Diabetes & Metabolism Journal

Original Articles

Risk Factors for the Progression of Intima-Media Thickness of Carotid Arteries: A 2-Year Follow-Up Study in Patients with Newly Diagnosed Type 2 Diabetes: Sang Ouk Chin, Jin Kyung Hwang, Sang Youl Rhee, Suk Chon, You-Cheol Hwang, Seungjoon Oh, Kyu Jeung Ahn, Ho Yeon Chung, Jeong-taek Woo, Sung-Woon Kim, Young Seol Kim, Ja-Heon Kang, In-Kyung Jeong; Diabetes Metab J. 2013;37(5):365-374. Published online October 17, 2013; DOI: https://doi.org/10.4093/dmj.2013.37.5.365

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Abstract PDF Supplementary Material PubReader

Background

Intima-media thickness (IMT) of the carotid arteries is known to have a positive correlation with the risk of cardiovascular disease. This study was designed to identify risk factors affecting the progression of carotid IMT in patients with type 2 diabetes mellitus (T2DM).

Methods

Patients with newly diagnosed T2DM with carotid IMT measurements were enrolled, and their clinical data and carotid IMT results at baseline and 2 years later were compared.

Results

Of the 171 patients, 67.2% of males and 50.8% of females had abnormal baseline IMT of the left common carotid artery. At baseline, systolic blood pressure, body mass index and smoking in male participants, and fasting plasma glucose and glycated hemoglobin levels in females were significantly higher in patients with abnormal IMT than in those with normal IMT. Low density lipoprotein cholesterol (LDL-C) levels in males and high density lipoprotein cholesterol (HDL-C) levels in females at the 2-year follow-up were significantly different between the nonprogression and the progression groups. Reduction of the United Kingdom Prospective Diabetes Study (UKPDS) 10-year coronary heart disease (CHD) risk score after 2 years was generally higher in the nonprogression group than the progression group.

Conclusion

LDL-C levels in males and HDL-C levels in females at the 2-year follow-up were significantly different between participants with and without progression of carotid IMT. Furthermore, a reduction in the UKPDS 10-year CHD risk score appeared to delay the advancement of atherosclerosis. Therefore, the importance of establishing the therapeutic goal of lipid profiles should be emphasized to prevent the progression of carotid IMT in newly diagnosed T2DM patients.

Citations

Citations to this article as recorded by

Comparison of the Effectiveness of Low Carbohydrate Versus Low Fat Diets, in Type 2 Diabetes: Systematic Review and Meta-Analysis of Randomized Controlled Trials
Tanefa A. Apekey, Maria J. Maynard, Monia Kittana, Setor K. Kunutsor
Nutrients.2022; 14(20): 4391. CrossRef
Nomogram Based on Risk Factors for Type 2 Diabetes Mellitus Patients with Coronary Heart Disease

Rong Shi, Birong Wu, Zheyun Niu, Hui Sun, Fan Hu
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy.2020; Volume 13: 5025. CrossRef
HMGA1 Mediated High-Glucose-Induced Vascular Smooth Muscle Cell Proliferation in Diabetes Mellitus: Association Between PI3K/Akt Signaling and HMGA1 Expression
Qinghai Zhang, Ling Chen, Zhibo Zhao, Ying Wu, Jing Zhong, Gebo Wen, Renxian Cao, Xuyu Zu, Jianghua Liu
DNA and Cell Biology.2018; 37(4): 389. CrossRef
Relationship between frequency of hypoglycemic episodes and changes in carotid atherosclerosis in insulin-treated patients with type 2 diabetes mellitus
Tomoya Mita, Naoto Katakami, Toshihiko Shiraiwa, Hidenori Yoshii, Nobuichi Kuribayashi, Takeshi Osonoi, Hideaki Kaneto, Keisuke Kosugi, Yutaka Umayahara, Masahiko Gosho, Iichiro Shimomura, Hirotaka Watada
Scientific Reports.2017;[Epub] CrossRef
Impact of carotid atherosclerosis detection on physician and patient behavior in the management of type 2 diabetes mellitus: a prospective, observational, multicenter study
In-Kyung Jeong, Sin-Gon Kim, Dong Hyeok Cho, Chong Hwa Kim, Chul Sik Kim, Won-Young Lee, Kyu-Chang Won, Doo-Man Kim
BMC Cardiovascular Disorders.2016;[Epub] CrossRef
The effect of fibroblast growth factors and advanced glycation end-products on the intima-media complex thickness in patients with coronary heart disease and type 2 diabetes
Ekaterina Vladimirovna Ivannikova, Victor Yurievich Kalashnikov, Olga Mikhailovna Smirnova, Alexander Borisovich Kuznetsov, Сергей Anatolievich Terekhin, Alexander Viktorovich Il'in
Diabetes mellitus.2014; 17(2): 47. CrossRef

Effects of Anti-Vascular Endothelial Growth Factor (VEGF) on Pancreatic Islets in Mouse Model of Type 2 Diabetes Mellitus.: Ji Won Kim, Dong Sik Ham, Heon Seok Park, Yu Bai Ahn, Ki Ho Song, Kun Ho Yoon, Ki Dong Yoo, Myung Jun Kim, In Kyung Jeong, Seung Hyun Ko; Korean Diabetes J. 2009;33(3):185-197. Published online June 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.3.185

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Abstract PDF: BACKGROUND
Vascular endothelial growth factor (VEGF) is associated with the development of diabetic complications. However, it is unknown whether systemic VEGF treatment has any effects on the pancreatic islets in an animal model of type 2 diabetes mellitus. METHODS: Anti-VEGF peptide (synthetic ATWLPPR, VEGF receptor type 2 antagonist) was injected into db/db mice for 12 weeks. We analyzed pancreatic islet morphology and quantified beta-cell mass. Endothelial cell proliferation and the severity of islet fibrosis were also measured. VEGF expression in isolated islets was determined using Western blot analysis. RESULTS: When anti-VEGF was administered, db/db mice exhibited more severe hyperglycemia and associated delayed weight gain than non-treated db/db mice. Pancreas weight and pancreatic beta-cell mass were also significantly decreased in the anti-VEGF-treated group. VEGF and VEGF receptor proteins (types 1 and 2) were expressed in the pancreatic islets, and their expression was significantly increased in the db/db group compared with the db/dm group. However, the elevated VEGF expression was significantly reduced by anti-VEGF treatment compared with the db/db group. The anti-VEGF-treated group had more prominent islet fibrosis and islet destruction than db/db mice. Intra-islet endothelial cell proliferation was also remarkably reduced by the anti-VEGF peptide. CONCLUSION: Inhibition of VEGF action by the VEGF receptor 2 antagonist not only suppressed the proliferation of intra-islet endothelial cells but also accelerated pancreatic islet destruction and aggravated hyperglycemia in a type 2 diabetes mouse model. Therefore, the potential effects of anti-VEGF treatment on pancreatic beta cell damage should be considered.

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