, 1.66; 95% CI, 1.13 to 2.44). The infection risk was higher in diabetic insulin users with 2 to 4 years of morbidity (OR, 1.744; 95% CI, 1.003 to 3.044).
Conclusion
Some diabetic patients with certain conditions would be associated with a higher risk of acquiring COVID-19, highlighting their need for special attention. Efforts are warranted to ensure that diabetic patients have minimal exposure to the virus. It is important to establish proactive care and screening tests for diabetic patients suspected with COVID-19 for timely disease diagnosis and management.

Citations

Citations to this article as recorded by  
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    Endocrinology and Metabolism.2024; 39(5): 813.     CrossRef
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    Frontiers in Public Health.2023;[Epub]     CrossRef
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    Evangelia Tzeravini, Eleftherios Stratigakos, Chris Siafarikas, Anastasios Tentolouris, Nikolaos Tentolouris
    Frontiers in Clinical Diabetes and Healthcare.2022;[Epub]     CrossRef
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    Norma Latif Fitriyani, Muhammad Syafrudin, Siti Maghfirotul Ulyah, Ganjar Alfian, Syifa Latif Qolbiyani, Muhammad Anshari
    Mathematics.2022; 10(21): 4027.     CrossRef
  • The World-Wide Adaptations of Diabetic Management in the Face of COVID-19 and Socioeconomic Disparities: A Scoping Review
    Jaafar Abou-Ghaida, Annalia Foster, Sarah Klein, Massah Bassie, Khloe Gu, Chloe Hille, Cody Brown, Michael Daniel, Caitlin Drakeley, Alek Jahnke, Abrar Karim, Omar Altabbakh, Luzan Phillpotts
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    Journal of Diabetes & Metabolic Disorders.2021; 20(2): 1919.     CrossRef
Intracerebroventricular Injection of Metformin Induces Anorexia in Rats
Chang Koo Lee, Yoon Jung Choi, So Young Park, Jong Yeon Kim, Kyu Chang Won, Yong Woon Kim
Diabetes Metab J. 2012;36(4):293-299.   Published online August 20, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.4.293
  • 5,217 View
  • 45 Download
  • 28 Crossref
AbstractAbstract PDFPubReader   
Background

Metformin, an oral biguanide insulin-sensitizing agent, is well known to decrease appetite. Although there is evidence that metformin could affect the brain directly, the exact mechanism is not yet known.

Methods

To evaluate whether metformin induces anorexia via the hypothalamus, various concentrations of metformin were injected into the lateral ventricle of rats through a chronically implanted catheter and food intake was measured for 24 hours. The hypothalamic neuropeptides associated with regulation of food intake were also analyzed following 1 hour of intracerebroventricular (ICV) injections of metformin.

Results

An ICV injection of metformin decreased food intake in a dose-dependent manner in unrestrained conscious rats. Hypothalamic phosphorylated AMP-activated protein kinase (pAMPK) increased by 3 µg with metformin treatment, but there was no further increase in pAMPK with increases in metformin dosage. The hypothalamic phosphorylated signal transducer and activator of transcription 3 (pSTAT3) increased by 3 µg with metformin treatment, but, there was no further increase in pSTAT3 level following increases of metformin dosage. Hypothalamic proopiomelanocortin was elevated with metformin treatment, while neuropeptide Y was not significantly changed.

Conclusion

Our results suggest that metformin induces anorexia via direct action in the hypothalamus and the increase in pSTAT3, at least in part, is involved in the process. However, hypothalamic pAMPK appears not to contribute to metformin-induced appetite reduction in normal rats. Further studies exploring new pathways connecting metformin and feeding regulation are needed.

Citations

Citations to this article as recorded by  
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    European Journal of Pharmacology.2024; 984: 177021.     CrossRef
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    Nutrition and Cancer.2023; 75(3): 1014.     CrossRef
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