Long-term effects intensive medical therapy on the development and progression of subclinical atherosclerosis and the metabolic syndrome in Chinese patients with type 2 diabetes mellitus

Abstract

Background:Few studies have investigated the progression of subclinical atherosclerosis and metabolic syndrome (MetS) in Chinese patients with type 2 diabetes mellitus (T2DM). This study was to compare the long-term effects of intensive medical therapy on the development and progression of subclinical atherosclerosis and MetS in Chinese T2DM patients with that of a conventional treatment regimen.Methods:A total of 316 T2DM patients were randomized to receive conventional pharmacological treatment or intensive medical therapy, consisting of diet and exercise counseling, from 2002 to 2014 at our hospital in Changsha, China. Clinical indicators of subclinical atherosclerosis and MetS were evaluated over the 12-year follow-up period. A χ2 analysis or t tests was used to compare the data between the 2 groups. Risk factors for subclinical atherosclerosis were identified using Cox proportional hazard models.Results:The incidence of subclinical atherosclerosis increased in both groups over time, and did not differ significantly between the 2 groups at the end of the study. However, after 6 years of treatment, the risk of subclinical atherosclerosis was significantly lower in the intensive medical therapy group, based on intima-media thickness (IMT) measurements, compared with that in the conventional treatment (44.2% vs. 69.7%; P < 0.01). Age, creatinine, and IMT of the common iliac artery were significantly associated with subclinical atherosclerosis. Although the indicators of MetS did not differ significantly at the end of study, the success rate for the management of MetS in the intensive medical therapy group was significantly higher than that in the conventional treatment group in 2006, 2008, 2010, and 2012.Conclusions:The incidence of atherosclerosis in the intensive medical therapy group was significantly lower than that in the conventional treatment group from 2006 to 2010 (P < 0.05), and the incidence of MetS in the intensive medical therapy group was significantly higher than that in the conventional treatment group from 2006 to 2012. Kaplan–Meier estimations showed that the risk of subclinical atherosclerosis in the intensive medical therapy group was significantly lower than that in the conventional treatment group (P < 0.001), whereas the risk of MetS was not significantly different between the treatment groups (P > 0.05).

Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters Show Stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It

“…Human gene INS (insulin) contains a known SNP marker (rs5505) of neonatal diabetes mellitus mediated by hyperinsulinemia [15], which in turn is a well-known physiological marker of atherosclerosis [103,104]. Around rs5505, we selected three more unannotated SNPs able to cause the same hyperinsulinemia (e.g., rs1389349459) and thereby atherogenesis (Table 4).…”

Age- and sex-specific profiles of temporal fasting plasma glucose variability in a population undergoing routine health screening

“…Generally, blood sugar levels between 70 mg/dL (3.9 mmol/l) and 100 mg/dL l (5.6 mmol/) are considered normal. It is evident that glucose variability (GV) plays a role in the development of diabetic complications, particularly cardiovascular events [ 4 , 5 ]. FPG variability is an important predictor of mortality, especially in patients with poor glycemic control [ 6 ].…”

The proliferation and migration of atherosclerosis‐related HVSMCs were inhibited by downregulation of lncRNA XIST via regulation of the miR‐761/BMP9 axis

“…VSMCs play a crucial role in the development and progression of AS 24,25 since VSMCs regain their proliferative properties when they are activated by certain pathological conditions, such as a variety of proinflammatory stimuli 26,27 . Several studies have shown that the proliferation and migration of VSMCs are significantly promoted in AS and contribute to AS progression 3,4,28 . Therefore, inhibiting the proliferation and migration of VSMCs might be a potential strategy for curing AS.…”

“…Both vascular endothelial cells and vascular smooth muscle cells (VSMCs) play major roles in the development of AS. Previous studies showed that the proliferation and migration of VSMCs was significantly promoted in AS, which might accelerate pathological processes 3,4 . However, comprehensive molecular investigations have not been fully reported regarding preventing VSMCs from highly proliferating and migrating.…”