Relationship between adipose tissue insulin resistance and subclinical atherosclerosis in patients with newly diagnosed type 2 diabetes mellitus

2019 
Objective To investigate the relationship between adipose tissue insulin resistance and subclinical atherosclerosis in patients with newly diagnosed type 2 diabetes mellitus. Methods The clinical data of 102 patients with newly diagnosed type 2 diabetes mellitus from March 2012 to March 2013 in Beijing Friendship Hospital, Capital Medical University were retrospectively analyzed. According to the carotid artery intima media thickness (cIMT) by ultrasonography, the patients were divided into cIMT thickening group (cIMT ≥ 0.9 mm, 44 cases) and cIMT normal group (cIMT<0.9 mm, 58 cases). The fasting insulin (FINS), free fatty acids (FFA), fasting blood glucose (FBG) and blood lipids were measured, and the adipose tissue insulin resistance index (Adipo-IR) and homeostatic model assessment insulin resistance index (HOMA-IR) were calculated. Results The cIMT of 102 patients with newly diagnosed type 2 diabetic mellitus was (0.85 ± 0.15) mm. The age, triglyceride, FFA, HOMA-IR and Adipo-IR in cIMT thickening group were significantly higher than those in cIMT normal group: (50.82 ± 12.45) years vs. (41.41 ± 10.61) years, (2.43 ± 0.78) mmol/L vs. (2.14 ± 0.70) mmol/L, (0.58 ± 0.09) mmol/L vs. (0.48 ± 0.10) mmol/L, 5.57 ± 2.88 vs. 4.11 ± 1.93 and 8.39 ± 3.72 vs. 5.69 ± 3.05, and there were statistical differences (P<0.01 or <0.05). Logistic regression analysis result showed that cIMT thickening was independently associated with age and Adipo-IR in patients with newly diagnosed type 2 diabetes mellitus (OR= 1.119 and 1.473, P= 0.002 and 0.003, 95% CI 1.041 to 1.201 and 1.144 to 1.895). Conclusions Adipose tissue insulin resistance is an independent risk factor for subclinical atherosclerosis in patients with newly diagnosed type 2 diabetic mellitus. Key words: Diabetes mellitus, type 2; Adipose tissue; Atherosclerosis; Insulin resistance; Retrospective studies
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []