Triglyceride/low-density-lipoprotein cholesterol ratio is the most valuable predictor for increased small, dense LDL in type 2 diabetes patients

Abstract

Background Small, dense low-density lipoprotein (sd-LDL) increases in type 2 diabetes patients and causes arteriosclerosis. Non–high-density-lipoprotein cholesterol (non–HDL-C) is thought to be useful for predicting arteriosclerosis and sd-LDL elevation; however, there are no data about whether the triglyceride /low-density-lipoprotein cholesterol (TG/LDL-C) ratio is a valuable predictor for sd-LDL. Methods A total of 110 type 2 diabetes patients with hypertriglyceridemia were analyzed. No patients were treated with fibrates, but 47 patients were treated with statins. LDL-C was measured by the direct method. LDL-migration index (LDL-MI) using electrophoresis (polyacrylamide gel, PAG) was calculated, and a value ≥0.400 was determined to indicate an increase in sd-LDL. Simple regression analyses were carried out between LDL-MI and lipid markers. Receiver operating characteristic curves of lipid markers for predicting high LDL-MI were applied to determine the area under the curve (AUC), sensitivity, specificity, and cut-off point. Results LDL-MI correlated negatively with LDL-C (P = 0.0027) and PAG LDL fraction (P < 0.0001) and correlated positively with TGs, non–HDL-C, TG/LDL-C ratio, TG/HDL-C ratio, and non–HDL-C/HDL-C ratio among all study patients. Similar results were obtained for patients analyzed according to statin treatment. The AUCs (95% confidence interval) were 0.945 (0.884-1.000) for TG/LDL-C ratio and 0.614 (0.463-0.765) for non–HDL-C in patients without statins (P = 0.0002). The AUCs were 0.697 (0.507-0.887) for TG/LDL-C and 0.682 (0.500-0.863) for non–HDL-C in patients treated with statins. The optimal cut-off point for TG/LDL-C ratio for increased LDL-MI was 1.1 (molar ratio) regardless of statin treatment. The sensitivity and specificity of the TG/LDL-C ratio (90.0 and 93.9%, respectively) were higher than those of non–HDL-C (56.7 and 78.8%, respectively) in patients without statins. Conclusions The TG/LDL-C ratio is a reliable surrogate lipid marker of sd-LDL and superior to non–HDL-C in type 2 diabetes patients not treated with statins.

Effect of Peanut Consumption on Cardiovascular Risk Factors: A Randomized Clinical Trial and Meta-Analysis

“…Moreover, a recent systematic review and meta-analysis found an enhancement of HDL-cholesterol in healthy subjects consuming peanut products, particularly high-oleic peanuts, for periods longer than 12 weeks (9). In a parallel study with 118 adults who randomly consumed 56 g of peanuts in different forms, an increase in HDL-cholesterol and a reduction of the triglycerides/HDL-cholesterol ratio (considered a predictive marker for higher small dense (sd)-LDL-cholesterol and an independent predictor of cardiovascular risk) were reported Post-intervention compared to baseline (7,29,30). Notably, the participants with high total cholesterol, mainly those who had a high LDL-cholesterol level, experienced a significantly greater reduction in total cholesterol and LDL-cholesterol than those with normal cholesterol values.…”

Diabetic dyslipidemia impairs coronary collateral formation: An update

“…TyG was significantly associated with poor collateral formation even after adjusting for various confounders ( 16 ). Triglyceride to HDL-C ratio (TG/HDL-C ratio) and atherogenic index of plasma (logarithmic transformation of TG/HDL-C ratio) reflect the comprehensive situation of blood lipids and severity of insulin resistance ( 17 ). An observational study of elderly patients with acute myocardial infarction showed that an elevated TG/HDL ratio was independently associated with poor development of coronary collateral circulation ( 18 ).…”

Correlation between the triglyceride-to-high-density lipoprotein cholesterol ratio and other unconventional lipid parameters with the risk of prediabetes and Type 2 diabetes in patients with coronary heart disease: a RCSCD-TCM study in China

“…The reason may be that excess cholesterol accumulation leads to β-cell dysfunction, thereby impairing glucose tolerance and affecting insulin secretion. In addition, islet cholesterol deposition may lead to increased islet amyloid polypeptide aggregation and increased islet amyloid formation, further deteriorating β-cell function and affecting glucose homeostasis [ 9 – 12 ]. More importantly, they are also considered more predictive of CHD than conventional lipid parameters.…”