Insulin resistance surrogates and left ventricular hypertrophy in normotensive obese children

Abstract

Background: The relationship between different surrogates of insulin resistance and left ventricular geometry in obese children is still unclear. Objective: We sought to explore the relationship between commonly used measures of insulin sensitivity/resistance (homeostatic model assessment index, serum uric acid, and triglycerides to high-density lipoprotein cholesterol ratio) and left ventricular geometry in normotensive obese children. Methods: In this cross-sectional study, 32 normotensive obese children were examined. Transthoracic echocardiography was used to measure left ventricular mass index and relative wall thickness. Homeostasis model assessment index, serum uric acid level, and a ratio of triglycerides to high-density lipoprotein cholesterol were used as markers of the insulin resistance. Simple and partial correlation analyses (to control for the effects of body mass index) were conducted to explore relationship between studied variables and left ventricular mass index or relative wall thickness as outcome variables. Results: We found positive correlations between homeostasis model assessment index and relative wall thickness (r = 0.47, p = 0.03) which remained significant after controlling for the effect of body mass index, z-score (r = 0.48, p = 0.03). The cutoff level of homeostasis model assessment index with the optimum sensitivity (Sn) and specificity (Sp) derived from the receiver operating characteristic (ROC) curves for predicting concentric remodelling was ≥5.51 with Sn = 83.33 and Sp = 68.75. Conclusion: There is a positive relationship between homeostasis model assessment index and relative wall thickness of obese normotensive children which may help to distinguish at risk obese normotensive children for the development of concentric left ventricular remodelling.

Combined superposition effect of hypertension and dyslipidemia on left ventricular hypertrophy

“…At present, abnormal lipid metabolism leading to left ventricular hypertrophy was explained by the accumulation of lipids in or around myocytes. A study on the human heart showed that fat deposition in the left ventricle constituted a direct risk of myocardial hypertrophy 34 ; abnormal lipid metabolism can be manifested by strong systemic or local inflammation and mitochondrial oxidative stress 35 and/or increased production of reactive oxygen species in NADPH oxidase complex, resulting in oxidative modification of LDL, thereby amplifying the inflammatory potential 36 ; abnormal lipid metabolism was usually accompanied by insulin resistance in the animal model of high‐fat feeding 37 and promoted LVH 38 ; neurohumoral effects 39 included the effects of the sympathetic nervous system, 9 renal angiotensin aldosterone system (RAAS), and other hormones. In addition, other signaling pathways caused by dyslipidemia also played important roles in the development of myocardial hypertrophy.…”

“…AI, atherosclerosis index; CI, confidence interval; HT, hypertension; OR, odds ratio; TC/HDL-C, ratio of total cholesterol to high-density lipoprotein cholesterol. (−) represents no or low percentile or low range; (+) represents yes or high percentile or high range.inflammatory potential36 ; abnormal lipid metabolism was usually accompanied by insulin resistance in the animal model of high-fat feeding37 and promoted LVH38 ; neurohumoral effects 39 included the effects of the sympathetic nervous system,9 renal angiotensin aldosterone system (RAAS), and other hormones. In addition, other signaling pathways caused by dyslipidemia also played important roles in the development of myocardial hypertrophy.…”